Alterations in protein synthesis in primary cultured rat liver parenchymal cells were examined after their exposure to the potent carcinogens, polychlorinated biphenyl (PCB) congeners. Co-planar PCB congeners (3,4,5,3′,4′-PCB and 3,4,5,3′,4′,5′-PCB) (10 nM) induced a protein, the Mr of which was 25,000 (25 k protein) under denaturing conditions. However, non-co-planar PCB congeners and several xenobiotics, which induce microsomal proteins, did not induce the 25 k protein. By using immunoblotting, the 25 k protein was identified as glutathione S-transferase P-form (GST-P, 7-7, EC 2.5.1.18).. ...
TY - CHAP. T1 - Report on liver cell transplantation using human fetal liver cells. AU - Pietrosi, Giada. AU - Chinnici, Cinzia. PY - 2017. Y1 - 2017. N2 - In an era of organ shortage, human fetuses donated after medically indicated abortion could be considered a potential liver donor for hepatic cell isolation. We investigated transplantation of fetal liver cells as a strategy to support liver functionality in end-stage liver disease. Here, we report our protocol of human fetal liver cells (hFLC) isolation in fetuses from 17 to 22 gestational weeks, and our clinical procedure of hFLC transplantation through the splenic artery.. AB - In an era of organ shortage, human fetuses donated after medically indicated abortion could be considered a potential liver donor for hepatic cell isolation. We investigated transplantation of fetal liver cells as a strategy to support liver functionality in end-stage liver disease. Here, we report our protocol of human fetal liver cells (hFLC) isolation in fetuses ...
Rat liver parenchymal cells express Na+-dependent and Na+-independent nucleoside transport activity. The Na+-dependent component shows kinetic properties and substrate specificity similar to those reported for plasma membrane vesicles [Ruiz-Montasell, Casado, Felipe and Pastor-Anglada (1992) J. Membr. Biol. 128, 227-233]. This transport activity shows apparent Km values for uridine in the range 8-13 μM and a Vmax of 246 pmol of uridine per 3 min per 106 cells. Most nucleosides, including the analogue formycin B, cis-inhibit Na+-dependent uridine transport, although thymidine and cytidine are poor inhibitors. Inosine and adenosine inhibit Na+-dependent uridine uptake in a dose-dependent manner, reaching total inhibition. Guanosine also inhibits Na+-dependent uridine uptake, although there is some residual transport activity (35% of the control values) that is resistant to high concentrations of guanosine but may be inhibited by low concentrations of adenosine. The transport activity that is ...
The general perception that catabolism and inflammation are associated with a high synthesis rate of total liver protein and a low albumin synthesis rate has been challenged in recent years by several studies in man, indicating that the synthesis rate of albumin in response to a catabolic insult is increased rather than decreased. Thus changes in liver protein synthesis rates in conjunction with catabolism and acute inflammation in man need to be characterized better. The aim of the present study was to measure protein synthesis rates of total liver protein and albumin during a state of acute inflammation. Patients (n=10) undergoing acute laparoscopic cholecystectomy due to acute cholecystitis were investigated. FSRs (fractional synthesis rates) of total liver protein (liver biopsy specimens) and albumin (plasma samples) were investigated as early as possible during the surgical procedure, using a flooding dose of L-[2H5]phenylalanine. The results were compared with a reference group of patients ...
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Expression of ECM proteins fibulin-1 and -2 in acute and chronic liver disease and in cultured rat liver cells. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Introduction: Liver perfusion has been the standard method to digest and isolate liver cells including liver sinusoidal endothelial cells (LSEC). Poor cannulating skills through portal vein results in a waste of animal resource. Familiarization of both liver perfusion technique and adhering strictly to aseptic technique during cell handling ensure high cell yield, minimum morphology disruption and cell contamination. We aimed to present a method of liver perfusion procedure followed by the isolation of LSEC. Materials and method: The study was conducted with the approval of IACUC committee. Seven Sprague Dawley rats underwent these procedures under anaesthesia. Liver perfusion was done as previously described. Briefly, LSEC were isolated by liberase enzyme perfusion of the liver, isopycnic sedimentation in a two- step Percoll gradient and selective adherence. The purification and cultivation of LSEC was evaluated by light and electron microscopy. Results: Purity and viability of LSEC after ...
A liver sinusoid is a type of sinusoidal blood vessel (with fenestrated, discontinuous endothelium) that serves as a location for mixing of the oxygen-rich blood from the hepatic artery and the nutrient-rich blood from the portal vein. Hepatocytes are separated from the sinusoids by the space of Disse. Kupffer cells are located inside the sinusoids and can take up and destroy foreign material such as bacteria. Hepatic stellate cells are present in the space of Disse and are involved in scar formation in response to liver damage. The sinusoidal endothelial cells are cultured for a variety of research purposes. The utility of these cells are of particular interest. One problem to overcome is the reversing of cellular differentiation that has made these cells highly specialized phenotypically in vitro. Human liver sinusoid A single lobule of the liver of a pig. X 60. SIU SOM Histology GI Sellaro TL, Ravindra AK, Stolz DB, Badylak SF. (September 2007). Maintenance of hepatic sinusoidal endothelial ...
Similar to the well-recognized phenotypical heterogeneity of hepatocytes, in situ sublobular variations have recently been detected in the cell structure, fenestration patterns, filtrating efficiency, surface glycosylation, scavenger function and pathological responses of the sinusoidal lining endothelium. However, unlike other liver cell populations, until now no endothelial cell subpopulations had been isolated or defined with clarity, much less with sublobular/acinar zone-related differential properties. On the basis of our previous studies showing that periportal segments of mouse liver sinusoids express a significantly higher number of wheat germ agglutinin-binding sites than do perivenous ones, we used this differential feature for in vitro labeling of the specific sublobular derivation of isolated sinusoidal lining endothelial cells to correlate their original lobular position with other features determined on flow cytometry, centrifugal elutriation, discontinuous arabinogalactan density ...
TY - JOUR. T1 - SIRT7 controls hepatic lipid metabolism by regulating the ubiquitin-proteasome pathway. AU - Yoshizawa, Tatsuya. AU - Karim, Md Fazlul. AU - Sato, Yoshifumi. AU - Senokuchi, Takafumi. AU - Miyata, Keishi. AU - Fukuda, Takaichi. AU - Go, Chisa. AU - Tasaki, Masayoshi. AU - Uchimura, Kohei. AU - Kadomatsu, Tsuyoshi. AU - Tian, Zhe. AU - Smolka, Christian. AU - Sawa, Tomohiro. AU - Takeya, Motohiro. AU - Tomizawa, Kazuhito. AU - Ando, Yukio. AU - Araki, Eiichi. AU - Akaike, Takaaki. AU - Braun, Thomas. AU - Oike, Yuichi. AU - Bober, Eva. AU - Yamagata, Kazuya. PY - 2014/4/1. Y1 - 2014/4/1. N2 - Sirtuins (SIRT1-7) have attracted considerable attention as regulators of metabolism over the past decade. However, the physiological functions and molecular mechanisms of SIRT7 are poorly understood. Here we demonstrate that Sirt7 knockout mice were resistant to high-fat diet-induced fatty liver, obesity, and glucose intolerance, and that hepatic triglyceride accumulation was also attenuated ...
The marker enzymes, alanine aminotransferase and glutamine synthetase, verified that enriched periportal and perivenous hepatocytes were isolated from different lobular origin within the rat liver. Our finding that alanine aminotransferase activity was higher in periportal hepatocytes (with a ratio of 1.9 for periportal to perivenous activities, Table 1) was in agreement with histochemical evidence on the enzyme in rat liver (Gorgens et al., 1988) and what was observed in other studies (Sillau et al., 1996; Tosh et al., 1996). The dramatic difference in glutamine synthetase activity between the perivenous and periportal regions (Table 1) was also shown by Stoll et al. (1991) and provided evidence on the successful preparation of enriched populations of periportal and perivenous cells. In addition, glutamate uptake, mediated by the sodium-dependent transporter, System G, in the perivenous region (Stoll et al., 1991) as well as the sodium-independent system in both periportal and perivenous ...
In chronic active hepatitis, very strong alpha-SMA staining was detected at the site of piecemeal necrosis and adjacent lobules. A-SMA expression was decreased in some cases after interferon treatment. In cases of transplanted liver biopsies, expression of intralobular alpha-SMA was diffusely increased but showed no correlation with degree of acute rejection. Cirrhotic livers revealed strong alpha-SMA positivity in fibrous septae as well as in the perisinusoidal space of intact hepatocytes at the leading edge of fibrosis. Interlobular bile ducts were concentrically circumscribed by alpha-SMA positive cells in cases of intrahepatic cholelithiasis. In trabecular type hepatocellular carcinomas, most sinusoidal lining cells were positive for alpha-SMA. Most intralobular alpha-SMA positive cells represent, if not all, perisinusoidal cells (PSCs) which are involved in intralobular fibrogenesis in various liver diseases. PMID: 8305144. ...
It is known that obesity and/or physical inactivity greatly increase a persons risk of developing heart disease and other serious health problems. This is partly because diabetes is associated with inflammation, oxidative stress, and insulin resistance. Diabetes is also associated with high levels of triglycerides in the blood and tissues such as the liver (known as fatty liver or steatosis). This elevation of fat in the liver is known to cause liver insulin resistance and impair the function of the liver and this impairment contributes to the development of diabetes.. Studies have shown that both aerobic exercise and weight loss have beneficial results on insulin resistance. However, the cause of this benefit remains unclear. We know that both aerobic exercise and/or weight loss can improve how muscle responds to insulin. However, it is also known that aerobic exercise and/or weight loss lowers liver fat content, thereby making it possible that the livers response to insulin is also improved ...
Preparation of Recombinant Adenoviruses. All first-generation recombinant adenoviruses were constructed according to Becker et al. (18). Generation of Ad-RIP-GFP and the bifunctional recombinant Ad-RIP-GFP-CMV-PDX-1 adenoviruses is described in Supporting Methods, which is published as supporting information on the PNAS web site.. Human Liver Cells. Adult human liver (AHL) tissues were obtained from eight different liver transplantation surgeries from 4- to 10-year-old children and three individuals ,40 years old. Fetal human livers were obtained from four deliberate abortions of 20-22 weeks of gestation. Both adult and fetal liver tissues were used with approval from the Committee on Clinical Investigations (Institutional Review Boards of Sheba Medical Center and Rabin Medical Center).. Cell Harvest and Culture Conditions. Isolation of human liver cells was performed as described (19). Briefly, liver samples were cut into thin slices (1- to 2-mm thickness), and digested by 0.03% collagenase ...
Although flow through portal vein and hepatic artery is readily accessible using Doppler sonography, (22,23) in vivo studies on human hepatic (parenchymal) perfusion are limited due to the often (highly) invasive methodology required. Indirect methods for measuring hepatic blood flow have been used and include the assessment of clearance or dilution of a dye or marker (gas or microspheres), which have a wider range of clinical applicability than the direct methods (38). Moreover, noninvasive measurements of hepatic perfusion using PET with the freely diffusible flow tracer [15O]H2O have been shown to provide reliable estimates of hepatic blood flow, when taking into account the dual input from hepatic artery and vena porta (27,28). In the current study, decreased hepatic parenchymal perfusion was observed in type 2 diabetic patients with increased liver triglyceride content but not in those type 2 diabetic patients with low liver triglyceride content, as compared with control subjects, implying ...
Background: Numerous studies in rats and a few other mammalian species, including man, have shown that the sinusoidal cells constitute an important part of liver function. In the pig, however, which is frequently used in studies on liver transplantation and liver failure models, our knowledge about the function of hepatic sinusoidal cells is scarce. We have explored the scavenger function of pig liver sinusoidal endothelial cells (LSEC), a cell type that in other mammals performs vital elimination of an array of waste macromolecules from the circulation. Results: 125I-macromolecules known to be cleared in the rat via the scavenger and mannose receptors were rapidly removed from the pig circulation, 50% of the injected dose being removed within the first 2-5 min following injection. Fluorescently labeled microbeads (2 μm in diameter) used to probe phagocytosis accumulated in Kupffer cells only, whereas fluorescently labeled soluble macromolecular ligands for the mannose and scavenger receptors ...
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The global human liver models market size is expected to reach USD 5.5 Billion in 2028 and register a CAGR of 13.9% over the forecast period, according to the latest report by Reports and Data. Some key factors such as rising incidence of liver infections, cancer, and increasing research on these liver diseases are driving global market revenue growth. The liver is an essential organ in the human system that performs various functions such as production of bile for digestion, glucose synthesis, detoxification, and production of various proteins. Moreover, it has capability of regenerating the damaged liver tissue. This ability of liver tissues to regenerate has encouraged researchers to develop liver models to help them explore molecular and cellular connectivity of the liver. Liver models, also called organoids, are obtained from single fetal liver progenitor cells to generate a specific environment to mimic liver functioning. Growing focus on developing and introducing alternatives to animal ...
Abstract: The study of the dynamics of adaptation to the rations containing casein and wheat protein showed some accumulation of hepatic protein on days 4-9. Evaluation of 14C-Leucine and protein turnover from the kinetics of precursor elimination from the pool and that of incorporation into proteins, demonstrated that there were no significant differences in the rate of endogenous protein synthesis, and the higher protein levels are associated with the lower secretion of these export proteins from the liver. In another experiment after adaptation to the casein feed, the animals were fed a wheat protein-containing feed, there were no changes in protein levels, yet the rate of total liver protein turnover was significantly increased on day 5, as shown by massive label estimation and calculation using the modified equation. Adaptation to new rations is accompanied by the initial accumulation of protein in the liver tissue and the subsequent adaptation to proteins of low biological value may be ...
The critical role of the liver in the resolution of systemic bacterial infections is well documented. In the case of Listeria monocytogenes, approximately 60% of bacteria inoculated i.v. into mice are recovered in the liver at 10 min after infection. Here we report that the Listeria recovered at 10 min were distributed equally among the hepatocyte and nonparenchymal liver cell populations. The majority (,/= 75%) of these organisms were bound extracellularly as judged by their sensitivity to gentamicin. In contrast, ,/= 93% of Listeria recovered in the liver at 6 h were located within hepatocytes. The listerial burden of the liver decreased 0.5 to 1.0 log, between 10 min and 6 h after infection. This decrease correlated with a sevenfold increase in the percentage of neutrophils that constituted the nonparenchymal cell population. Mice rendered neutrophil deficient by pretreatment with anti-granulocyte (RB6-8C5) mAb exhibited a significant increase (,300%) rather than a decrease in liver Listeria ...
Hepatitis C virus (HCV) is the leading cause of liver disease. HCV productively infects hepatocytes to impart liver inflammation and progressive tissue damage leading to fibrosis and cirrhosis. These processes underlie liver dysfunction and are thought to drive the onset of liver cancer. However, the molecular mechanism(s) by which HCV confers hepatic inflammation are not defined. Now, there is growing evidence that liver sinusoidal endothelial cells (LSEC) and Kupffer cells (KC), may play key roles in regulating immune responses and facilitating tolerance induction. These cells are playing a pivotal role in blood-borne virus clearance (>90%), leaving only a small fraction of infectious virus that escapes clearance in a manner peculiar to each individual pathogen. The biology of HCV, specifically regarding non-parenchymal liver cells, has been largely neglected. LSEC account for the 20% and KC for 15% of the hepatic cells, and are a unique organ-resident cell population with diverse functions, ...
Hepatitis C virus (HCV) is the leading cause of liver disease. HCV productively infects hepatocytes to impart liver inflammation and progressive tissue damage leading to fibrosis and cirrhosis. These processes underlie liver dysfunction and are thought to drive the onset of liver cancer. However, the molecular mechanism(s) by which HCV confers hepatic inflammation are not defined. Now, there is growing evidence that liver sinusoidal endothelial cells (LSEC) and Kupffer cells (KC), may play key roles in regulating immune responses and facilitating tolerance induction. These cells are playing a pivotal role in blood-borne virus clearance (>90%), leaving only a small fraction of infectious virus that escapes clearance in a manner peculiar to each individual pathogen. The biology of HCV, specifically regarding non-parenchymal liver cells, has been largely neglected. LSEC account for the 20% and KC for 15% of the hepatic cells, and are a unique organ-resident cell population with diverse functions, ...
There is great interest in the biology of liver progenitor cells (LPCs) because of their stem cell-like ability to regenerate the liver when the hepatocyte pool is exhausted. Barely detectable in healthy tissue, they emerge upon chronic insult in periportal regions, proliferate and migrate to injury sites in the parenchyma and eventually differentiate into hepatocytes and cholangiocytes to restore liver mass, morphology and function. The increasing worldwide shortage of livers for orthotopic transplantation means LPCs have assumed more prominence as candidates for cell therapy as an alternative therapeutic approach for the treatment of various liver diseases. However, an LPC response is usually seen in pre-cancerous liver pathologies and their high proliferation potential makes them possible transformation targets; associations that overshadow their restorative capability. This mandates that we continue to investigate the factors that govern their activation, proliferation and especially their ...
Custom 3D InSight™ Animal Liver Microtissues are available only on request for research partners, who perform translational toxicology studies on a regular basis. We offer fully tested and highly standardized monkey, dog, and rat liver toxicology models produced using species-specific primary hepatocytes and non-parenchymal liver cells. Ideal for studying species-specific effects of liver function and toxicity these custom animal liver toxicology models can be delivered assay-ready to your lab, or used in tailored in vitro toxicology services.. ...
Hepatic histology and expressions of VLDL, L-FABP and FATP4 in liver tissues.(A) Representative images (200×magnification, haematoxylin and eosin stain) of hep
The exposure of Nigerians to House Hold Kerosene (HHK) is on the increase following carelessness from handling the product and proliferation of sales outlet. Against this backdrop, hepatotoxicity of HHK on liver enzyme markers and its effect on hematological and oxidative stress parameters on wistar albino rats were investigated. Preliminary toxicity study to determine the volume of HHK that could cause toxicity was carried out using 30 healthy albino rats. Another set of 20 albino rats were grouped into two groups and used for the biochemical analysis: Group I animals were the control group and Group II animals were administered with 1ml/kg body weight of HHK. The results of this study shows that HGB, RBC and HCT values were significantly reduced (P,0.05) in the group administered with kerosene compared to the healthy group. WBC, lymphocyte# count, MCV and MCH values were significantly increased (P,0.05) in the treated group compared to the control group. All the liver enzyme markers: AST, ALT, ...
During the last few years, considerable progress has been made in the dissection of cellular and molecular mechanisms of hepatic fibrogenesis. The disease, initiated by hepatocellular damage and perpe
High-fat diets are known to negatively impact liver health and metabolism, but the mechanisms behind it are unclear. A new study takes an in-depth look.
The mechanisms controlling mammalian organ size have long been a source of fascination for biologists. These controls are needed to both ensure the integrity of the body plan and to restrict inappropriate proliferation that could lead to cancer. Regulation of liver size is of particular interest inasmuch as this organ maintains the capacity for regeneration throughout life, and is able to regain precisely its original mass after partial surgical resection. Recent studies using genetically engineered mouse strains have shed new light on this problem; the Hippo signalling pathway, first elucidated as a regulator of organ size in \(Drosophila\), has been identified as dominant determinant of liver growth. Defects in this pathway in mouse liver lead to sustained liver overgrowth and the eventual development of both major types of liver cancer, hepatocellular carcinoma and cholangiocarcinoma. In this review, we discuss the role of Hippo signalling in liver biology and the contribution of this pathway ...
The liver plays a major role for the metabolism, but it is also of general importance for the immune system, e.g. for the deletion of activated T cells or the induction of peripheral tolerance. Under physiological conditions T cells and other leukocytes can be found in the liver, in the sinusoids as well as in the parenchyma. This hepatic accumulation of T cells might be due to immunosurveillance, but it would also be a prerequisite for modulation of T cells by hepatic cells. The present study investigated two different aspects of the interaction of liver sinusoidal endothelial cells (LSEC), the barrier between the sinusoidal lumen and the hepatic parenchyma, and CD4+ T cells. In the first part of the study it could be demonstrated that LSEC support the spontaneous transmigration of CD4+ T cells as well as their chemotaxis to CXCL12 and CXCL9 more efficiently than other endothelial cells. Whereas a direct endothelial activation by chemokines could be excluded the efficient chemokine presentation ...
Cause of NAFLD: physical inactivity: while exercise predominantly enhances muscle insulin sensitivity, studies suggest exercise may decrease liver fat.
TY - JOUR. T1 - Expression and regulation of leukotriene-synthesis enzymes in rat liver cells. AU - Shimada, Kazuo. AU - Navarro, Javier. AU - Goeger, Douglas E.. AU - Mustafa, Shamimunisa B.. AU - Weigel, Paul H.. AU - Weinman, Steven A.. PY - 1998. Y1 - 1998. N2 - The liver plays a major role in metabolism and elimination of leukotrienes (LT). It produces cysteinyl leukotrienes (cLT), and cLT have been implicated in hepatocellular toxicity in several models of lipopolysaccharide (LPS)associated liver injury. However, the liver cell types responsible for cLT production are poorly defined, and the expression of the LT-synthesis enzymes, 5-lipoxygenase (5-LO) and LTC4 synthase (LTC4- S), in liver cells has never been demonstrated. The aim of the present study was to examine the ability of rat liver cells to produce cLT by determining whether hepatocytes, Kupffer cells, and sinusoidal endothelial cells express mRNA and enzyme activities of the LT-synthesis enzymes and whether expression is altered ...
A volume in the popular Pattern Recognition Series, Practical Hepatic Pathology: A Diagnostic Approach features completely updated and reorganized content, resulting in a truly practical guide to understanding liver pathology. Dr. Romil Saxena presents interpretation of liver biopsies according to a pattern-based approach that begins with recognition of the predominant histological pattern of injury, followed by identification of secondary features and appropriate work-up that lead you away from pitfalls to the best diagnosis.. ...
The authors concluded that PFOA modulates at least the PPARα, PPARγ and constitutive androstane receptor (CAR) pathways in liver of hPPARα mice, as well as multiple genes involved in cholesterol metabolism and homeostasis. PPARγ is another member of the PPAR subfamily of nuclear receptors and CAR is a transcriptional regulator of certain metabolic functions. They also found that not all effects were PPARα-dependent and that the hepatic response to PFOA exposure is sexually dimorphic.. Essential New Information. The research provides essential new information to understand the mechanism(s) by which PFAS can affect the amount of lipids in blood. The crucial role of hPPARα in basal cholesterol homeostasis, as well as fatty acid homeostasis, and known species differences in ligand binding gene components support the BU researchers conclusion that this model is an important new tool in exploring multiple, interacting mechanisms of PFOA action on cholesterol homeostasis.. Additionally, a ...
Guildford, UK, 30 November 2006: ReNeuron Group plc (LSE: RENE.L) and CellSeed Inc., a privately owned tissue engineering company based in Tokyo, Japan, today announce the signing of a collaboration agreement to develop novel, patented liver cell culture systems for drug safety screening in the pharmaceutical industry. The development work, to be conducted in CellSeeds laboratories in Tokyo, will establish protocols for efficiently developing ReNeurons patented ReNcellTM HEP hepatocyte cell lines in combination with CellSeeds UpCell and HydroCell temperature-sensitive polymer products for 3-dimensional functional liver tissue. 3-D liver culture systems represent the most effective way to assay for human liver toxicity of new drugs. The collaboration will enable the joint development of new, high-value, human cell-based drug discovery products for use in the pharmaceutical industry. If the collaboration is successful, these products are expected to be launched in 2007. ReNeurons ReNcellTM HEP ...
View Stock Photo of Human Liver Tissue Showing Origins Of The Bile Duct Lm X95. Find premium, high-resolution photos at Getty Images.
IL-10 ameliorates hepatic pathology during PyL and PyNL infection.Liver pathology was examined (A) in WT and IL-10−/− mice that were either uninfected or ha
The mechanisms that regulate vascular resistance in the liver are an area of active investigation. Previously, we have shown that nitric oxide (NO) modulates hepatic vascular tone in the normal rat liver. In this study, the production of NO is examined in further detail by isolating sinusoidal endot …
TY - JOUR. T1 - Sirt1. T2 - A metabolic master switch that modulates lifespan. AU - Leibiger, Ingo B.. AU - Berggren, Per Olof. PY - 2006/1. Y1 - 2006/1. N2 - Sirt1, an enzyme that removes acetyl groups from specific nuclear proteins, has been linked to the regulation of aging. It is now clear that Sirt1 also controls hepatic glucose metabolism by serving as a sensor of the metabolic status in hepatocytes.. AB - Sirt1, an enzyme that removes acetyl groups from specific nuclear proteins, has been linked to the regulation of aging. It is now clear that Sirt1 also controls hepatic glucose metabolism by serving as a sensor of the metabolic status in hepatocytes.. UR - http://www.scopus.com/inward/record.url?scp=30044440497&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=30044440497&partnerID=8YFLogxK. U2 - 10.1038/nm0106-34. DO - 10.1038/nm0106-34. M3 - Short survey. C2 - 16397557. AN - SCOPUS:30044440497. VL - 12. SP - 34. EP - 36. JO - Nature Medicine. JF - Nature ...
The ability to incorporate three-dimensional (3D) hepatocyte-laden hydrogel constructs using layered fabrication approaches into devices that can be perfused with drugs enables the creation of dynamic microorgan devices (DMDs) that offer an optimal analog of the in vivo liver metabolism scenario. The dynamic nature of such in vitro metabolism models demands reliable numerical tools to determine the optimum process, material, and geometric parameters for the most effective metabolic conversion of the perfused drug into the liver microenvironment. However, there is a current lack of literature that integrates computational approaches to guide the optimum design of such devices. The groundwork of the present numerical study has been laid by our previous study [1], where the authors modeled in 2D an in vitro DMD of arbitrary dimensions and identified the modeling challenges towards meaningful results. These constructs are hosted in the chamber of the microfluidic device serving as walls of the ...
The majority of cells in the liver are hepatocytes, which constitute two-thirds of the mass of the liver. The remaining cell types are Kupffer cells (members of the reticuloendothelial system), stellate (Ito or fat-storing) cells, endothelial cells and blood vessels, bile ductular cells, and supporting structures. Viewed by light microscopy, the liver appears to be organized in lobules, with portal areas at the periphery and central veins in the center of each lobule. However, from a functional point of view, the liver is organized into acini, with both hepatic arterial and portal venous blood entering the acinus from the portal areas (zone 1) and then flowing through the sinusoids to the terminal hepatic veins (zone 3); the intervening hepatocytes constituting zone 2. The advantage of viewing the acinus as the physiologic unit of the liver is that it helps to explain the morphologic patterns and zonality of many vascular and biliary diseases not explained by the lobular arrangement. ...
The major findings described here establish that GATA4 is the molecular master regulator that orchestrates specification of discontinuous sinusoidal endothelium during liver development. This GATA4-dependent transcriptional program determines the functional competence of the hepatic sinusoidal endothelium. As suggested by the fact that the gene expression signatures of fetal LSECs and ectopically GATA4-expressing cultured continuous ECs only partially overlap, organ-specific vascular functions differ in a context-dependent manner: (a) liver endothelial-associated angiokines such as WNT2, HGF, RSPO3, ANG2, and BMP2 do not seem to play a major role in liver development, while they do in establishing metabolic zonation in adult liver (18, 19) or in regulating adult liver regeneration (10, 11); (b) GATA4-expressing LSECs are permissive for transmigration of HSCs during early fetal development, while they become non-permissive during later fetal development despite continued expression of ...
Liver sinusoidal endothelial cells (LSECs) are very thin cells that line the liver sinusoids and separate blood from the hepatocytes. The blood flow through the sinusoid is slow giving LSECs a perfect condition to eliminate macromolecules from the blood. Representing one of the most actively endocytosing cell types in the body the LSEC is regarded as a professional pinocyte and very efficiently eliminates soluble macromolecules and small particles (colloids) from the blood circulation. In fact, the most important site of elimination of nearly all tested soluble waste macromolecules and nanoparticles injected into animals are the LSECs. The LSECs make up only 3,3 % of the total liver volume, but 21 % of the total number of liver cells. ...
The discovery by researchers in Hopkins Institute of Basic Biomedical Sciences and McKusick-Nathans Institute for Genetic Medicine reveals that a protein called GCN5 is critical for controlling a domino-like cascade of molecular events that lead to the release of sugar from liver cells into the bloodstream. Understanding the role of GCN5 in maintaining blood sugar levels is leading to a clearer picture of how the body uses sugar and other nutrients to make, store and spend energy ...
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In this study we focused on the hepatic αβ T cells found in perfused donor organs. The hepatic αβ-TCRpos population contains more than twice as many CD8pos cells and 4 times as many double-negative cells as the corresponding population in matched peripheral blood. As evidenced by the absence of CD45RO (26), almost half of the peripheral blood and one-third of hepatic αβ T cells have a naive-like phenotype. The majority of αβposCD45ROneg cells in the periphery coexpress CD4, whereas ,5% of αβposCD45ROneg hepatic cells coexpress CD4. This suggests that naive CD4 expressing αβ T cells are rare in the liver and abundant in the periphery. In contrast, CD8 coexpressing αβposCD45ROneg cells are more abundant in the liver than in matched blood. This suggests that the normal liver may contain a significant population of naive αβposCD8pos cells.. However, although CD45RO defines a memory population, up to 20% of CD8posCD45ROneg T cells in the periphery represent a recently activated ...
The liver is one of the bodys most important organs which is why you need to eat the best foods for a healthy liver. Your liver helps in flushing out toxins and assisting in digestion but more importantly, the liver is the main part of our body where ingredients are metabolized or processed. Medicines and all harmful substances are metabolized in the liver. Continuous pressure on the liver can lead to number of liver related disease such as fatty liver, jaundice, hepatitis and even liver cirrhosis or liver failure.. Lipoproteins are synthesized in the liver which also converts excess carbohydrates and proteins into fatty acids and triglycerides. These are again stored in adipose tissue. This is also why you need to decrease unhealthy fatty acids in your body by avoiding foods bad for your liver. The liver also synthesizes cholesterol and phospholipids. The key to maintain a healthy liver is diet and eating the right foods for a healthy liver. Here are the 8 best foods for a healthy ...
Background/Aims Certain liver diseases have been associated with depletion of glutathione (GSH) the major antioxidant in liver. and attenuated mitochondrial damage accompanied with diminished hepatic steatosis; however abnormal liver biochemical tests hepatocytes death and hepatic oxidative stress persisted in the rescued mice. At age 50 days the liver from rescued mice started to display characteristics of fibrosis and at age 120 days macronodular cirrhosis was observed. Immunohistostaining for liver-specific markers and the expression profile of hepatic cytokines indicated that the repopulation of hepatocytes in the cirrhotic nodules involves the expansion of oval cells. Conclusions Replenishment of mitochondrial GSH and restoration of mitochondrial function by NAC prevent mortality caused by loss of hepatocyte GSH synthesis allowing the progression of steatosis to a chronic stage. Thus with NAC supplementation mice provide a model for the development of liver fibrosis and cirrhosis. ...
TY - JOUR. T1 - Hepatic protein synthesis rate of liver specimens as a predictor of viability in rat cold ischemia liver transplantation model. AU - Matsui, Yoshifumi. AU - Asano, Takehide. AU - Nakagohri, Toshio. AU - Yokoro, Yoshiharu. AU - Kainuma, Osamu. AU - Kenmochi, Takashi. AU - Isono, Kaich. PY - 1997/11. Y1 - 1997/11. N2 - Background/Aims: We have previously reported that the hepatic protein synthesis rate, calculated as the uptake rate of L-[4.5 3H] leucine by the fraction during a 10-min incubation of a 16-G needle biopsy specimen of liver tissue, represents a high level of liver function and is therefore useful for evaluating liver function. We investigated the hepatic protein synthesis rate level in a pretransplant liver to learn if it might predict the outcome in a rat orthotopic liver transplantation model. Methods: Grafts were stored, liver specimens were obtained using a 21-G Chiba type II skinny needle, and the hepatic protein synthesis rate was calculated. Subsequently, liver ...
We examined whether superoxide is a factor responsible for paraquat-induced liver injury in terms of superoxide dismutase using cultured rat liver slices exposed to various concentrations of paraquat. The degree of liver injury was assessed by measurement of percentage of lactate dehydrogenase leakage into the medium and lipid hydroperoxides in the liver slices and by direct histopathological observation. Paraquat produced concentration- and time-related liver injury in the cultured rat liver slices. Notably, after exposure to 5 mmol/L paraquat, a significant increase of the percentage of lactate dehydrogenase leakage occurred from 4 hr (p , 0.05 vs. control group), and this gradually increased up to 8 hr (p , 0.01 and p , 0.001 vs. control group at 6 and 8 hr, respectively). Changes in lipid hydroperoxides in the liver slices were similar to those in percentage of lactate dehydrogenase leakage (p , 0.05 and p , 0.01 vs. control group at 6 and 8 hr, respectively). Liver injury was located around ...
TY - JOUR. T1 - The repopulation potential of fetal liver hematopoietic stem cells in mice exceeds that of their adult bone marrow counterparts. AU - Rebel, Vivienne I.. AU - Miller, Cindy L.. AU - Eaves, Connie J.. AU - Lansdorp, Peter M.. PY - 1996/4/15. Y1 - 1996/4/15. N2 - Varying, limiting numbers of unseparated or purified cells (Ly-5.1), either from 14.5-day-old fetal liver (FL) or from adult bone marrow (BM) were coinjected with 105 unseparated BM cells (Ly-5.2) into lethally irradiated adult C57B1/6 recipients (Ly-5.2). The kinetics of donor cell repopulation of the lymphoid and myeloid compartments by Ly-5.1+ donor hematopoietic stem cells (ie, competitive repopulation units [CRU]) were monitored at various time points after the transplantation by Ly-5 analysis of the peripheral white blood cells (WBC). Recipients that had received on average less than 2 adult BM or FL CRU did not show a significant difference in the level of donor-reconstitution when analyzed 4 weeks after the ...
TY - JOUR. T1 - Nonalcoholic fatty liver disease. T2 - Diagnosis and management. AU - Wilkins, Thad. AU - Tadkod, Altaf. AU - Hepburn, Iryna. AU - Schade, Robert R.. PY - 2013/7/1. Y1 - 2013/7/1. N2 - Nonalcoholic fatty liver disease is characterized by excessive fat accumulation in the liver (hepatic steatosis). Nonalcoholic steatohepatitis is characterized by steatosis, liver cell injury, and inflammation. The mechanism of nonalcoholic fatty liver disease is unknown but involves the development of insulin resistance, steatosis, inflammatory cytokines, and oxidative stress. Nonalcoholic fatty liver disease is associated with physical inactivity, obesity, and metabolic syndrome. Screening is not recommended in the general population. The diagnosis is usually made after an incidental discovery of unexplained elevation of liver enzyme levels or when steatosis is noted on imaging (e.g., ultrasonography). Patients are often asymptomatic and the physical examination is often unremarkable. No single ...
If your recent blood test results showed signs of elevated liver enzymes or if you want to know about high liver levels out of curiosity, you should first learn about the possible causes of high liver levels.
TY - JOUR. T1 - Recent Concepts in Non-alcoholic Fatty Liver Disease. AU - Adams, Leon. AU - Angulo, P.. PY - 2005. Y1 - 2005. N2 - Non-alcoholic fatty liver disease (NAFLD) is present in up to one-third of the general population and in the majority of patients with metabolic risk factors such as obesity and diabetes. Insulin resistance is a key pathogenic factor resulting in hepatic fat accumulation. Recent evidence demonstrates NAFLD in turn exacerbates hepatic insulin resistance and often precedes glucose intolerance. Once hepatic steatosis is established, other factors, including oxidative stress, mitochondrial dysfunction, gut-derived lipopolysaccharide and adipocytokines, may promote hepatocellular damage, inflammation and progressive liver disease. Confirmation of the diagnosis of NAFLD can usually be achieved by imaging studies, however, staging the disease requires a liver biopsy. NAFLD is associated with an increased risk of all-cause death, probably because of complications of insulin ...
Youngs research team demonstrated that UPR activation in the brain, specifically in the forebrain, is causally linked to non-alcoholic fatty liver disease. Also known as hepatic steatosis, the research shows that brain ER stress can cause the disease independent of changes in body weight, food intake, and other factors.. Non-alcoholic fatty liver disease impairs normal liver function and is linked to other diseases such as diabetes and cardiovascular disease. The next step is to determine how and why ER stress occurs in the brain and how it causes fat build up in the liver.. Further research may give us another possible avenue for targeting fatty liver disease, said Young. The field has been focused on how we can improve the liver, for example, by developing drugs that target the liver. Our research suggests that we may also need to think about targeting the brain to treat non-alcoholic fatty liver disease.. ###. The study, Obesity-induced Hepatic Steatosis is Mediated by Endoplasmic ...
Non-alcoholic fatty liver disease is a condition in which there is excess fat stored in the liver, not because of heavy alcohol use. There are two forms of NAFLD: non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH). People will generally be diagnosed with one form or the other, however, it is possible for someone to be diagnosed with one and then later, the other.. Non-alcoholic fatty liver:. A form of NAFLD in which there is fat stored in the liver, however, there is little or no inflammation. This form of NAFLD typically will not progress to cause liver damage or complications, though enlargement of the liver can cause pain.. Non-alcoholic steatohepatitis:. A form of NAFLD where in addition to fat stored in the liver, there is also inflammation and liver damage. This inflammation and tissue damage can result in fibrosis or scarring of the liver. NASH may lead to permanent scarring of the liver, known as cirrhosis.. Risk Factors:. ...
Definition of massive hepatic necrosis in the Legal Dictionary - by Free online English dictionary and encyclopedia. What is massive hepatic necrosis? Meaning of massive hepatic necrosis as a legal term. What does massive hepatic necrosis mean in law?
AIM: Non-invasive steatosis-quantifying methods are required for non-alcoholic fatty liver disease (NAFLD) patients in order to monitor disease severity and assess therapeutic efficacy. Controlled attenuation parameter (CAP) evaluated with vibration-controlled transient elastography can predict the presence of steatosis, but its application to absolute hepatic fat quantitation remains unclear. The aim of this study was to examine whether CAP is correlated with real hepatic fat content in NAFLD patients. METHODS: Eighty-two NAFLD patients who had undergone percutaneous liver biopsy were enrolled. CAP was measured using FibroScan(R) just before liver biopsy. The percentage of fat droplet area to hepatocyte area in biopsied specimen was determined morphometrically using computerized optical image analyzing system. The correlation between CAP and liver histology was examined. RESULTS: CAP showed an excellent correlation with actual liver fat percentage in the NAFLD patients with body mass index ...
TY - JOUR. T1 - Updated thresholds for serum alanine aminotransferase level in a large-scale population study composed of 34 346 subjects. AU - Wu, W. C.. AU - Wu, C. Y.. AU - Wang, Y. J.. AU - Hung, H. H.. AU - Yang, H. I.. AU - Kao, W. Y.. AU - Su, C. W.. AU - Wu, J. C.. AU - Chan, W. L.. AU - Lin, H. C.. AU - Lee, F. Y.. AU - Lee, S. D.. PY - 2012/9/1. Y1 - 2012/9/1. N2 - Background: The sensitivity of current upper limit of normal (ULN) of serum alanine aminotransferase (ALT) levels for detecting chronic liver disease has been challenged recently. Aim: To identify modulating factors for serum ALT levels and to refine its ULN threshold. Methods: We enrolled 34 346 consecutive subjects who completed the health check-up at Taipei Veterans General Hospital from 2002 to 2009. ULN was set for healthy ALT level to the 95th percentile of the reference healthy population. Results: A group of 21 282 subjects were used as a training set to define an ULN with the highest sensitivity; afterwards, this ...
Non-alcoholic fatty liver disease (NAFLD) incorporates an extensive spectrum of histologic liver abnormalities, varying from simple triglyceride accumulation in hepatocytes non-alcoholic fatty liver (NAFL) to non-alcoholic steatohepatitis (NASH), and it is the most frequent chronic liver disease in the industrialized world. Beyond liver related complications such as cirrhosis and hepatocellular carcinoma, NAFLD is also an emerging risk factor for type 2 diabetes and cardiovascular disease. Currently, lifestyle intervention including strategies to reduce body weight and to increase regular physical activity represents the mainstay of NAFLD management. Total caloric intake plays a very important role in both the development and the treatment of NAFLD; however, apart from the caloric restriction alone, modifying the quality of the diet and modulating either the macro- or micronutrient composition can also markedly affect the clinical evolution of NAFLD, offering a more realistic and feasible treatment
Dichlorodiphenyltrichloroethane (DDT) is a persistent estrogenic organochlorine pesticide that is a rodent hepatic tumor promoter, with inconclusive carcinogenicity in humans. We have previously reported that o, p-DDT elicits primarily PXR/CAR-mediated activity, rather than ER-mediated hepatic responses, and suggested that CAR-mediated effects, as opposed to ER-mediated effects, may be more important in tumor promotion in the rat liver. To further characterize species-specific hepatic responses, gene expression analysis, with complementary histopathology and tissue level analyses were investigated in immature, ovariectomized C57BL/6 mice treated with 300 mg/kg o, p-DDT, and compared to Sprague-Dawley rat data. Rats and mice exhibited negligible histopathology with rapid o, p-DDT metabolism. Gene expression profiles were also similar, exhibiting PXR/CAR regulation with the characteristic induction of Cyp2b10 and Cyp3a11. However, PXR-specific target genes such as Apoa4 or Insig2 exhibited more
Non-alcoholic fatty liver disease (NAFLD) associates with abnormal mitochondrial capacity. While oxidative capacity can be increased in steatosis, hepatic adenosine triphosphate (ATP) descreases in long-standing diabetes. However, longitudinal studies of diabetes-related NAFLD and its relationship to hepatic energy metabolism are lacking.This prospective study comprised volunteers with type 1 (T1DM, n=30) and type 2 (T2DM, n=37) diabetes. At diagnosis and 5 years later, they underwent 1H/31P magnetic resonance spectroscopy for measurements of hepatic lipid (HCL), γATP, inorganic phosphate (Pi) concentrations and imaging for adipose tissue volumes. Insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamps.At diagnosis, T2DM individuals had higher HCL and adipose tissue volumes, but lower whole-body insulin sensitivity than T1DM, despite comparable glycemic control. NAFLD was present in 38% of T2DM and 7% of T1DM. After 5 years, only persons with T2DM had increased their visceral ...
Abstract: A major concern in drug development is the potential for chemical injury to the liver. Drugs account for 1/3~1/2 of acute liver failures, yet underlying toxicity mechanisms are poorly understood. Adverse reactions are often detected too late, as with troglitazone, an antidiabetic drug introduced in 1997 and withdrawn in 2000 after several cases of liver failure. Predictions are more limi... read moreted with multi-drug interactions, common among patients with chronic ailments like diabetes. Here we develop a microfluidic reactor for the culture of HepG2 cells and the establishment of a steady state drug gradient. Traditional in vitro experiments explore the metabolic effects of troglitazone on HepG2 cells and the interactions between rosiglitazone and metformin (common antidiabetic compounds). LC-MS methods are developed for the detection of drugs and key metabolites. This research expands our knowledge drug metabolism in the liver and introduces a physiologically relevant platform for ...
Objective To evaluate the impact of miR-148a on hepatic ischemia/reperfusion (I/R) injury via inhibiting Ca(2+)/calmodulin-dependent protein kinase IIα (CaMKIIα), and analyze the potential mechanism. Methods Liver I/R model was built in mice. Expression of CaMKIIα was detected in the hepatic tissues by Western blotting. The mRNA levels of miR-148a, CaMKIIα, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were analyzed by quantitative real-time PCR (qRT-PCR). HE staining was performed to observe morphological changes of the livers in each group. TUNEL was used to evaluate the degree of hepatocellular apoptosis in each group. Results After hepatic I/R injury, the expression of miR-148a increased, and it was negatively correlated with CaMKIIα. After therapy with exogenous miR-148a mimics, the protein expression of CaMKIIα, the mRNA levels of TNF-α and IL-1β, the degree of inflammatory cell infiltration and liver cell necrosis, and the level of hepatocellular apoptosis were all
Hepatic steatosis is an abnormal lipid accumulation within hepatocytes, generally present in non-alcoholic fatty liver disease (NAFLD) patients, a starting-point pathology currently associated with other clinical manifestations such as metabolic syndrome, non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and eventually hepatocellular carcinoma. Hepatic steatosis in NAFLD may be induced by mechanisms such as insulin resistance, increased fatty acid uptake, a higher de novo lipogenesis from glucose or acetate, lower fatty acids oxidation and a decrease in fatty acid mobilization from liver. Among different therapeutic strategies appropriate for these patients, exercise has shown to be effective in reversing hepatic steatosis. However, the specific mechanisms involved in this response remain unclear. Therefore, the aim of this review is (1) to describe the mechanisms whereby exercise reverts hepatic steatosis, and (2) review the clinical outcomes of different exercise modalities in NAFLD ...
Ischemia/reperfusion injury (IRI) remains a major problem in organ transplantation, which represents the main cause of graft dysfunction posttransplantation. Hepatic IRI is characterized by an excessive inflammatory response within the liver. Mesenchymal stem cells (MSCs) have been shown to be immunomodulatory cells and have the therapeutic action on IRI in several organs. However, the mechanism of regulatory effect of MSCs on IRI remains unclear. In the present study, we examined the impact of MSCs on hepatic inflammatory response such as neutrophil influx and liver damage in a rat model of 70% hepatic IRI. Treatment with MSCs protected rat against hepatic IRI, with significantly decreased serum levels of liver enzymes, attenuated hepatic neutrophil infiltration, reduced expression of apoptosis-associated proteins, and ameliorated liver pathological injury. MSCs also significantly enhanced the intracellular activation of p38 MAPK phosphorylation, which led to decreased expression of CXCR2 on the
Abstract: An Assessment of Serum Metabolites, Liver Enzymes Activities and Relative Organ Characteristics in Rabbits Fed Varying Levels of Chromolaena Odorata
The increasing burden and risk of non-alcoholic fatty liver disease (NAFLD) associated with HIV infection have today been highlighted in two studies presented at The International Liver Congress 2019 in Vienna, Austria. These studies found that, whilst prevalence and mortality rates associated with viral hepatitis in HIV-infected individuals have been declining, rates associated with NAFLD are increasing, leading to a risk of progressive liver disease.
TY - JOUR. T1 - Isolation of CD133+ liver stem cells for clonal expansion. AU - Bart Rountree, C.. AU - Ding, Wei. AU - Dang, Hein. AU - van Kirk, Colleen. AU - Crooks, Gay M.. PY - 2011/10. Y1 - 2011/10. N2 - Liver stem cell, or oval cells, proliferate during chronic liver injury, and are proposed to differentiate into both hepatocytes and cholangiocytes. In addition, liver stem cells are hypothesized to be the precursors for a subset of liver cancer, Hepatocellular carcinoma. One of the primary challenges to stem cell work in any solid organ like the liver is the isolation of a rare population of cells for detailed analysis. For example, the vast majority of cells in the liver are hepatocytes (parenchymal fraction), which are significantly larger than non-parenchymal cells. By enriching the specific cellular compartments of the liver (i.e. parenchymal and non-parenchymal fractions), and selecting for CD45 negative cells, we are able to enrich the starting population of stem cells by over ...
Do you know what non-alcoholic fatty liver disease symptoms look like? Discover 10 common non-alcoholic fatty liver disease symptoms at 10FAQ Health and stay better informed to make healthy living decisions.
1. R. Blomhoff, T. Gjøen, G. Skretting, H.K. Blomhoff, K.R. Norum and T. Berg (1986). Uptake of retinol and retinol binding protein in hepatic parenchymal cells and perisinusoidal stellate cells. In Cells of the hepatic sinusoid (A. Kirn, D.L. Knook and E. Wisse eds.) Pasmans, Netherlands.. 2. Kaare R. Norum, Rune Blomhoff, Michael H. Green, Joanne B. Green, karl-Olof Wathne, Tor Gjøen, Marie Botilsrud and Trond Berg (1986). Metabolism of retinol in the intestine and liver. In Proceedings from 618th Meeting of Biochemical Society Transactions: Biological Roles of Retinol and other Retinoids.. 3. T. Gjøen, R. Seljelid and S.O. Kolset 1989. Binding of metastatic colon carcinoma cells to liver macrophages. In Cells of the hepatic sinusoid Vol 2 (E. Wisse, D.L. Knook and K. Decker eds) The Kupffer cell foundation. Rijswijk, The Netherlands pp245-246.. 4. Gjøen, T., Holtz, E., Strande, P., Klaveness, J., Leander, P. and Berg, A. Particulate biodegradable contrast medium for CT of the liver. 1991. ...
Effects of In Vivo Hepatic Ischemia-Reperfusion Injury on the Hepatobiliary Disposition of Rhodamine 123 and its Metabolites in Isolated Perfused Rat Livers
Hepatic NADPH-cytochrome P450 oxidoreductase null (HRN™) mice exhibit no functional expression of hepatic cytochrome P450 (P450) when compared to wild type (WT) mice, but have normal hepatic and extrahepatic expression of other biotransformation enzymes. We have assessed the utility of HRN™ mice for investigation of the role of metabolic bioactivation in liver toxicity caused by the nonsteroidal anti-inflammatory drug (NSAID) fenclozic acid. In vitro studies revealed significant NADPH-dependent (i.e. P450-mediated) covalent binding of [14C]-fenclozic acid to liver microsomes from WT mice and HRN™ mice, whereas no in vitro covalent binding was observed in the presence of the UDP-glucuronyltransferase cofactor UDPGA. Oral fenclozic acid administration did not alter the liver histopathology or elevate the plasma liver enzyme activities of WT mice, or affect their hepatic miRNA contents. Livers from HRN™ mice exhibited abnormal liver histopathology (enhanced lipid accumulation, bile duct ...
TY - JOUR. T1 - AAV8-mediated Sirt1 gene transfer to the liver prevents high carbohydrate diet-induced nonalcoholic fatty liver disease. AU - Vilà, Laia. AU - Elias, Ivet. AU - Roca, Carles. AU - Ribera, Albert. AU - Ferré, Tura. AU - Casellas, Alba. AU - Lage, Ricardo. AU - Franckhauser, Sylvie. AU - Bosch, Fatima. PY - 2014/1/8. Y1 - 2014/1/8. N2 - © 2014 American Society of Gene & Cell Therapy Nonalcoholic fatty liver disease (NAFLD) is the most common hepatic disease worldwide, and evidence suggests that it promotes insulin resistance and type 2 diabetes. Caloric restriction (CR) is the only available strategy for NAFLD treatment. The protein deacetylase Sirtuin1 (SIRT1), which is activated by CR, increases catabolic metabolism and decreases lipogenesis and inflammation, both involved in the development of NAFLD. Here we show that adeno-associated viral vectors of serotype 8 (AAV8)-mediated liver-specific Sirt1 gene transfer prevents the development of NAFLD induced by a high carbohydrate ...
Synonyms for focal necrosis in Free Thesaurus. Antonyms for focal necrosis. 3 synonyms for necrosis: gangrene, mortification, sphacelus. What are synonyms for focal necrosis?
Bioarray offers an assortment of various human and non-human hepatic derived cells. These include Hepatocytes, Total Liver Cell Population (TLC), Stellates, Progenitors and Intra-hepatic biliary epithelial cells. We offer these as cryopreserved cells for convenience. Cryopreserved cells are suitable for a variety of assays including induction, toxicity, drug metabolism and systems biology. Both adherent and suspension cells are available. Custom configurations are available upon request ...
Replied on 04/19/2011 Liver changes are one of the known side effects of Lysodren (generically known as mitotane). According to the prescriberinformation for Lysodren, liver changes associated with the drug are not usually symptomatic. Usually these changes occur in dogs that have been receiving Lysodren on a long term basis, which implies a course of treatment generally longer than two months. Liver changes can also be seen in dogs that had preexisting liver problems. Even if bloodwork done before the treatment was started showed normal liver enzymes, this is no guarantee that the liver did not have the beginnings of disease. Lysodren is not known to cause liver cancer. The symptom of poor appetite that you mention is also a common side effect of Lysodren therapy, but is usually a separate problem from the liver changes. As Lysodren is intended to kill parts of the adrenal gland in the treatment of Cushings, it will lower the levels of cortisone (a steroid hormone produced by the adrenal ...
Human liver sinusoidal endothelial cell line with tailored liver endothelial cell culture medium. Cryopreserved liver sinusoidal endothelial cells.
BioAssay record AID 1340971 submitted by ChEMBL: Hepatic extraction ratio in mouse liver microsomes at 1 uM in presence of NADPH by LC-MS/MS method.
Preliminary evidence suggests that exenatide (Byetta®) may have several beneficial direct and indirect effects on NAFLD and liver lipid metabolism. Ad hoc analysis of phase III studies has shown that exenatide treatment is associated with improvement and normalization of alanine aminotransferase (ALT), a marker of liver injury, and that this effect is most pronounced in those with the greatest weight loss. In addition, treatment of leptin deficient ob/ob mice with exenatide reduced weight, liver lipid content, serum ALT and liver lipid peroxidation. Additional evidence suggests that the effects of exenatide on the liver are not simply a result of weight loss, but rather due to direct effects on the liver. Hepatocytes express GLP-1 receptors that are responsive to both GLP-1 and exenatide. Furthermore, exenatide treatment of ob/ob mice or isolated hepatocytes reduces mRNA for stearoyl-CoA desaturase-1 (SCD-1) and SREBP-1c, which would be expected to reduce DNL.. Based upon this data, we ...
A growing number of studies reported the connection between the level of serum ferritin (SFL) and non-alcoholic fatty liver disease (NAFLD). However, such connection was still disputable. The aim of our meta-analysis was to estimate SFL between the groups as below: patients with NAFLD against control group; non-alcoholic steatohepatitis (NASH) patients against control group; non-alcoholic fatty liver (NAFL) patients against a control group and NASH patients vs NAFL patients. We screened the studies in PubMed, EMBASE, the Cochrane Database and the Cochrane Central register controlled trials from the beginning to July 10, 2016 to find the studies indicated the connection between SFL and NAFLD (NAFL and/or NASH). Fourteen published studies which evaluate the SFL in NAFLD patients were selected. Higher SFL was noticed in NAFLD patients against control group (standardized mean difference [SMD] 1.01; 95% CI 0.89, 1.13), NASH patients against control group (SMD 1.21; 95% CI 1.00, 1.42), NAFL patients against
Kupffer cells (KC), the resident liver macrophages, constitute the liver sinusoids together with other cells such as sinusoidal endothelial cells, hepatic stellate cells, liver-specific natural killer cells and dendritic cells. KC account for approximately 10-15% of the total liver cell population and represent 80-90% of tissue macrophages in the reticuloendothelial system. KC represent an important component of innate immunity.1 2 One characteristic of innate immunity is the rapid response to potentially dangerous stimuli. This suggests a central role of the liver in systemic and regional immune response, because KC come in contact with all the microbiological debris from the gastrointestinal tract reaching the liver via the portal vein.3. KC express the scavenger receptor CD163; CD163 is involved in the clearance and endocytosis of the haemoglobin-haptoglobin complex.4 Once erythrocytes or the haemoglobin-haptoglobin complex has been taken up by KC, the heme delivered from haemoglobin is ...
A subset of patients with non-alcoholic fatty liver disease develop an inflammatory condition, termed non-alcoholic steatohepatitis (NASH). NASH is characterised by hepatocellular injury, innate immune cell-mediated inflammation and progressive liver fibrosis. The mechanisms whereby hepatic inflammation occurs in NASH remain incompletely understood, but appear to be linked to the proinflammatory microenvironment created by toxic lipid-induced hepatocyte injury, termed lipotoxicity. In this review, we discuss the signalling pathways induced by sublethal hepatocyte lipid overload that contribute to the pathogenesis of NASH. Furthermore, we will review the role of proinflammatory, proangiogenic and profibrotic hepatocyte-derived extracellular vesicles as disease biomarkers and pathogenic mediators during lipotoxicity. We also review the potential therapeutic strategies to block the feed-forward loop between sublethal hepatocyte injury and liver inflammation. ...
TY - JOUR. T1 - Lack of therapeutic improvement of liver fibrosis in rats by dexamethasone in spite of ascites amelioration. AU - Ki, Sung Hwan. AU - Choi, DalWoong. AU - Kim, Choon Won. AU - Kim, Sang Geon. PY - 2005/2/28. Y1 - 2005/2/28. N2 - Pathophysiology of liver fibrosis (LF) includes hepatic parenchymal cell destruction and connective tissue formation. Although dexamethasone has been used in the liver diseases, there is controversy over the beneficial effects of dexamethasone on LF. Previous studies showed that CCAAT/enhancer binding protein-β (C/EBPβ) activation contributes to hepatocyte regeneration and dissolution of fibrosis and that dexamethasone activates C/EBPβ whereas C/EBPβ-mediated gene induction by dexamethasone is antagonized by a corepressor. The present study investigated the possible therapeutic effect of dexamethasone for the treatment of LF in rats. We injected rats with multiple doses of dimethylnitrosamine (DMN) for 4 weeks and then used the LF rats to determine ...
The liver is the main metabolic organ in the body especially in lipometabolism and glycometabolism. Carbohydrates and fats disorders can result in insulin resistance in the liver. Metabolic imbalance can even lead to life-threatening conditions. Therefore, it is essential to maintain the normal metabolic function of the liver. When the liver is in a pathological state, liver metabolism homeostasis is damaged, and metabolic disorders will further aggravate liver disease. Consequently, it is essential to determine the relationship between liver diseases and metabolic disorders. Here we review a lot of evidence that liver diseases are closely related to lipometabolism and glycometabolism. Although the disorder of the liver metabolism is caused by different liver diseases, the break of metabolic balance is determined by changes in the state of the liver. We discuss the relationship between liver disease and metabolic changes, outline the process of how metabolic changes are regulated by liver diseases, and
Non-alcoholic fatty liver disease (NAFLD) is one of the most common conditions worldwide that targets the liver parenchyma. NAFLD represents an intrahepatic triglyceride accumulation in the absence of excessive alcohol consumption and other diseases that affect the liver parenchyma. The current gold standard for evaluating the amount of intrahepatic fat is represented by liver biopsy, but many patients are reluctant and hardly accept undergoing this procedure due to its invasive nature. The current study addresses this aspect by evaluating the reliability of liver magnetic resonance spectroscopy (MRS) in diagnosing NAFLD, compared to the traditional invasive liver biopsy. The present study included a total of 38 patients based on several well-defined inclusion and exclusion criteria. We used the same NAFLD grading system for both liver MRS and liver biopsy: grade 0 ...
Nonalcoholic fatty liver disease (NAFLD) is a hepatic ailment with a rapidly increasing incidence due to dietary hypernutrition and subsequent obesity. Fatty liver disease can lead to steatohepatitis, fibrosis, cirrhosis, and even cancer, which is associated with various complications. Discovering effective natural materials and herbs can provide alternative and complementary medical treatments to current chemical pharmaceuticals. To develop an effective natural agent for NAFLD, we formulated a combination of four herb mixtures (KIOM2012H) and observed lipid-lowering efficacy. The inhibitory effects of KIOM2012H on free fatty acid-induced lipid accumulation, triglyceride contents, and gene expressions were analyzed in HepG2 cells. Using high fat diet-fed mice, body weight changes, gross liver appearances, hepatic triglyceride contents, and gene expressions were evaluated. KIOM2012H dose-dependently inhibited lipid accumulation and gene expressions involved in lipogenesis and related regulators.
ALT: 15,360 (rat normal 29-65). Contributors Diagnosis and Comments: Moderate to severe, acute, multifocal to coalescing centrilobular hepatic necrosis.. Acute coagulative necrosis of the centrilobular region (Zone 3 of the liver acinus) is present throughout this section of rat liver. The necrosis of hepatocytes is most severe in zone 3, with complete dissolution of cytoplasmic components, karyorrhexis and karyolysis, and breakdown of sinusoidal endothelium with blood-filled lakes in the immediate vicinity of central veins. Phagocytosis by large cells assumed to be Kupffer cells is evident in the centrilobular region, and by Kupffer cells and intact hepatocytes at the periphery of the necrotic zones. Large numbers of neutrophils and lesser numbers of other mononuclear cells are abundant in or at the periphery of the necrotic zone (often approximating the Zone 2-3 boundary). Increased homogeneity of the hepatocytic cytoplasm with increased finely granular basophilia exists in the midzonal to ...
TY - JOUR. T1 - Sinusoidal endothelial cells direct traffic at the intersection of regeneration and fibrosis. AU - Huebert, Robert C.. AU - Shah, Vijay H.. PY - 2014/8. Y1 - 2014/8. N2 - Chemical or traumatic damage to the liver is frequently associated with aberrant healing (fibrosis) that overrides liver regeneration. The mechanism by which hepatic niche cells differentially modulate regeneration and fibrosis during liver repair remains to be defined. Hepatic vascular niche predominantly represented by liver sinusoidal endothelial cells deploys paracrine trophogens, known as angiocrine factors, to stimulate regeneration. Nevertheless, it is not known how pro-regenerative angiocrine signals from liver sinusoidal endothelial cells is subverted to promote fibrosis. Here, by combining an inducible endothelial-cell-specific mouse gene deletion strategy and complementary models of acute and chronic liver injury, we show that divergent angiocrine signals from liver sinusoidal endothelial cells ...
Get the best treatment for nonalcoholic fatty liver disease in Chennai, Non-alcoholic fatty liver disease (NAFLD) is a very common liver disease that results in fat accumulation in the liver. Dr.Rela Institute and Medical Centre is the most sought after destination for Fatty Liver Treatment and all medical problems concerning liver.
Non-alcoholic fatty liver disease (NAFLD) represents a spectrum ranging from simple steatosis to more severe steatohepatitis with hepatic inflammation and fibrosis, known as nonalcoholic steatohepatitis (NASH). NASH may further lead to cirrhosis and hepatocellular carcinoma (HCC). This map shows a stage-dependent progression of NAFLD. In the first stage of NAFLD, excess lipid accumulation has been demonstrated. The main cause is the induction of insulin resistance, which leads to a defect in insulin suppression of free fatty acids (FAAs) disposal. In addition, two transcription factors, SREBP-1c and PPAR-alpha, activate key enzymes of lipogenesis and increase the synthesis of FAAs in liver. In the second stage, as a consequence of the progression to NASH, the production of reactive oxygen species (ROS) is enhanced due to oxidation stress through mitochondrial beta-oxidation of fatty acids and endoplamic reticulum (ER) stress, leading to lipid peroxidation. The lipid peroxidation can further ...
There is a peroxidase quench that will block ALL forms of peroxidase, totally. This is the glucose oxidase method. Hsu H-M, et al Am J Pathology 188:209-217,1984 Andrew SM and Jasani G Histchem J 19:426-430, 1987 Vector provided me with the exact protocol ,Date: Mon, 10 Jul 2000 14:43:03 -0400 ,From: Jeff Crews ,[email protected], ,Subject: Re: IH on Liver Tissue ,To: kkdu[email protected], [email protected] , , With extremely bloody tissue like spleen or liver, it is sometimes , impossible to quench all of the peroxidase present in the blood. Try , an alkaline-phoshatase detection system. , , Jeffrey Crews, HTL (ASCP) , Organogenesis, Inc. , , ,______________________________ Reply Separator _________________________________ ,Subject: IH on Liver Tissue ,Author: ,[email protected], at internet ,Date: 07/10/2000 11:03 AM , , ,How can you successfully perform immunohistochemistry on slides of liver ,tissue using horse-radish peroxidase and DAB? How do you quench the ,endogenous peroxidase ...
The content and structure of glycogen in hepatocytes of normal and cirrhotic rat liver were examined at different time intervals after glucose administration to starving animals. We used an original...
Non-alcoholic fatty liver disease (NAFLD) represents a spectrum ranging from simple steatosis to more severe steatohepatitis with hepatic inflammation and fibrosis, known as nonalcoholic steatohepatitis (NASH). NASH may further lead to cirrhosis and hepatocellular carcinoma (HCC). This map shows a stage-dependent progression of NAFLD. In the first stage of NAFLD, excess lipid accumulation has been demonstrated. The main cause is the induction of insulin resistance, which leads to a defect in insulin suppression of free fatty acids (FAAs) disposal. In addition, two transcription factors, SREBP-1c and PPAR-alpha, activate key enzymes of lipogenesis and increase the synthesis of FAAs in liver. In the second stage, as a consequence of the progression to NASH, the production of reactive oxygen species (ROS) is enhanced due to oxidation stress through mitochondrial beta-oxidation of fatty acids and endoplamic reticulum (ER) stress, leading to lipid peroxidation. The lipid peroxidation can further ...