Gerin I, Bommer GT, McCoin CS, Sousa KM, Krishnan V, MacDougald OA. Roles for miRNA-378/378* in adipocyte gene expression and lipogenesis. Am J Physiol Endocrinol Metab 299: E198-E206, 2010. First published May 18, 2010; doi:10.1152/ajpendo.00179.2010.-In this study, we explored the roles of microRNAs in adipocyte differentiation and metabolism. We first knocked down Argonaute2 (Ago2), a key enzyme in the processing of micro-RNAs (miRNAs), to investigate a potential role for miRNAs in adipocyte differentiation and/or metabolism. Although we did not observe dramatic differences in adipogenesis between Ago2 knock-down and control 3T3-L1 cells, incorporation of [C-14] glucose or acetate into triacylglycerol, and steady-state levels of triacyglycerol were all reduced, suggesting a role for miRNAs in adipocyte metabolism. To study roles of specific miRNAs in adipocyte biology, we screened for miRNAs that are differentially expressed between preadipocytes and adipocytes for the 3T3-L1 and ST2 cell ...
The mechanism of activation for protein kinase B (PKB), an important target for insulin signaling, has been scarcely investigated in primary cells. In this study, we have characterized the insulin-induced phosphorylation and activation of PKB beta in primary rat adipocytes. Insulin stimulation resulted in a translocation of PKB beta from cytosol to membranes, and phosphorylation and activation of PKB beta. Phosphoamino acid analysis and phosphopeptide mapping demonstrated that the phosphorylation occurred mainly on serines, also when using calyculin A, and that these were localized within one major phosphopeptide. Radiosequencing showed that the radioactivity was released in Cycle No. 7. In addition, the peptide was specifically immunoprecipitated from a tryptic digest of PKB beta using the anti-phospho-PKB (Ser-473) antibody. Taken together, these results show that rat adipocyte PKB beta mainly is phosphorylated on Ser-474 in response to insulin stimulation, in contrast to previous studies in ...
Several studies in mice indicate a role for apolipoprotein E (APOE) in lipid accumulation and adipogenic differentiation in adipose tissue. However, little is yet known if APOE functions in a similar manner in human adipocytes. This prompted us to compare lipid loading and expression of adipocyte differentiation markers in APOE-deficient and control adipocytes using the differentiated human mesenchymal stem cell line hMSC-Tert as well as primary human and mouse adipocytes as model systems. Differentiated hMSC-Tert were stably transduced with or without siRNA targeting APOE while murine adipocytes were isolated from wild type and Apoe knockout mice. Human APOE knockdown hMSC-Tert adipocytes accumulated markedly less triglycerides compared to control cells. This correlated with strongly decreased gene expression levels of adipocyte markers such as adiponectin (ADIPOQ) and fatty acid binding protein 4 (FABP4) as well as the key transcription factor driving adipocyte differentiation, peroxisome ...
One of the major findings in the current report is that PIKE-A is critical for adipocyte differentiation. Several lines of evidence support the role of PIKE-A in terminal adipocyte differentiation instead of preadipocyte formation. First, the mature adipocyte marker aP2 is significantly decreased during in vitro adipocyte differentiation in PIKE−/− MEFs, indicating PIKE-A is important for adipocyte differentiation (Fig. 3B and C). Second, PIKE-A expression is increased in fat tissue development of HFD-fed and ob/ob mice, which highlights its function in the process (Fig. 2H). Lastly, HFD induced comparable preadipocyte marker Pref-1 expression in both wild-type and PIKE−/− mice, indicating that formation of new adipocytes is normal in PIKE-null adipose tissue (Fig. 3A). Interestingly, we found a small portion of PIKE−/− MEFs was able to differentiate into mature adipocytes (Fig. 3B), and quantitative analysis revealed a small but statistically significant increment of lipid ...
AIMS/HYPOTHESIS: Salt-inducible kinase 2 (SIK2) is downregulated in adipose tissue from obese or insulin-resistant individuals and inhibition of SIK isoforms results in reduced glucose uptake and insulin signalling in adipocytes. However, the regulation of SIK2 itself in response to insulin in adipocytes has not been studied in detail. The aim of our work was to investigate effects of insulin on various aspects of SIK2 function in adipocytes.. METHODS: Primary adipocytes were isolated from human subcutaneous and rat epididymal adipose tissue. Insulin-induced phosphorylation of SIK2 and HDAC4 was analyzed using phosphospecific antibodies and changes in the catalytic activity of SIK2 with in vitro kinase assay. SIK2 protein levels were analyzed in primary adipocytes treated with the proteasome inhibitor MG132.. RESULTS: We have identified a novel regulatory pathway of SIK2 in adipocytes, which involves insulin-induced phosphorylation at Thr484. This phosphorylation is impaired in individuals with ...
The Ca2+-insensitive protein kinase C (PKC) isoforms ε, η, δ and ζ are possible direct downstream targets of phosphatidylinositol 3-kinase (PI3-K), and might therefore be involved in insulin signalling. Although isoform-specific changes in PKC expression have been reported for skeletal muscle and liver in insulin-resistant states, little is known about these isoforms in adipocytes. Therefore we studied (1) expression and subcellular localization of these isoforms in murine adipocytes, (2) translocation of specific isoforms to membranes in response to treatment with insulin and phorbol 12-myristate 13-acetate (PMA) and (3) regulation of expression in insulin-resistant states. The PKC isoforms ε, η, δ and ζ are expressed in adipocytes. Immunoreactivity for all isoforms is higher in the membranes than in the cytosol, but subcellular fractionation by differential centrifugation shows an isoform-specific distribution within the membrane fractions. PMA treatment of adipocytes induces ...
TY - JOUR. T1 - Beta-mecaptoethanol suppresses inflammation and induces adipogenic differentiation in 3T3-F442A murine preadipocytes. AU - Guo, Wen. AU - Li, Yahui. AU - Liang, Wentao. AU - Wong, Siu. AU - Apovian, Caroline. AU - Kirkland, James L.. AU - Corkey, Barbara E.. PY - 2012/7/23. Y1 - 2012/7/23. N2 - Preadipocytes are present in adipose tissues throughout adult life that can proliferate and differentiate into mature adipocytes in response to environmental cues. Abnormal increase in adipocyte number or size leads to fat tissue expansion. However, it is now recognized that adipocyte hypertrophy is a greater risk factor for metabolic syndrome whereas fat tissue that continues to produce newer and smaller fat cells through preadipocyte differentiation is "metabolically healthy". Because adipocyte hypertrophy is often associated with increased oxidant stress and low grade inflammation, both are linked to disturbed cellular redox, we tested how preadipocyte differentiation may be regulated ...
The retinoblastoma protein (RB) has previously been shown to facilitate adipocyte differentiation by inducing cell cycle arrest and enhancing the transactivation by the adipogenic CCAAT/enhancer binding proteins (C/EBP). We show here that the peroxisome proliferator-activated receptor gamma (PPARgamma), a nuclear receptor pivotal for adipogenesis, promotes adipocyte differentiation more efficiently in the absence of RB. PPARgamma and RB were shown to coimmunoprecipitate, and this PPARgamma-RB complex also contains the histone deacetylase HDAC3, thereby attenuating PPARgammas capacity to drive gene expression and adipocyte differentiation. Dissociation of the PPARgamma-RB-HDAC3 complex by RB phosphorylation or by inhibition of HDAC activity stimulates adipocyte differentiation. These observations underscore an important function of both RB and HDAC3 in fine-tuning PPARgamma activity and adipocyte differentiation.. Keywords: Thiazolidinediones. ...
Uncoupling protein 1 (UCP-1), the specific marker of brown adipose tissue, is transcriptionally activated in response to adrenergic stimuli and thyroid hormones are necessary for its full expression. We describe differences in the regulation of UCP-1 mRNA expression between rat and mouse brown adipocytes in culture, using norepinephrine (NE), triiodothyronine (T3), insulin and retinoic acid (RA). Results: NE and cAMP-elevating agents strongly increase UCP-1 mRNA levels in cultures of mouse adipocytes, but increases are low in those from rat. In rat adipocytes NE poorly increases UCP-1 mRNA expression and T3 markedly increases the adrenergic response of UCP-1, an effect not observed in mouse adipocytes. In the absence of insulin, T3 itself increases UCP-1 mRNA in rat adipocytes and enhances the response to NE, while in mouse adipocytes no effect of T3 is observed. RA by itself stimulates UCP-1 mRNA in mouse adipocytes, but not in those from rat. In rat cultures, RA requires the presence of NE ...
TY - JOUR. T1 - Regulation of gene expression during adipocyte differentiation. T2 - a review.. AU - Gaskins, H. R.. AU - Hausman, G. J.. AU - Martin, R. J.. PY - 1989/9. Y1 - 1989/9. N2 - The differentiation of adipose precursor cells is accompanied by the acquisition of adipocyte-specific messenger (m) RNAs allowing characteristic changes in protein composition. The development of methods for cloning and characterizing individual genes has provided the opportunity to study selective gene expression by adipocytes at the molecular level. In this review, the information obtained to date regarding transcriptional and post-transcriptional regulatory mechanisms utilized by adipocytes is summarized. Included are descriptions of conserved DNA sequences found in noncoding regions of adipose genes and of how protein-DNA interactions at these regions are thought to regulate the initiation of transcription. Among the transcription factors implemented in regulation of adipocyte-specific gene expression are ...
Tumor necrosis factor (TNF)-alpha is postulated to play a major role in the pathogenesis of obesity-linked insulin resistance, probably resulting from an interaction with insulin signaling pathways. This cross talk has now been investigated in human adipocytes at the level of phosphatidylinositol (PI) 3-kinase, and the TNF receptors (TNFRs) mediating these processes have been identified. Equilibrium binding studies using human adipocytes from mammary tissue indicated the presence of two populations of TNFR with apparent affinity constants of 13 pmol/l and 1.6 nmol/l, respectively. Interaction of TNF-alpha with insulin signaling was determined by quantification of insulin receptor substrate (IRS)-1-associated PI 3-kinase activity. Under control conditions, PI 3-kinase was activated about 10-fold in response to insulin (10[-7] mol/l, 5 min). Preincubation of adipocytes with 5 nmol/l TNF-alpha for 15 min resulted in a 60-70% reduction of insulin action, reaching a stable inhibition (40%) after ...
In contrast to the published studies, which demonstrated associations between average adipocyte size and serum levels or secretion, our study is unique because it investigated the secretory capacity of adipocyte fractions from the same individual separated by cell size. The results obtained by the technique clearly suggest that only the very large adipocytes are dysregulated. Adipocyte hypertrophy appears to cause a differentially impaired secretion between pro- and antiinflammatory adipokines shifting the immunological balance toward the expression of proinflammatory proteins. Thisabnormal function of adipocytes may play an important role in the development of a chronic low-grade proinflammatory state in obesity, which is considered to build the common soil for the development of insulin resistance, type 2 diabetes, and atherosclerosis (5, 68 ...
There is a physiologic limit to adipocyte cell size. Adipocytes in the mouse inguinal and epididymal fat pads can increase in size three- and seven-fold, respectively, during 12 weeks of HFF (62). Cell size correlates strongly with the frequency of adipocyte death. The percentage of dead epididymal adipocytes increases progressively from 0.1% at one week to as much as 16% at 12 weeks of HFF (62). Independent of how adipocytes die - from necrosis or apoptosis - the reaction of AT to adipocyte death can be likened to the initiation of a wound healing response, triggering a considerable increase in immune cell infiltration. Monocyte recruitment and differentiation to proinflammatory macrophages are of particular importance. These macrophages surround the dead adipocytes, forming what is described histologically as "crown-like structures" (62-64). Concomitantly, activated myofibroblasts in the area secrete collagen to maintain the integrity of the damaged tissue (65). As macrophages and neutrophils ...
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Dermal adipose tissue (also known as dermal white adipose tissue and herein referred to as dWAT) has been the focus of much discussion in recent years. However, dWAT remains poorly characterized. The fate of the mature dermal adipocytes and the origin of the rapidly reappearing dermal adipocytes at different stages remain unclear. Here, we isolated dermal adipocytes and characterized dermal fat at the cellular and molecular level. Together with dWATs dynamic responses to external stimuli, we established that dermal adipocytes are a distinct class of white adipocytes with high plasticity. By combining pulse-chase lineage tracing and single-cell RNA sequencing, we observed that mature dermal adipocytes undergo dedifferentiation and redifferentiation under physiological and pathophysiological conditions. Upon various challenges, the dedifferentiated cells proliferate and redifferentiate into adipocytes. In addition, manipulation of dWAT highlighted an important role for mature dermal adipocytes ...
It is a desirable goal to stimulate fuel oxidation in adipocytes and shift the balance toward less fuel storage and more burning. To understand this regulatory process, respiration was measured in primary rat adipocytes, mitochondria, and fat-fed mice. Maximum O(2) consumption, in vitro, was determi …
Adipocytes play an important role in energy storage and metabolism. Adipocyte differentiation is a developmental process that is critical for metabolic homeostasis and nutrient signaling. It is controlled by complex actions involving gene expression and signal transduction. Preadipocytes are present throughout adult life in adipose tissues and can proliferate and differentiate into mature adipocytes according to the energy balance. The proliferation and differentiation of these preadipocytes contribute to increases in adipose tissue mass. In vitro study indicates that different tissue-derived preadipocytes exhibit differently in lipid accumulation, adipogenic transcription factor expression, and TNF?-induced apoptosis. It has also been demonstrated that there is a close relationship between adipocyte differentiation and many physiological and pathological processes including fat metabolism, energy balance, obesity, diabetes, hyperlipidemia and breast cancer. HPA-s from Bioarray Research ...
In a previous study designed to understand the role of Myo1c in GLUT4 trafficking and membrane dynamics, we observed that Myo1c overexpression induced dramatic cortical actin remodeling (membrane ruffling) in 3T3-L1 adipocytes, in a serum- and insulin-independent manner (4). This observation suggested that Myo1c might mediate the effect of insulin on membrane ruffling in 3T3-L1 adipocytes, which is supported by our observation that Myo1c depletion in 3T3-L1 adipocytes does indeed attenuate insulin-induced membrane ruffling (data not shown). Interestingly, expression of Myo1c in cultured adipocytes induces membrane ruffling even in the presence of wortmannin, suggesting that Myo1c may function downstream or independent of PI3K in activating membrane ruffling. Our studies here suggest that formation and maintenance of the Rictor-Myo1c complex are not dependent on insulin, rapamycin, or wortmannin (Fig. 1, 2, and 4). Therefore, to determine the functional relevance of Rictors association with ...
CEBPA [ENSP00000427514]. CCAAT/enhancer binding protein (C/EBP), alpha; Transcription factor that coordinates proliferation arrest and the differentiation of myeloid progenitors, adipocytes, hepatocytes, and cells of the lung and the placenta. Binds directly to the consensus DNA sequence 5-T[TG]NNGNAA[TG]-3 acting as an activator on distinct target genes. During early embryogenesis, plays essential and redundant functions with CEBPB. Essential for the transition from common myeloid progenitors (CMP) to granulocyte/monocyte progenitors (GMP). Critical for the proper development of the liver and the lung (By similarity). Necessary for terminal adipocyte differentiation, is required for postnatal maintenance of systemic energy homeostasis and lipid storage (By similarity). To regulate these different processes at the proper moment and tissue, interplays with other transcription factors and modulators. Downregulates the expression of genes that maintain cells in an undifferentiated and ...
Obesity is an increasing health problem worldwide, and nonsurgical strategies to treat obesity have remained rather inefficient. We here show that acute loss of TGF-β-activated kinase 1 (TAK1) in adipocytes results in an increased rate of apoptotic adipocyte death and increased numbers of M2 macrophages in white adipose tissue. Mice with adipocyte-specific TAK1 deficiency have reduced adipocyte numbers and are resistant to obesity induced by a high-fat diet or leptin deficiency. In addition, adipocyte-specific TAK1-deficient mice under a high-fat diet showed increased energy expenditure, which was accompanied by enhanced expression of the uncoupling protein UCP1. Interestingly, acute induction of adipocyte-specific TAK1 deficiency in mice already under a high-fat diet was able to stop further weight gain and improved glucose tolerance. Thus, loss of TAK1 in adipocytes reduces the total number of adipocytes, increases browning of white adipose tissue, and may be an attractive strategy to treat ...
Introduction: Renin-Angiotensin System (RAS) induces oxidative stress and contributes to various pathological conditions including insulin resistance and the metabolic syndrome. Recent studies have shown the role of PPARδ-agonist in attenuation of Angiotensin II induced oxidative stress.The aim of this study was to explore the effectiveness of a PPARδ-agonist in the prevention of Ang II-induced vascular and adipocyte dysfunction and the possible interaction between PPARδ and HO-1 system in a model of enhanced oxidative stress, the Goldblatt 2K1C model.. Methods: We first established a direct stimulatory effect of the PPARδ-agonist (GW 501516) on the HO-1 gene by demonstrating increased luciferase activity in COS-7 cells transfected with a luciferase-HO-1 promoter construct. SD rats were divided in 4 groups: sham operated animals, 2K1C rats and 2K1C rats treated with GW 501516, in the absence or presence of the HO activity inhibitor, stannous mesoporphyrin (SnMP).. Results: 2K1C animals had ...
Chemerin is a leukocyte chemoattractant and adipokine with important immune and metabolic roles. Chemerin, secreted in an inactive form prochemerin, undergoes C-terminal proteolytic cleavage to generate active chemerin, a ligand for the chemokine-like receptor-1 (CMKLR1). We previously identified that adipocytes secrete and activate chemerin. Following treatment with the obesity-associated inflammatory mediator TNF alpha, unknown adipocyte mechanisms are altered resulting in an increased ratio of active to total chemerin production. Based on these findings we hypothesized adipocytes produce proteases capable of modifying chemerin and its ability to activate CMKRL1. 3T3-L1 adipocytes expressed mRNA of immunocyte and fibrinolytic proteases known to activate chemerin in vitro. Following treatment with a general protease inhibitor cocktail (PIC), the TNF alpha-stimulated increase in apparent active chemerin concentration in adipocyte media was amplified 10-fold, as measured by CMKLR1 activation. ...
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The number of overweight and obese individuals continues to increase in both the U.S. and worldwide. This increase has led to a significant increase in obesity-related medical problems including diabetes mellitus, cardiovascular disease and cancer. In obesity, the differentiation of adipocytes is suppressed. Although adipocyte differentiation is associated with changes in glucose metabolism, little is known about the potential of enzymes involved in glucose metabolism to modulate this process. Pyruvate kinase (PK) mediates the rate-limiting step of glycolysis. The M2 isoform of PK (PKM2) is expressed in adipocytes but its role in adipogenesis is unknown. Here we demonstrate that PKM2 regulates the differentiation of both human and mouse adipocytes. Silencing of PKM2 in preadipocytes led to increased lipid accumulation, enhanced expression of markers (FABP4, PPARgamma, C/EBPBeta) of adipocyte differentiation and caused a shift in the pattern of enzymes involved in glucose metabolism favoring the ...
Occurrence of hyperplasia (negative morphology value) or hypertrophy (positive morphology value) was independent of sex and body weight but correlated with fasting plasma insulin levels and insulin sensitivity, independent of adipocyte volume (β-coefficient = 0.3, P , 0.0001). Total adipocyte number and morphology were negatively related (r = −0.66); i.e., the total adipocyte number was greatest in pronounced hyperplasia and smallest in pronounced hypertrophy. The absolute number of new adipocytes generated each year was 70% lower (P , 0.001) in hypertrophy than in hyperplasia, and individual values for adipocyte generation and morphology were strongly related (r = 0.7, P , 0.001). The relative death rate (∼10% per year) or mean age of adipocytes (∼10 years) was not correlated with morphology. ...
Interestingly, the protein levels of GLUT4, PPARg and Leptin are independent of insulin. It would thus appear that insulin controls the translocation of GLUT4 to the cell surface, not the amount of GLUT4 in an adipocyte. The results of the PPARg and leptin also fly in the face of what I have blogged on before, even small adipocytes contain the same amount of leptin as large adipocytes. And PPARg does not appear to predict adipocyte size in this data set. ( I would of expected larger adipocytes to have higher PPARg, and vice versa for the small adipocytes. *shrug ...
Using a subtraction method, we have isolated genes that are induced early in the differentiation of mouse 3T3-L1 preadipocyte cells into adipocytes. These include the genes encoding transcription factors and signalling proteins, as well as unknown genes. Bach1, a transcription factor, and ARA70, a cofactor, were rapidly induced during differentiation. The induction of these two genes was observed only in growth-arrested 3T3-L1 cells, and not in proliferating cells. In NIH-3T3 cells, no induction was observed under either set of conditions. These results strongly indicate that Bach1 and ARA70 have valuable roles at the onset of adipocyte differentiation.. ...
Much of the research into obesity and diabetes is carried out using transgenic animal models. FRAMEs experience and that of many others is that such animal models are of little use when trying to study human diseases and responses to potential therapies. The FRAME Alternatives Laboratory cultures primary human adipocytes and skeletal muscle myotubes to study the effects of increased fat and carbohydrate levels on the metabolism and gene expression of human fat and muscle tissue.. ...
article{5d70646d-8df7-4e0f-a397-fb9a3b72cc4f, author = {Ridderstråle, Martin and Amstrup, J and Hilton, D J and Billestrup, N and Tornqvist, H}, issn = {1439-4286}, language = {eng}, number = {3}, pages = {169--177}, publisher = {Georg Thieme Verlag}, series = {Hormone and Metabolic Research}, title = {SOCS-3 is Involved in the Downregulation of the Acute Insulin-Like Effects of Growth Hormone in Rat Adipocytes by Inhibition of Jak2/IRS-1 Signaling.}, url = {http://dx.doi.org/10.1055/s-2003-39077}, volume = {35}, year = {2003 ...
Stimulation of lipogenesis in rat adipocytes by ATP, a ligand for P2-receptors.: The activation of P2-receptors has a wide range of diverse effects in many tiss
Adipocytes are key cells in metabolic homeostasis. They are very useful for creating models for studying metabolic diseases such as obesity and diabetes.
Obesity has spread worldwide and become a common health problem in modern society. One typical feature of obesity is the excessive accumulation of fat in adipocytes, which occurs through the following two physiological phenomena: hyperplasia (increase in quantity) and hypertrophy (increase in size) of adipocytes. In clinical and scientific research, the accurate quantification of the number and diameter of adipocytes is necessary for assessing obesity. In this study, we present a new automatic adipocyte counting system, AdipoCount, which is based on image processing algorithms. Comparing with other existing adipocyte counting tools, AdipoCount is more accurate and supports further manual correction. AdipoCount counts adipose cells by the following three-step process: 1) It detects the image edges, which are used to segment the membrane of adipose cells; 2) It uses a watershed-based algorithm to re-segment the missing dyed membrane; and 3) It applies a domain connectivity analysis to count the cells. The
Background Middle age weight problems is recognized as a risk factor for Alzheimers disease (AD) although a mechanistic linkage remains unclear. stimulation-dependent changes in macrophage and adipocyte culture phenotype were examined for comparison to the changes. CYT997 Conclusions/Significance Adipose brain and tissue from fat rich diet given pets demonstrated increased TNF- and microglial and macrophage activation. Both brains and adipose cells got raised APP amounts localizing to neurons and macrophage/adipocytes also, respectively. APP agonist antibody excitement of macrophage ethnicities improved particular cytokine secretion without obvious results on adipocyte tradition phenotype. These data support the hypothesis that high fats diet-dependent weight problems leads to concomitant pro-inflammatory adjustments in mind and adipose cells thats characterized, partly, by improved degrees of APP which may be adding specifically to inflammatory changes that occur. Introduction Obesity, ...
By stimulating the synthesis of AQP8 into adipocytes, Actiporine 8G maintains mitochondrial homeostasis and reactivates lipolysis by adipocytes. This action allows the decrease of adipocytes volume.
A combination of cellular, biochemical, genetic and genomic techniques have revealed a new molecular player in the production of fat cells in mice, which could improve our understanding of obesity.
Exposure of cultures of 3T3-L1 preadipose cells to nitrogen for 16 hours kills almost all of the cells, but after exposure to 5% oxygen for 16 hours most of the cells survive, and recover when culture is continued in 20 ...
The broad area of research that I am interested in is obesity and cardiovascular disease (CVD). My group is particularly focused on deciphering the cellular events and the molecular mechanisms regulating adipocyte energy dissipation in response to oxidative stress. The overreaching goal of our research is to understand the basic regulation of adipocyte function and to identify factors that can be used to reprogram these cells into energetically more active cells for the treatment of obesity.
Description - Human interleukin 1 receptor antagonist (IL1RN, IL1F3, IL1RA, IRAP; Gene ID: 3557) is a protein that is produced in at least two forms, one that stays inside the cell and one that is secreted. This assay is for the secreted version. IL-1RA is secreted by various cell types including epithelial cells, monocytes, and adipocytes. It binds to the IL-1 receptor thus preventing signaling by both IL-1α and IL 1β cytokines ...
Comments, concepts and statistics about Pancreatic Lipase Inhibitory Gallotannins from Galla Rhois with Inhibitory Effects on Adipocyte Differentiation in 3T3-L1 Cells.
TY - JOUR. T1 - microRNA-320/RUNX2 axis regulates adipocytic differentiation of human mesenchymal (skeletal) stem cells. AU - Hamam, D. AU - Ali, D. AU - Vishnubalaji, R. AU - Hamam, R. AU - Al-Nbaheen, M. AU - Chen, L. AU - Kassem, M. AU - Aldahmash, A. AU - Alajez, N M. PY - 2014. Y1 - 2014. N2 - The molecular mechanisms promoting lineage-specific commitment of human mesenchymal (skeletal or stromal) stem cells (hMSCs) into adipocytes (ADs) are not fully understood. Thus, we performed global microRNA (miRNA) and gene expression profiling during adipocytic differentiation of hMSC, and utilized bioinformatics as well as functional and biochemical assays, and identified several novel miRNAs differentially expressed during adipogenesis. Among these, miR-320 family (miR-320a, 320b, 320c, 320d and 320e) were ~2.2-3.0-fold upregulated. Overexpression of miR-320c in hMSC enhanced adipocytic differentiation and accelerated formation of mature ADs in ex vivo cultures. Integrated analysis of ...
The primary function of adipose tissue is to store energy in the form of triacylglycerol, which is hydrolyzed to fatty acids to supply other tissues with energy. While insulin promotes the storage of triacylglycerol, catecholamines stimulate its hydrolysis. The development of type II diabetes is strongly associated with obesity, indicating a role of triacylglycerol metabolism in the pathogenesis of diabetes. Caveolae are plasma membrane invaginations found in most cells but are highly abundant in adipocytes. Insulin receptors are localized in caveolae and their function depends on intact caveolae structures. In the present thesis work, mass spectrometry-based methodology allowed identification of a number of new proteins and their posttranslational modifications in caveolae of human adipocytes. Variable N-terminal acetylation and phosphorylation of caveolin-1α and caveolin-1β were identified, which might regulate the function of caveolae. The transcription regulator protein PTRF was identified ...
Stem cells are cells that can self-renew and differentiate into a variety of cell types under certain conditions. Stem cells have great potential in regenerative medicine and cell therapy for the treatment of certain diseases. To deliver knowledge about this frontier in science and technology to medical undergraduate students, we designed an innovative practical experiment for freshmen in their second semester. The lab exercise focused on rat bone marrow mesenchymal stem cell (BMSC) isolation, cell culture and differentiation, and it aimed to help students master the aseptic techniques for cell culture, the basic methods and procedures for the primary culture and passage of BMSCs, the basic procedure for the directional differentiation of BMSCs into adipocytes and their subsequent identification by oil-red-O staining ...
TY - JOUR. T1 - Effects of gut microbiota manipulation on ex vivo lipolysis in human abdominal subcutaneous adipocytes. AU - Jocken, Johan W. E.. AU - Reijnders, Dorien. AU - Canfora, Emanuel E.. AU - Boekschoten, Mark V.. AU - Plat, Joghum. AU - Goossens, Gijs H.. AU - Blaak, Ellen E.. PY - 2018/1/1. Y1 - 2018/1/1. KW - Microbiota. KW - Lipolysis. KW - Fatty acid metabolism. KW - Adipose Tissue. KW - Obesity. KW - Insulin resistance. KW - HORMONE-SENSITIVE LIPASE. KW - ADIPOSE TRIGLYCERIDE LIPASE. KW - DIET-INDUCED OBESITY. KW - FREE FATTY-ACIDS. KW - PROPIONIC-ACID. KW - ACETATE. KW - PROTEIN. KW - PHOSPHORYLATION. KW - DIFFERENTIATION. KW - EXPRESSION. U2 - 10.1080/21623945.2018.1464366. DO - 10.1080/21623945.2018.1464366. M3 - Article. VL - 7. SP - 106. EP - 112. JO - Adipocyte. JF - Adipocyte. SN - 2162-3945. IS - 2. ER - ...
TY - JOUR. T1 - Peroxisome proliferator-activated receptor γ and its role in adipocyte homeostasis and thiazolidinedione-mediated insulin sensitization. AU - Wang, Qiong A.. AU - Zhang, Fang. AU - Jiang, Lei. AU - Ye, Risheng. AU - An, Yu. AU - Shao, Mengle. AU - Tao, Caroline. AU - Gupta, Rana K. AU - Scherer, Philipp E. PY - 2018/5/1. Y1 - 2018/5/1. N2 - Adipose tissue is a dynamic organ that makes critical contributions to whole-body metabolic homeostasis. Although recent studies have revealed that different fat depots have distinct molecular signatures, metabolic functions and adipogenic mechanisms, peroxisome proliferator-activated receptor γ (PPARγ) is still widely viewed as the master regulator of adipogenesis and critical for maintaining mature adipocyte function. Using an inducible, adipocyte-specific knockout system, we explored the role of PPARγ in mature adipocytes in vivo. Short-term PPARγ deficiency in adipocytes reduces whole-body insulin sensitivity, but adipocytes are ...
TY - JOUR. T1 - Tumor necrosis factor increases the rate of lipolysis in primary cultures of adipocytes without altering levels of hormone-sensitive lipase. AU - Green, Allan. AU - Dobias, Susan B.. AU - Walters, Diedra J.A.. AU - Brasier, Allan R.. PY - 1994/6. Y1 - 1994/6. N2 - To investigate the effects of cytokines on adipocyte lipolysis, a macrophage cell line (RAW 264.7) was treated with Escherichia coli lipopolysaccharide (1 μg/ml) for 18 h to induce cytokine release. Conditioned medium (5%, vol/vol) from these cells was added to rat epididymal adipocytes isolated and incubated under sterile conditions. After incubation, the adipocytes were washed, and the rate of lipolysis (glycerol release) was determined after a further 1-h incubation. The conditioned medium caused an approximately 2.7-fold increase in lipolysis, detectable after 6-12 h, maximal by 24 h, and reversible by 48 h after washing the cells. The effect of conditioned medium was reversed by a neutralizing antibody to mouse ...
Saturated fatty acids have been shown to cause insulin resistance and low-grade chronic inflammation, whereas unsaturated fatty acids suppress inflammation via G-protein coupled receptor 120 (GPR120) in macrophages. However, the anti-inflammatory effects of unsaturated fatty acids in adipocytes have yet to be elucidated. Hence, the aims of the present study were to evaluate the anti-inflammatory effects of eicosapentaenoic acid (EPA) via GPR120 in adipocytes. We used 250 μM palmitate as a representative saturated fatty acid. 3T3-L1 adipocytes were used for in vitro studies. We further evaluated the effect of EPA supplementation in a high-fat/high-sucrose (HFHS) diet-induced adipose tissue inflammatory mouse model. EPA attenuated palmitate-induced increases in inflammatory gene expression and NF-κB phosphorylation in 3T3-L1 adipocytes. Silencing of GPR120 abolished the anti-inflammatory effects of EPA. In GPR120 downstream signal analysis, EPA was found to decrease palmitate-induced increases in TAK1
Intramuscular fat or marbling is critical for the palatability of beef. In mice, very recent studies show that adipocytes and fibroblasts share a common pool of progenitor cells, with Zinc finger protein 423 (Zfp423) as a key initiator of adipogenic differentiation. To evaluate the role of Zfp423 in intramuscular adipogenesis and marbling in beef cattle, we sampled beef muscle for separation of stromal vascular cells. These cells were immortalized with pCI neo-hEST2 and individual clones were selected by G418. A total of 288 clones (3×96 well plates) were isolated and induced to adipogenesis. The presence of adipocytes was assessed by Oil-Red-O staining. Three clones with high and low adipogenic potential respectively were selected for further analyses. In addition, fibro/adipogenic progenitor cells were selected using a surface marker, platelet derived growth factor receptor (PDGFR) α. The expression of Zfp423 was much higher (307.4±61.9%, P|0.05) in high adipogenic cells, while transforming growth
TY - JOUR. T1 - Zinc-α2-glycoprotein, a lipid mobilizing factor, is expressed in adipocytes and is up-regulated in mice with cancer cachexia. AU - Bing, Chen. AU - Bao, Yi. AU - Jenkins, John. AU - Sanders, Paul. AU - Manieri, Monia. AU - Cinti, Saverio. AU - Tisdale, Michael J.. AU - Trayhurn, Paul. PY - 2004/2/24. Y1 - 2004/2/24. N2 - Zinc-α2-glycoprotein (ZAG), a 43-kDa protein, is overexpressed in certain human malignant tumors and acts as a lipid-mobilizing factor to stimulate lipolysis in adipocytes leading to cachexia in mice implanted with ZAG-producing tumors. Because white adipose tissue (WAT) is an endocrine organ secreting a wide range of protein factors, including those involved in lipid metabolism, we have investigated whether ZAG is produced locally by adipocytes. ZAG mRNA was detected by RT-PCR in the mouse WAT depots examined (epididymal, perirenal, s.c., and mammary gland) and in interscapular brown fat. In WAT, ZAG gene expression was evident in mature adipocytes and in ...
Our findings presented herein have uncovered a previously unappreciated transcription factor pathway, mediated by HIF-2 in adipocytes, that plays a critical role in the regulation of adipocyte functions. Chronic activation of HIF-2, but not HIF-1, in adipocytes leads to adipose inflammation and pathological hypertrophy in the heart. The hypertrophic heart conditions presented by our mouse models are reminiscent of the cardiac hypertrophy observed in severely obese persons.2 Our solid genetic evidence strongly suggests that adipose hypoxia, observed under the condition of pathological obesity,5-7 may facilitate the development of obesity-related cardiac hypertrophy via sustained activation of HIF-2 in adipocytes.. Our findings demonstrate that HIF activation in adipocytes exerts its cardiac effects in a manner distinct from other purported mechanisms linked to obesity-associated cardiomyopathy. The pathological cardiomegaly observed herein occurs in the absence of lipid accumulation in blood ...
Preadipocyte factor-1 (Pref-1) is a transmembrane protein highly expressed in preadipocytes. Pref-1 expression is, however, completely abolished in adipocytes. The extracellular domain of Pref-1 undergoes two proteolytic cleavage events that generate 50 and 25 kDa soluble products. To understand the function of Pref-1, we generated transgenic mice that express the full ectodomain corresponding to the large cleavage product of Pref-1 fused to human immunoglobulin-γ constant region. Mice expressing the Pref-1/hFc transgene in adipose tissue, driven by the adipocyte fatty acid-binding protein (aP2, also known as aFABP) promoter, showed a substantial decrease in total fat pad weight. Moreover, adipose tissue from transgenic mice showed reduced expression of adipocyte markers and adipocyte-secreted factors, including leptin and adiponectin, whereas the preadipocyte marker Pref-1 was increased. Pref-1 transgenic mice with a substantial, but not complete, loss of adipose tissue exhibited ...