Adiposity is known to be related to asthma. Although a causal link between adiponectin (a protein produced by adipose tissue) and asthma has been demonstrated in mice,. Low serum adiponectin levels predict an increased future risk for developing asthma in middle-aged women, particularly among smokers, according to a new study.. the evidence in humans has been conflicting," said lead author Akshay Sood, MD, MPH, associate professor in the Division of Pulmonary and Critical Care Medicine at the University of New Mexico Health Sciences Center School of Medicine.. "In an earlier cross-sectional study, we found an association between low serum adiponectin levels and prevalent asthma among women, but the direction of this association is not known," Dr. Sood continued. "In the current study, we examined the longitudinal association between asthma and adiponectin and found that low serum adiponectin concentrations, independent of obesity, predicted a higher risk for developing asthma.". The findings ...
Insulin resistance (IR) and related metabolic disturbances are characterized by low levels of adiponectin. High molecular weight adiponectin (HMWA) is considered the active form of adiponectin and a better marker of IR than total adiponectin. The objective of this study is to compare the utility of total adiponectin, HMWA and the HMWA/total adiponectin index (SA index) for the identification of IR and related metabolic conditions. A cross-sectional analysis was performed in a group of ambulatory subjects, aged 20 to 70 years, in Mexico City. Areas under the receiver operator characteristic (ROC) curve for total, HMWA and the SA index were plotted for the identification of metabolic disturbances. Sensitivity and specificity, positive and negative predictive values, and accuracy for the identification of IR were calculated. The study included 101 men and 168 women. The areas under the ROC curve for total and HMWA for the identification of IR (0.664 vs. 0.669, P = 0.74), obesity (0.592 vs. 0.610, P = 0.32)
Murine models have also shown that subcutaneous injection of adiponectin in ovalbumin-sensitised mice prevents the subsequent development of increased airway responsiveness on exposure to ovalbumin.10 31 Taken together, the known anti-inflammatory effects of adiponectin in both mice and humans and the prevention of both allergen-induced airway responsiveness and airway smooth muscle proliferation in murine models has led to the hypothesis that the decreased serum concentrations of adiponectin in obese humans may contribute to the propensity towards asthma in this population.30. This study suggests that a higher serum adiponectin concentration may be a protective factor for current asthma in women, particularly those who are premenopausal. The observed association was independent of adiposity. These results are consistent with a previous cross-sectional study from a different population that suggested that high serum concentrations of leptin, another adipokine, are an independent risk factor for ...
Atherosclerosis is the primary cause of coronary artery disease (CAD). There is increasing recognition that lesion composition rather than size determines the acute complications of atherosclerotic disease. Low serum adiponectin levels were reported to be associated with coronary artery disease and future incidence of acute coronary syndrome (ACS). The impact of adiponectin on lesion composition still remains to be determined. We measured serum adiponectin levels in 303 patients with stable typical or atypical chest pain, who underwent dual-source multi-slice CT-angiography to exclude coronary artery stenosis. Atherosclerotic plaques were classified as calcified, mixed or non-calcified. In bivariate analysis adiponectin levels were inversely correlated with total coronary plaque burden (r = -0.21, p = 0.0004), mixed (r = -0.20, p = 0.0007) and non-calcified plaques (r = -0.18, p = 0.003). No correlation was seen with calcified plaques (r = -0.05, p = 0.39). In a fully adjusted multivariate model ...
As mentioned above, both antidiabetic treatments inhibited the development of hypoadiponectinemia during the animal experiment (Figure 1).. Generally, the effect of insulin on adiponectin serum levels is contentious. In vitro, insulin inhibits the expression of adiponectin at mRNA level [35], but then it leads to an increased adiponectin secretion from adipocytes [36, 37]. In vivo, there is a good documented association of hypoadiponectinemia with insulin resistance and diabetes mellitus type 2 [38], but the effect of insulin therapy on serum levels of adiponectin is not well studied so far. A study in five healthy male volunteers showed a decrease of adiponectin levels during a hyperinsulinemic euglycemic clamp [39]. Another study with insulin treatment in a murine model of obesity and diabetes mellitus type 2, the db/db mice, suggested no impact on adiponectin levels [40]. A recent study indicates an elevation of adiponectin levels in a hyperinsulinemia rat model [41]. In this respect, our ...
Adiponectin is an adipocyte-specific protein that plays a role in obesity, insulin resistant, lipid metabolism, and anti-inflammation. Hypoadiponectinemia may be associated with a higher risk for type 2 diabetes and cardiovascular disease. Some studies suggest that adiponectin levels are modulated by lifestyle factors, but little is known about the associations between lifestyle factors and plasma adiponectin levels in Japanese people. We therefore investigated the associations between lifestyle factors and plasma adiponectin levels in general Japanese men. The subjects were 202 Japanese male workers who participated in an annual health check. They provided details about anthropometrical data, blood collection, their use of prescribed medication, and the clinical history of their families. They also completed a self-administered questionnaire about their lifestyles. Subjects with plasma adiponectin levels below 4.0 μg/ml had significantly lower levels of HDL cholesterol and higher levels of BMI, SBP,
TY - JOUR. T1 - The Significance of Elevated Adiponectin in the Treatment of Type 2 Diabetes. AU - Combs, Terry P.. AU - Scherer, Philipp E.. PY - 2003/12/1. Y1 - 2003/12/1. N2 - Thiazolidinediones (TZDs) represent a new family of oral antihyperglycemic agents for insulin resistance and type 2 diabetes. A recently discovered effect of TZDs is the induction of a circulating protein produced exclusively in adipocytes, called Acrp30 or adiponectin. To date, 5 clinical studies have confirmed the induction of circulating adiponectin during TZD treatment. Subjects with type 2 diabetes have lower levels of adiponectin than those without diabetes, yet it is very unlikely that the induction of adiponectin during TZD treatment is a secondary effect of improved glycemia. Highly purified recombinant adiponectin showed very dramatic blood glucose (BG) -lowering effects. The increase in circulating adiponectin during TZD treatment is associated with elevated adiponectin levels in adipose tissue. There is ...
Two independent studies recently demonstrated that there is a modest level of adiponectin expression in C/EBPα-deficient adipocytes with ectopic expression of PPARγ, whereas expression of both PPARγ and C/EBPα led to production of abundant quantities of adiponectin (23,24). These studies suggest that C/EBPα and PPARγ are required to fully activate adiponectin gene expression. Our study indicates that the regulation of adiponectin gene transcription by C/EBPα and PPARγ is through different sites of the human adiponectin gene. C/EBPα increased adiponectin promoter activity only when the DNA encoding the first intron was present (Fig. 2C). In contrast, overexpression of PPARγ2 and its partner RXRα increased the activity of the adiponectin proximal promoter, and this was not enhanced in the presence of the DNA encoding the first intron (Fig. 2B). These data are consistent with the identification of a PPARγ response element within both the human and mouse adiponectin proximal promoter ...
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It is well known that circulating adiponectin concentrations are reduced in animal models of obesity and in patients with obesity or metabolic syndrome, despite adipocyte hypertrophy or increased body fat (2-6). However, the details of adiponectin production and release have varied among studies, especially in animal models (10,28,29,32,33). This is probably due to the apparently different etiology of the three types of obese animal models: genetic, diet-induced, and hypothalamic obesity (20,34).. VMH lesion-induced hypothalamic obesity in animals is the only obesity model that shows clear derangements of autonomic nervous activities (hyperactivity of the vagus nerve and hypoactivity of sympathetic nerves) compared with genetic (20), diet-induced obesity (34), and other types of hypothalamic obesity (19). Thus, there is a possibility that this animal model has different characteristics of adiponectin production and release, with resultant change of serum adiponectin, compared with those of other ...
Purpose: : A transgenic mouse model with overexpression of the adipokine adiponectin resulted in progressive expansion of the retrobulbar fat pad leading to fulminant exophthalmos. We undertook a pilot study to determine if adiponectin levels in patients with Graves Ophthalmopathy are elevated as found in the transgenic mouse model. Methods: : From a large urban ophthalmic plastics service 46 consecutive patients with Graves Ophthalmolopathy had their mean serum adiponectin levels determined through an adiponectin ELISA. Clinical data was recorded using standardized criteria. Results: : An ANOVA analysis found that mean adiponectin levels differed significantly between inactive and active Graves disease patients (p=0.0458) and presence of diabetes (p=0.0054). Mean adiponectin level in the active disease group was 15.78 mg/L (SD=8.51), and in the inactive group it was 11.36 mg/L (SD=6.29). Conclusions: : The adipokines such as adiponectin warrant further investigation regarding its role in the ...
A number of bioactive molecules secreted from fat tissue, referred to as adipokines, could participate in the development of obesity-related complications through regulation of inflammatory responses.9,10 Most adipokines are proinflammatory. In contrast, adiponectin, also referred to as adipocyte complement-related protein 30 (ACRP30), is an antiinflammatory adipokine that is abundantly present in blood stream. Whereas adiponectin is expressed almost exclusively in adipose tissue,11,12 plasma adiponectin levels are paradoxically decreased in obese individuals.13 This regulation of adiponectin results, at least in part, from the upregulation of tumor necrosis factor (TNF)-α and other proinflammatory cytokines which inhibits the synthesis of adiponectin in the obese state. Low plasma adiponectin levels, also known as hypoadiponectinemia, are closely associated with the increased prevalence of obesity-linked disorders including type 2 diabetes, coronary heart disease, and hypertension.9 Studies ...
BACKGROUND AND OBJECTIVES: Molecular data suggests that adiponectin may directly regulate urinary albumin excretion. In the Diabetes Prevention Program (DPP) we measured adiponectin and albuminuria before and after intervention, and we previously reported increases in adiponectin with interventions. Here we have used the DPP dataset to test the hypothesis that treatment-related increases in adiponectin may reduce albuminuria in obesity. DESIGN, SETTING, PARTICIPANTS AND METHODS: We evaluated cross-sectional correlations between plasma adiponectin and urinary albumin excretion at baseline, and the relationship of treatment-related changes in adiponectin and albuminuria. Baseline and follow-up urine albumin to creatinine ratios (ACR (albumin to creatinine ratio)) and plasma adiponectin concentration were available in 2553 subjects. RESULTS: Adjusting for age, sex and race/ethnicity, we observed a statistically significant but weak inverse relationship between adiponectin and ACR at baseline (conditional
Background: Adiponectin is an adipokine with beneficial effect on vascular function. Although adiponectin levels are decreased in patients with diabetes mellitus (DM), it is unclear whether impaired glucose tolerance (IGT) affects adiponectins release, or whether glucose intake modifies its release from adipocytes. We examined the effect of glucose on serum adiponectin/insulin and endothelial function, in subjects with IGT, patients with DM and healthy individuals.. Methods: The study population consisted of 113 subjects: 19 with IGT, 78 with DM and 16 controls. All subjects underwent glucose loading (75g oral glucose), and blood samples were obtained at baseline and after 3 hours. Endothelial function was evaluated by gauge-strain plethysmography at baseline and every 1h, and endothelium-dependent dilation (EDD) was determined. Adiponectin and insulin were measured at baseline and at 3h.. Results: Glucose loading increased adiponectin levels in healthy (70.1±8.5 to 80.8±11.4 ng/ml, p,0.05) ...
Abstract: Nitric oxide (NO) stimulates mitochondrial biogenesis. We recently reported that adiponectin synthesis is regulated by mitochondrial function in adipocytes. This study was undertaken to test the hypothesis that endothelial NO synthase (eNOS) plays an important role in adiponectin synthesis by producing NO and enhancing mitochondrial function in adipocytes. We examined the effects of eNOS knockdown on adiponectin synthesis in 3T3-L1 adipocytes and also examined plasma adiponectin levels and the mitochondria in adipose tissue of eNOS knockout (eNOS-/-) mice with and without chronic administration of a NO donor. In cultured 3T3-L1 adipocytes, eNOS siRNA decreased rosiglitazone-induced adiponectin secretion, which was associated with decreases in mitochondrial proteins and biogenesis factors. Plasma adiponectin concentrations were reduced in adult eNOS-/- mice compared with age-matched wild-type mice. Mitochondrial contents in adipose tissue were reduced in eNOS-/- mice, and this was ...
In the current study, we showed that in patients with AMI, low plasma adiponectin was associated independently with increased risk of developing T2DM in a linear dose-response relationship. Even in patients with low glucose, adiponectin still added significantly to the prognostic value, as the risk of developing T2DM was higher in patients with low adiponectin/low glucose compared with patients with high adiponectin/low glucose. However, the risk increased by ∼10-fold in patients who were characterized by the combination of low adiponectin and high blood glucose.. Low plasma adiponectin has been suggested to be causally involved in pathways leading to T2DM. The binding of adiponectin to its receptors (adiR1/R2) directly suppresses hepatic gluconeogenesis and stimulates fatty acid oxidation in liver and muscle, glucose uptake in skeletal muscle, and insulin secretion (1,10).. In a study of 335 cases of incident T2DM from the Whitehall II study, adiponectin was measured three times per ...
Adiponectin is an adipose-derived secreted protein containing 226 amino acid residues. It is relatively abundant in humans and rodents, accounting for about 0.01% of total plasma protein. The circulating levels of adiponectin are decreased under conditions of obesity, insulin resistance, and type II diabetes. Disruption of adiponectin in mice causes insulin resistance and neointimal formation. Conversely, administration of recombinant adiponectin suppresses hepatic glucose production, and reverses insulin resistance associated with both lipoatrophy and obesity. The protective role of adiponectin is attributed to its anti-inflammatory properties (e.g. ability to suppress expression of TNF-α and class A scavenger receptor in macrophages). Recombinant adiponectin is a multimeric glycoprotein containing amino acids Glu-19 to Asn-244 of the adiponectin precursor protein fused to an N-terminal histidine tag.. ...
Iranian Journal of Diabetes and Obesity is scientific quarterly journal published by Shahid Sadoughi University of Medical Sciences
Current epidemics of diabetes mellitus is largely caused by wide spread obesity. The best-established connection between obesity and insulin resistance is the elevated and/or dysregulated levels of circulating free fatty acids that cause and aggravate insulin resistance, type 2 diabetes, cardiovascular disease and other hazardous metabolic conditions. Here, we investigated the effect of a major dietary saturated fatty acid, palmitate, on the insulin-sensitizing adipokine adiponectin produced by cultured adipocytes. We have found that palmitate rapidly inhibits transcription of the adiponectin gene and the release of adiponectin from adipocytes. Adiponectin gene expression is controlled primarily by PPARγ and C/EBPα. Using mouse embryonic fibroblasts from C/EBPα-null mice, we have determined that the latter transcription factor may not solely mediate the inhibitory effect of palmitate on adiponectin transcription leaving PPARγ as a likely target of palmitate. In agreement with this model, palmitate
Adipose tissue is now accepted by the scientific and medical community to be a genuine endocrine organ, in addition to its classical role as an energy store. Adiponectin is one of the many adipocytokines that are secreted almost exclusively by adipose tissue. Alteration in blood adiponectin concentrations has been linked to many human diseases in numerous cross-sectional and prospective studies. In this review, we describe briefly the biological effects of adiponectin as revealed by basic scientific investigations. We also summarize the principles of blood adiponectin assays. Overall, lower blood adiponectin concentration is found in subjects with obesity, type 2 diabetes mellitus, dyslipidemia, and hypertension. These medical conditions are components of the metabolic syndrome and major risk factors for accelerated atherosclerosis. Plasma adiponectin levels are also expected to be lower in subjects with cardiovascular diseases, such as coronary artery disease, ischemic stroke and peripheral artery
Background: Adiponectin is a circulating adipose-derived cytokine with anti-inflammatory and antiatherosclerotic properties. Low adiponectin concentrations are related with endothelial dysfunction, hypertension, and incidence of type 2 diabetes. However the relationship of adiponectin concentrations and cardiovascular outcomes in patients with pre-existing cardiovascular disease is unclear.. Methods: We used data from patients enrolled in the prospective, multicentre French registry of Acute ST elevation or non-ST-elevation Myocardial Infarction(Fast-MI). Blood samples were drawn immediately at admission. Adiponectin concentrations were measured using a validated immunoassay (n= 932 patients, of whom 279 with diabetes). Cox proportional hazards regression models were used for assessing outcomes, e.g all-cause mortality and recurrent AMI during a 2-year follow-up, according to adiponectin levels as continuous variable and tertiles.. Results: During follow-up, 162(17%) patients died or had a ...
TY - JOUR. T1 - Inverse association between serum adiponectin level and transaminase activities in Japanese male workers. AU - Yokoyama, Hirokazu. AU - Hirose, Hiroshi. AU - Ohgo, Hideki. AU - Saito, Ikuo. PY - 2004/7. Y1 - 2004/7. N2 - Background/Aims Since a novel polypeptide named adiponectin was shown to prevent the development of steatosis and steatohepatitis in animal models, we studied whether it was also possible in a clinical situation. Methods Associations between serum adiponectin levels and serum transaminase activities were studied in 791 Japanese males who were not heavy drinkers, and had no autoimmune or HBV- or HCV-induced liver diseases. Results Various markers of metabolic diseases including levels of body mass index (BMI), serum triglyceride, total cholesterol, and insulin resistance assessed by the homeostasis model were significantly higher in subjects with increased transaminase activities when compared to those with normal activities. Single regression analyses ...
TY - JOUR. T1 - Association of low serum adiponectin levels with erosive esophagitis in men. T2 - An analysis of 2405 subjects undergoing physical check-ups. AU - Kato, Motohiko. AU - Watabe, Kenji. AU - Hamasaki, Toshimitsu. AU - Umeda, Miyuki. AU - Furubayashi, Aiko. AU - Kinoshita, Kazuo. AU - Kishida, Osamu. AU - Fujimoto, Takashi. AU - Yamada, Akira. AU - Tsukamoto, Yoshifumi. AU - Yamamoto, Shunsuke. AU - Kamada, Yoshihiro. AU - Yoshida, Yuichi. AU - Kiso, Shinichi. AU - Tsutsui, Shusaku. AU - Kihara, Shinji. AU - Hayashi, Norio. AU - Matsuzawa, Yuji. PY - 2011/12/1. Y1 - 2011/12/1. N2 - Obesity is a risk factor for gastro-esophageal reflux disease (GERD). It is generally considered that intra-abdominal pressure in obese subjects is involved in the pathogenesis of GERD through acid exposure to the esophagus. Recently, visceral fat has been recognized as an endocrine organ that secretes various adipocytokines including adiponectin. The aim of this study was to elucidate the relation between ...
The present study demonstrates that PPARγ-activating ARBs induce adiponectin protein expression at a post-transcriptional level, independently of their AT1R-blocking properties. In addition, AT2R activation resulted in adiponectin upregulation. The PPARγ-activating ARB irbesartan improved parameters of insulin sensitivity in obese Zucker rats, which was associated with the prevention of adiponectin serum depletion.. We and others could recently demonstrate that a subset of ARBs including irbesartan has the potential to activate the insulin-sensitizing nuclear hormone receptor PPARγ, completely independent from their AT1R blocking properties.8,10 PPARγ activation has been shown to stimulate adiponectin expression in adipocytes and to upregulate adiponectin plasma levels in animals and humans.6,11 In the present study, pharmacological antagonism of PPARγ completely blocked irbesartan-induced adiponectin expression in vitro. In addition, adiponectin expression in adipocytes and fat tissue was ...
Adiponectin (Ad) is an abundant protein hormone regulatory of numerous metabolic processes, anti-inflammatory, vascular protective, and anti-ischemic properties. Since its 1995 discovery, Ad has garnered considerable attention for its role in diabetic and cardiovascular pathology. Clinical observations have demonstrated the association of hypoadiponectinemia in patients with obesity, cardiovascular disease, and insulin resistance. There is growing evidence supporting Ad can act as a novel risk factor for cardiovascular and cerebrovascular injury. This 5 years follow-up study will focus on serum adiponectin concentration, activity and isoforms in Chinese population and its correlation to cardiovascular and cerebrovascular diseases ...
Adiponectin is the most abundant plasma adipokine, and is well known for its role in energy homeostasis and cardiac protection. In humans with dilated cardiomyopathy, myocardial adiponectin protein expression is reduced compared to normal hearts and has been implicated in the pathology of cardiomyopathy. Serum adiponectin levels are often conflicting, with higher levels associated with poor survival in humans with congestive heart failure (CHF). We evaluated adiponectin serum concentrations and myocardial protein expression in dogs with naturally occurring myxomatous mitral valve disease and CHF. We compared the findings to active and hibernating brown bears as bears are adapted to endure an extreme period of low cardiac output during their annual hibernation. Bears exhibited largely the active high-molecular weight (HMW) versus the low-molecular weight isoforms of myocardial adiponectin (HMW:LMW = 6.3) during both the active period and hibernation, while healthy dogs exhibited a more balanced mix of
Adiponectin, also referred to as Acrp30, AdipoQ, and GBP28, is a plasma protein exclusively produced by adipose tissue and a possible insulin-sensitizing agent (1-6). Serum adiponectin levels are negatively correlated to BMI in healthy individuals and decreased in type 2 diabetic patients (1-6). However, serum adiponectin levels in type 1 diabetes have not been elucidated.. We examined the serum adiponectin concentrations in 46 type 1 diabetic patients (21 males and 25 females) and compared them with those of BMI-matched healthy control subjects (17 males and 19 females). Mean age was 33 ± 3 and 33 ± 4 years, BMI was 19.8 ± 0.5 and 19.9 ± 0.6 kg/m2, HbA1c level was 9.7± 0.7 and 10.4 ± 0.6%, duration of diabetes was 3.2 ± 0.9 and 3.4 ± 1.3 years, and urinary C-peptide excretion was 18.4 ± 4.3 and 18.0 ± 2.4 μg/day in male and female patients, respectively. High prevalence of GAD antibody or islet cell antibodies (91.3%) indicated autoimmune-associated β-cell destruction in those ...
Introduction: Adiponectin is anti-inflammatory and anti-tumor cytokine secreted exclusively from adipocytes. Thereis a growing evidence of association between adiponectin gene polymorphism and development of pancreatic cancer.The current study aimed at evaluation of the possible association between selected adiponectin gene polymorphism andthe risk of pancreatic cancer. Methods: Prospective case-control study included 77 patients (29 women and 48 men)with biopsy-proven pancreatic adenocarcinoma and 97 healthy control. Blood samples from all included participantswere genotyped for 3 single nucleotide polymorphism (SNPs) of adiponectin genes (rs1501299C|A, rs266729C|G andrs2241766G|T) by PCR. Clinical, biochemical, and radiological data analyzed. Results: We demonstrated a significantassociation between the three studied SNPs (rs1501299, rs266729, and rs2241766) and increased risk of pancreaticadenocarcinoma (p|0.001). Furthermore, in clinical correlation analysis, Patients with rs2241766 polymorphismhave
TY - JOUR. T1 - Systemic fate of the adipocyte-derived factor adiponectin. AU - Halberg, Nils. AU - Schraw, Todd D.. AU - Wang, Zhao V.. AU - Kim, Ja Young. AU - Yi, James. AU - Hamilton, Mark P.. AU - Luby-Phelps, Kate. AU - Scherer, Philipp E.. PY - 2009/9. Y1 - 2009/9. N2 - OBJECTIVE - The adipocyte-derived secretory protein adiponectin has been widely studied and shown to have potent insulin-sensitizing, antiapoptotic, and anti-inflammatory properties. While its biosynthesis is well understood, its fate, once in circulation, is less well established. RESEARCH DESIGN AND METHODS - Here, we examine the half-life of adiponectin in circulation by tracking fluorescently labeled recombinant adiponectin in the circulation, following it to its final destination in the hepatocyte. RESULTS - Despite its abundant presence in plasma, adiponectin is cleared rapidly with a half-life of ∼75 min. A more bioactive version carrying a mutation at cysteine 39 is cleared within minutes. Even though ...
Studies have shown that single-nucleotide polymorphisms (SNPs) on the ADIPOQ gene have been linked with obesity and with adiponectin levels in various populations. Here, we aimed to investigate the association of ADIPOQ rs17366568 and rs3774261 SNPs with obesity and with adiponectin levels in Malaysian Malays. Obesity parameters and adiponectin levels were measured in 574 subjects. Genotyping was performed using real-time polymerase chain reaction and Sequenom MassARRAY. A significant genotypic association was observed between ADIPOQ rs17366568 and obesity. The frequencies of AG and AA genotypes were significantly higher in the obese group (11%) than in the non-obese group (5%) (P=0.024). The odds of A alleles occurring among the obese group were twice those among the non-obese group (odds ratio 2.15; 95% confidence interval 1.13-4.09). However, no significant association was found between allelic frequencies of ADIPOQ rs17366568 and obesity after Bonferroni correction (P>0.025) or between ...
BACKGROUND: Insulin resistance is the major pathogenesis underlying type 2 diabetes mellitus (T2DM) and these patients have doubled risk of Alzheimers disease (AD). Increasing evidence suggests that insulin resistance plays an important role in AD pathogenesis, possibly due to abnormal GSK3β activation, causing intra- and extracellular amyloid-beta (Aβ) accumulation. Adiponectin (APN) is an adipokine with insulin-sensitizing and anti-inflammatory effects. Reduced circulatory APN level is associated with insulin resistance and T2DM. The role of APN in AD has not been elucidated. In this study, we aim to examine if adiponectin deficiency would lead to cerebral insulin resistance, cognitive decline and Alzheimers-like pathology in mice. METHODS: To study the role of adiponectin in cognitive functions, we employed adiponectin-knockout (APN-KO) mice and demonstrated chronic APN deficiency in their CNS. Behavioral tests were performed to study the cognitions of male APN-KO mice. Brains and tissue ...
Purpose : To validate earlier found physiologic response patterns explaining retinopathy of prematurity (ROP) development in infants born very preterm. Generally adiponectin production is up-regulated by weight loss and down regulated by weight gain, oxidative stress as well as pro-inflammatory cytokines. Disturbed homeostasis, impaired growth and inflammation are factors closely related to ROP development. This study assessed the longitudinal postnatal development of serum adiponectin levels and ROP development in a new cohort of very preterm infants. Methods : A study was performed in 90 infants with gestational age (GA) , 28 weeks with a mean (SD) gestational age at birth of 25.2 (1.4) weeks and mean (SD) birth weight of 882 (220) g. Cord blood samples and thereafter venous blood samples were obtained at postnatal day 1, 7, 14, 28 days and at postmenstrual age 32, 36 and 40 weeks. Serum adiponectin levels were assayed using a human adiponectin ELISA kit (E091M, Mediagnost, Germany). The ...
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AIMS/HYPOTHESIS: Pregnancy, a state of insulin resistance, is associated with elevated levels of cytokines and profound alterations in metabolism. Serum adiponectin, an adipokine with anti-inflammatory and insulin-sensitising properties, has been shown to be lower in patients with gestational diabetes mellitus, a state of greater insulin resistance than normal pregnancies. Hypothesising that the human placenta is a source of adiponectin, we investigated its expression and secretion, and the regulation by cytokines of adiponectin and its receptors. METHODS: Real-time RT-PCR, radioimmunoassay, Western blotting, radioligand binding and immunofluorescent analyses were applied to demonstrate the expression, secretion and functionality of placental adiponectin. RESULTS: Adiponectin gene expression and protein were found in the human term placenta, with expression primarily in the syncytiotrophoblast. RIA of conditioned media from explant experiments revealed that the placenta can secrete adiponectin in vitro.
On the basis of the above-reported properties unraveled by basic science studies, it would be conceivable to hypothesize that adiponectin exerts beneficial effects on metabolic and cardiovascular traits in human beings. In fact, in pioneering cross-sectional studies carried out in Pima Indians, circulating adiponectin levels correlated positively with both skeletal muscle (21) and liver (22) insulin sensitivity. In addition, in this same population, adiponectin was negatively correlated with inflammatory markers (23). Along the same line is the observation that insulin-sensitizing agents increase adiponectin concentrations in humans (24). In addition, a prospective study has also shown that low plasma adiponectin concentration predicts the deterioration of insulin sensitivity over time (25).. Unfortunately, the observational design of all such studies could not address whether the reported associations were due to a positive effect of adiponectin on insulin sensitivity. In this regard, it must ...
The hormone adiponectin is secreted from fat cells. Overweight and obese people are known to have less adiponectin secreted and they are definitely at higher risk for suffering from cancers. The mechanism linking hormone existence to overall health is the following: high adiponectin levels in blood are able to suppress blood vessels inflammation, this leads to increased metabolism.. Therefore, higher adiponectin levels decrease the risk of obesity, diabetes, heart disease, breast cancer and now it is also linked to colorectal cancer. It is clear that hormone adiponectin makes people healthier, but how exactly the hormone is being secreted from fat cells is yet unclear.. According to American Cancer Society statistics, colorectal cancer affects 1.2 million and kills 630000 people worldwide each year. This year is estimated to have 149000 newly diagnosed and 50000 cases in US. About 1/3 of cases are associated with family history, other factors causing the disease are believed to be diet reach in ...
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Adiponectin is a protein hormone that modulates a number of metabolic processes, including glucose regulation and fatty acid oxidation.[7] Adiponectin is secreted from adipose tissue (and also from the placenta in pregnancy[8]) into the bloodstream and is very abundant in plasma relative to many hormones. Many studies have found adiponectin to be inversely correlated with body mass index in patient populations.[9] However, a meta analysis was not able to confirm this association in healthy adults.[10] Circulating adiponectin concentrations increase during caloric restriction in animals and humans, such as in patients with anorexia nervosa. This observation is surprising, given that adiponectin is produced by adipose tissue. However, a recent study suggests that adipose tissue within bone marrow, which increases during caloric restriction, contributes to elevated circulating adiponectin in this context.[11]. Transgenic mice with increased adiponectin show reduced adipocyte differentiation and ...
ABSTRACT. Background and aims: Non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome (MS) are well-recognized complications of obesity. This study was designed to evaluate the role of the UCP1 -3826 A,G polymorphism, adiponectin levels, leptin/adiponectin ratio (L/A), and main biochemical parameters in 102 unrelated severely obese adults [61 females and 41 males, median body mass index (BMI) = 47.8 kg/m2] with NAFLD, with (MS+) or without MS (MS-) from Southern Italy. Subject and methods: The UCP1 polymorphism was tested by the TaqMan method, main biochemical parameters by routinary methods, adiponectin, and leptin serum levels by enzyme-linked immunosorbent assay. MS was diagnosed according to the American Heart Association criteria, liver steatosis was detected by ultrasound. Results: MS was present in 53% male and 66% female obese patients. Only total cholesterol (p=0.04 males and p=0.002 females) and L/A ratio (p=0.03 males) differed between MS+ and MS- obese patients. At ...
Adiponectin, also referred to as Acrp30, AdipoQ and GBP-28, is a recently discovered 244 amino acid protein, the product of the apM1 gene, which is physiologically active and specifically and highly expressed in adipose cells (adipokine). The protein belongs to the soluble defence collagen superfamily; it has a collagen-like domain structurally homologous with collagen VIII and X and complement factor C1q-like globular domain. Adiponectin forms homotrimers, which are the building blocks for higher order complexes found circulating in serum. The human Adiponectin is expressed in E. coli as a recombinant 25.1 kDa sinle, non-glycosylated polypeptide chain containing 231 amino acid residues ...
Results MN and CD4+T cells from RA patients showed a higher proliferative effect when exposed to leptin and adiponectin in comparison with healthy donors. Interesting, the level of proliferation correlated with the DAS28 of patients. Similarly, cells from patients were more sensitive to leptin and adiponectin treatment when evaluating CD25+/CD69+ cell expression and IL-2, TNF secretion, in comparison to healthy donor cells. Comparatively, adiponectin treatment was more effective to induce the expression of CD25, CD69 and IL-6, whereas leptin was a better inductor of IL-2 and TNF-a on the RA patient cells. Comparing this with the clinical activity of patients, we only observed a significant correlation between the DAS28 and the IL-2 induction when exposed to leptin. Preliminary assays showed that leptin was also capable to rescue MN cells from an apoptotic environment by a mechanism related to IL-2 secretion. On the other hand, MN cells from RA patients incubated for several days with leptin ...
In the present study, we found that the I164T mutation of adiponectin gene was associated with CAD prevalence and hypoadiponectinemia in the Japanese population. In contrast, the genotypes of SNP94 and SNP276, which were reported to be present in type 2 diabetes, influenced neither the prevalence of CAD nor the plasma adiponectin level. Importantly, all subjects carrying I164T in the present study including CAD and non-CAD subjects had at least one or more metabolic disorders including diabetes mellitus, hypertension, and dyslipidemia. Among CAD patients, the prevalence of the metabolic syndrome was significantly higher in I164T mutation than that in wild type. These findings suggest that the I164T mutation of adiponectin gene is associated with the development of the metabolic syndrome-linked CAD. Importantly, the severe hypoadiponectinemia in subjects with the I164T mutation was independent of BMI. Recently, we have demonstrated that intimal thickening was accelerated in mechanically injured ...
Recently, adipose tissue has been implicated in the regulation of vascular function in humans. This regulatory function is mediated via the release of vasoactive cytokines called adipokines. Adiponectin is an adipokine with powerful anti-inflammatory and antioxidant properties being dysregulated in obesity and in insulin resistance states. In both in vitro and in vivo models adiponectin has been shown to increase nitric oxide bioavailability, improve endothelial function, and exert beneficial effects on vascular smooth muscle cell function. Strategies to upregulate adiponectin expression or to potentiate adiponectin signalling may favourably modulate vascular redox state and therefore reduce cardiovascular risk. Various drug classes such as glitazones, newer sulfonylureas, angiotensin receptor blockers, ACE inhibitors and nicotinic acid exert beneficial effects on insulin resistance partly by increasing plasma adiponectin levels. Others such as tetrahydrobiopterin or certain antioxidants are also
Adiponectin is the most abundant peptide secreted by adipocytes, whose reduction plays a central role in obesity-related diseases, including insulin resistance/type 2 diabetes and cardiovascular disease. In addition to adipocytes, other cell types, such as skeletal and cardiac myocytes and endothelial cells, can also produce this adipocytokine. Adiponectin effects are mediated by adiponectin receptors, which occur as two isoforms (AdipoR1 and AdipoR2). Adiponectin has direct actions in liver, skeletal muscle, and the vasculature.Adiponectin exists in the circulation as varying molecular weight forms, produced by multimerization. Several endoplasmic reticulum ER-associated proteins, including ER oxidoreductase 1-α (Ero1-α), ER resident protein 44 (ERp44), disulfide-bond A oxidoreductase-like protein (DsbA-L), and glucose-regulated protein 94 (GPR94), have recently been found to be involved in the assembly and secretion of higher-order adiponectin complexes. Recent data indicate that the high-molecular
Mouse Adiponectin (Acrp30) ELISA Kit, 96 tests, Quantitative Kit 100-150-ADM Mouse Adiponectin (Acrp30) ELISA Kit Enzyme-linked immunosorbent assay (ELISA Kit); enzyme immunoassay (EIA); animal (mouse;; rat;; human;; monkey etc) crossreactivity; serum plasma and biolgoical fluids; peptide;; proteins;; ELISA Kit;; antibody;; Acrp30 (adipocyte complement-related protein of 30 kDa);; also known as AdipoQ;; APM1;; Adiponectin;; Gelatin binding protein 28 kDa/GBP28 or adipocyte most abundant protein Mouse Adiponectin (Acrp30) ELISA Kit, 96 tests, Quantitative Kit 100-150-ADM Mouse Adiponectin (Acrp30) ELISA Kit Enzyme-linked immunosorbent assay (ELISA Kit); enzyme immunoassay (EIA); animal (mouse;; rat;; human;; monkey etc) crossreactivity; serum plasma and biolgoical fluids; peptide;; proteins;; ELISA Kit;; antibody;; Acrp30 (adipocyte complement-related protein of 30 kDa);; also known as AdipoQ;; APM1;; Adiponectin;; Gelatin binding protein 28 kDa/GBP28 or adipocyte most abundant protein
Adiponectin, an adipokine predominantly secreted from adipocytes, has been shown to play protective roles against chronic alcohol consumption. While excessive ROS production in macrophages is considered one of the critical events for ethanol-induced damage in various target tissues, the effect of adiponectin on ethanol-induced ROS production is not clearly understood. In the present study, we investigated the effect of globular adiponectin (gAcrp) on ethanol-induced ROS production and the potential mechanisms underlying these effects of gAcrp in macrophages. Here, we demonstrated that gAcrp prevented ethanol-induced ROS production both in RAW 264.7 macrophages and primary murine peritoneal macrophages. Globular adiponectin also inhibited ethanol-induced activation of NADPH oxidase. In addition, gAcrp suppressed ethanol-induced increase in expression of NADPH oxidase subunits, including Nox2 and p22phox, via modulation of NF-κB pathway. Furthermore, pretreatment with Compound C, a selective ...
Objective. To explore the relationship between adiponectin and albuminuria in a large group of overweight and obese nondiabetic individuals after controlling for potential confounders. Material and Methods. Detailed anthropometiy, computed tomography-measured visceral abdominal adipose tissue, 24-h albuminuria, adiponectin and a series of biochemical parameters were assessed. Four hundred forty patients, predominantly of Caucasian origin, were included (80.2% female). A multiple linear regression model was developed, with albuminuria as the dependent variable and potential predictors as independent variables. Results. The mean age was 40 +/- 13 years, the mean body mass index was 35.7 +/- 6.6 kg/m(2), and the median visceral abdominal adipose tissue was 142.4 (92.3-194.0) cm(2). 10.9% of subjects exhibited microalbuminuria. The median adiponectin level was 9.08 (6.23-12.94) mu g/ml, and the median fasting serum glucose level was 83 (77-89) mg/dl. The strongest significant univariate correlations ...
Common genetic variants at the ARL15 locus are associated with plasma adiponectin, insulin and HDL cholesterol concentrations, obesity, and coronary atherosclerosis. The ARL15 gene encodes a small GTP-binding protein whose function is currently unknown. In this study adipocyte-autonomous roles for ARL15 were investigated using conditional knockdown of Arl15 in murine 3T3-L1 (pre)adipocytes. Arl15 knockdown in differentiated adipocytes impaired adiponectin secretion but not adipsin secretion or insulin action, while in preadipocytes it impaired adipogenesis. In differentiated adipocytes GFP-tagged ARL15 localized predominantly to the Golgi with lower levels detected at the plasma membrane and intracellular vesicles, suggesting involvement in intracellular trafficking. Sequencing of ARL15 in 375 severely insulin resistant patients identified four rare heterozygous variants, including an early nonsense mutation in a proband with femorogluteal lipodystrophy and non classical congenital adrenal ...
Introduction: The interleukin 28B (IL28B) genotype is associated with changes of lipid metabolism in patients infected with hepatitis C virus (HCV). The association of steatosis with serum levels of adiponectin in chronic hepatitis C (CHC) patients has also been documented. This study aimed for the evaluation of serum levels of IL28B and adiponectin as well as the association of IL28B SNPs with different clinicopathological parameters in HCV-infected patients.. Methodology: All 142 HCV-infected patients received peg-interferon plus ribavirin. Detection of rs8099917 and rs12979860 IL-28B genotypes was done with specific primers. Serum IL28 and adiponectin levels were measured using commercial ELISA kits.. Results: Higher levels of both IL28 and adiponectin were found in patients. In Genotype 3a (G3a) -infected patients, IL28 and adiponectin serum levels were significantly higher than those infected with G1a. A correlation was found between increasing levels of AST and ALT in G3a-infected patients ...