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PubMed2005

The stimulatory effect of globular adiponectin on insulin-stimulated glucose uptake and fatty acid oxidation is impaired in skeletal muscle from obese subjects.

Adiponectin is an adipose-derived hormone that plays an important role in regulating insulin sensitivity in rodents. However, little is known regarding the effect of adiponectin on metabolism in human skeletal muscle. Therefore, we examined whether the globular head of adiponectin, gAcrp30, acutely activates fatty acid oxidation and glucose uptake in isolated human skeletal muscle. Furthermore, we aimed to determine whether these effects would differ in muscle from lean versus obese individuals. Treatment with gAcrp30 (2.5 microg/ml) increased fatty acid oxidation in lean muscle (70%, P < 0.0001) and to a lesser extent in obese muscle (30%, P < 0.01). In the absence of insulin, gAcrp30 increased glucose uptake 37% in lean (P < 0.05) and 33% in obese muscle (P < 0.05). Combined exposure of insulin and gAcrp30 demonstrated an additive effect on glucose uptake in lean and obese individuals, but this effect was reduced by 50% in obese muscle (P < 0.05). These metabolic effects were attributable to an increase in AMP-activated protein kinase-alpha1 (AMPKalpha1) and AMPKalpha2 activity. However, in obese muscle the activation of AMPKalpha2 by gAcrp30 was blunted. This study provides evidence that gAcrp30 plays a role in regulating fatty acid and glucose metabolism in human skeletal muscle. However, the effects are blunted in obesity, indicating the possible development of adiponectin resistance.

AMP-Activated Protein Kinases↗
PubMed2003

Plasma adiponectin plays an important role in improving insulin resistance with glimepiride in elderly type 2 diabetic subjects.

OBJECTIVE: We investigated the effect of glimepiride, a third-generation sulfonylurea hypoglycemic agent, on insulin resistance in elderly patients with type 2 diabetes, in connection with plasma adiponectin and 8-epi-prostagrandin F2alpha (8-epi-PGF2alpha), an oxidative stress marker. RESEARCH DESIGN AND METHODS: A total of 17 elderly patients with type 2 diabetes received 12 weeks of treatment with glimepiride. Homeostasis assessment model of insulin resistance (HOMA-IR), homeostasis assessment model of beta-cell function, HbA(1c), C-peptide in 24-h pooled urine (urine CPR), and plasma concentrations of 8-epi-PGF2alpha, tumor necrosis factor-alpha (TNF-alpha), plasminogen activator inhibitor type 1, and adiponectin were measured at various times. The metabolic clearance rate of glucose (MCR-g) was also assessed by a hyperinsulinemic-euglycemic clamp. RESULTS: After 8 weeks of glimepiride treatment, significant reductions were observed in HbA(1c) (from 8.4 +/- 1.9 to 6.9 +/- 1.0%), HOMA-IR (from 2.54 +/- 2.25 to 1.69 +/- 0.95%), and plasma TNF-alpha concentrations (from 4.0 +/- 2.0 to 2.6 +/- 2.5 pg/ml). MCR-g was significantly increased from 3.92 +/- 1.09 to 5.73 +/- 1.47 mg. kg(-1). min(-1). Plasma adiponectin increased from 6.61 +/- 3.06 to 10.2 +/- 7.14 micro g/ml. In control subjects, who maintained conventional treatment, no significant changes were observed in any of these markers. CONCLUSIONS: Glimepiride remarkably improved insulin resistance, suggested by a significant reduction in HOMA-IR, an increase in MCR-g, and a reduction in HbA(1c) without changing extrapancreatic beta-cell function and urine CPR. Increased plasma adiponectin and decreased plasma TNF-alpha may underlie the improvement of insulin resistance with glimepiride.

Adiponectin↗
PubMed2005

Beneficial effects of fenofibrate to improve endothelial dysfunction and raise adiponectin levels in patients with primary hypertriglyceridemia.

OBJECTIVE: Improvement in endothelial function is predicted to improve insulin sensitivity, and this may be one mechanism by which fenofibrate decreases the incidence of coronary heart disease. We hypothesize fenofibrate improves endothelial function by enhancing insulin sensitivity. RESEARCH DESIGN AND METHODS: We administered placebo or fenofibrate 200 mg daily for 8 weeks to 46 patients with primary hypertriglyceridemia (24 had metabolic syndrome). This study was randomized, double blind, placebo controlled, and crossover in design. RESULTS: Compared with placebo, fenofibrate decreased total cholesterol, non-HDL cholesterol, apolipoprotein B, and triglycerides and increased HDL cholesterol and apolipoprotein A-I (all P < 0.001) while tending to decrease LDL cholesterol (P = 0.069). Fenofibrate significantly improved percent flow-mediated dilator response to hyperemia by 48 +/- 5% (P < 0.001) and lowered plasma levels of high-sensitivity C-reactive protein (hsCRP) relative to baseline measurements from 0.80 to 0.70 mg/l (P = 0.001) and fibrinogen levels by 16 +/- 3% (P < 0.001). Compared with placebo, fenofibrate therapy significantly increased plasma levels of adiponectin by 14 +/- 5% (P = 0.008) and increased insulin sensitivity (assessed by quantitative insulin sensitivity check index [QUICKI]) by 6 +/- 2% (P = 0.048). There were significant correlations between percent changes in adiponectin levels and percent changes in flow-mediated dilation (r = 0.401, P = 0.006), hsCRP (r = -0.443, P = 0.002), or QUICKI (r = 0.292, P = 0.049). Multivariate regression analysis showed that only changes in adiponectin levels persisted as an independent predictor of changes in flow-mediated dilation (r = 0.504, P = 0.013). Overall, we observed similar results in 24 patients with metabolic syndrome. CONCLUSIONS: Fenofibrate therapy significantly improved percent flow-mediated dilator response to hyperemia, reduced inflammation marker levels, increased adiponectin levels, and improved insulin sensitivity in hypertriglyceridemic or metabolic syndrome patients.

Adiponectin↗
PubMed2005

The influence of very-low-calorie-diet on serum leptin, soluble leptin receptor, adiponectin and resistin levels in obese women.

The aim of our study was to determine whether adipocyte-derived hormones leptin, adiponectin and resistin contribute to the improvement of insulin sensitivity after very-low calorie diet (VLCD). Therefore, serum levels of these hormones were measured in fourteen obese females before and after three weeks VLCD and in seventeen age- and sex-matched healthy controls. Body mass index, HOMA index, serum insulin and leptin levels in obese women before VLCD were significantly higher than in control group (BMI 48.01+/-2.02 vs. 21.38+/-0.42 kg/m(2), HOMA 10.72+/-2.03 vs. 4.69+/-0.42, insulin 38.63+/-5.10 vs. 18.76+/-1.90 microIU/ml, leptin 77.87+/-8.98 vs. 8.82+/-1.52 ng/ml). In contrast, serum adiponectin and soluble leptin receptors levels were significantly lower in obese women before VLCD than in the control group. No differences were found in serum glucose and resistin levels between the obese group before VLCD and the control group. VLCD significantly decreased BMI, HOMA index, serum glucose, insulin and leptin levels and increased soluble leptin receptor levels. The changes in serum adiponectin and resistin levels in obese women after VLCD did not reach statistical significance. We conclude that leptin and soluble leptin receptor levels were affected by VLCD while adiponectin and resistin concentrations were not. Therefore, other mechanisms rather than changes in the endocrine function of the adipose tissue are probably involved in the VLCD-induced improvement of insulin sensitivity.

Adiponectin↗
PubMed2006

Effect of walking with a pedometer on serum lipid and adiponectin levels in Japanese middle-aged men.

OBJECTIVE: To clarify the effects of walking with a pedometer on metabolic parameters, including adiponectin (APN). METHODS: We recruited 44 male Japanese volunteers (age, 37 +/- 9 yrs; body mass index (BMI), 24.2 +/- 2.9 kg/m2; fasting plasma glucose (FPG), 96 +/- 11 mg/dL; total cholesterol (TC) 190 +/- 26 mg/dL; triglycerides (TG) 119 +/- 80 mg/dL; HDL-C56 +/- 14 mg/dL). Subjects were instructed to walk with a pedometer and record the number of steps they walked every day for 50 days. Serum adiponectin (APN) levels were measured by enzyme immunoassay. Treatment effects were examined by Wilcoxon's rank test. RESULTS: The average number of steps was 8211 +/- 2084 per day. There were significant reductions in BMI, sBP, TG and TNF-alpha levels after 50 days, but no changes in adiponectin levels. We then divided the subjects into 2 groups according to the steps walked per day, namely, more than 8000 steps (MT group, n = 22) and less than 8000 steps (LT group, n = 22) and found that the reduction in TG and BP was observed only in the MT group. CONCLUSIONS: Walking with a pedometer is effective for improving metabolic parameters, such as TG and blood pressure, but is not sufficient to increase adiponectin levels in Japanese men.

Adiponectin↗
PubMed2003

[Role of adiponectin--a protein secreted by adipose tissue in preventing atherosclerosis].

Adiponectin is an adipocyte-specific secretory protein, which seems to play a protective role in different models of vascular injury. Adiponectin infiltrates in the subendothelial space of injured vascular walls and suppresses the expression of adhesion molecules on endothelial cells, thus inhibiting the inflammatory processes that occur during the early phases of atherosclerosis. Adiponectin also suppresses lipid accumulation in macrophages and macrophage-to-foam cell transformation. The ability of adiponectin to act as an anti-inflammatory and anti-atherogenic factor has made this novel adipocytokine a promising therapeutic tool for the future.

Adiponectin↗
PubMed2004

Adiponectin and its role in the obesity-induced insulin resistance and related complications.

It is now generally accepted that adipose tissue acts as an endocrine organ producing a number of substances with an important role in the regulation of food intake, energy expenditure and a series of metabolic processes. Adiponectin is a recently discovered protein produced exclusively by adipocytes. A number of studies have shown that obesity, insulin resistance and atherosclerosis are accompanied by decreased adiponectin levels and that adiponectin replacement under experimental settings is able to diminish both insulin resistance and atherosclerosis. The aim of this review is to summarize the current knowledge about the physiology and pathophysiology of adiponectin and to discuss its potential in the treatment of insulin resistance and atherosclerosis.

Adiponectin↗
PubMed2004

[Adiponectin knockout mice].

Here we investigated the biological functions of adiponectin, a fat-derived hormone, by disrupting the gene encodes it in mice. Adiponectin knockout mice (KO) exhibited severe diet-induced insulin resistance with reduced IRS-1-associated P13-kinase activity in muscle. KO also revealed severe neo-intimal thickening in response to vascular-injury and hypertension induced by salt diet. Carbon-tetrachloride induced severe liver fibrosis in KO with the elevated gene expression of growth factors. These phenotypes in KO were reversed by viral-mediated production of adiponectin. Our results indicate that adiponectin should be one of key molecule of the metabolic syndrome and may be a new therapeutic target for the metabolic syndrome.

Adiponectin↗
PubMed2005

[Effect of conjugated linoleic acid on gene expression of adiponectin of obese rat fed with high fat diet].

OBJECTIVE: To study the effect of conjugated linoleic acid (CLA) on expression of adiponectin in white adipose tissue of obese rats. METHODS: Male Wistar rats were randomly divided into control group, high-fat group and high fat + CLA group (0.75 g, 1.50 g, 3.00 g per hundred gram diet weight), we observed the effect of CLA on serum insulin and glucose levels of obese rats, and the reverse transcription polymerase chain reaction (RT-PCR) technique was used to measure the expression level of adiponectin and peroxisome proliferator-activated receptor-gamma (PPARgamma) mRNA. RESULTS: The serum insulin and glucose levels of obese rats were (11.11 +/- 2.73) microIU/ml, (5.09 +/- 0.66) mmol/L. The supplement of CLA decreased the hyperinsulinemia and hyperglycemia, the serum insulin in CLA group (0.75 g, 1.50 g, 3.00 g per hundred gram diet weight) were (6.99 +/- 1.77) microIU/ml, (7.36 +/- 1.48) microIU/ml, (7.85 +/- 1.60) microIU/ml (P < 0.05), and glucose were (4.28 +/- 0.72) mmol/L, (4.18 +/- 0.55) mmol/L (P < 0.05), (4.06 +/- 0.63) mmol/L (P < 0.05), CLA can increase the expression of adiponectin and PPARgamma in adipose tissue of obese rat. CONCLUSION: The CLA might improve the insulin resistance of the obese rat and increase the expression of adiponectin mRNA, which might possibly act through activating PPARgamma.

Adiponectin↗
PubMed2006

Adiponectin receptor expression in the human adrenal cortex and aldosterone-producing adenomas.

Adiponectin is an adipocyte-derived circulating peptide that plays an important role in adipose tissue metabolism, insulin sensitivity and cardiovascular disease. The adrenal gland, by secreting glucorticoid and mineralocorticoid hormones, intervenes in cardiovascular and glucose metabolism regulation and is surrounded by adipose tissue. Hence, we investigated the hypothesis that adiponectin receptor types 1 and 2 (adipo-R1 and adipo-R2) are expressed in the human adrenal gland and in adrenocortical zona glomerulosa cell-derived aldosterone-producing adenoma (APA) tissue. We used real-time reverse transcription-polymerase chain reaction to demonstrate the mRNA of adipo-R1 and adipo-R2 in 10 histologically normal human adrenal cortexes that were obtained from patients with renal cancer undergoing nephrectomy with ipsilateral adrenalectomy and in 10 APAs. Melting curve analysis and sequencing were used to confirm the specificity of the amplicons obtained. Results consistently showed the expression of specific mRNAs of adiponectin receptors in all histologically normal human adrenal cortexes and APAs. This novel finding suggests that adiponectin could play a regulatory role in adrenocortical function and growth in humans.

Adrenal Cortex↗
PubMed2006

[The relationship between serum adiponectin level and serum alanine aminotransferase elevation in Korean male with nonalcoholic fatty liver disease].

BACKGROUND/AIMS: Nonalcoholic fatty liver disease (NAFLD) comprises a large part of chronic liver diseases. Recently it was reported that adipokines are closely associated with the common risk factors for NAFLD, such as obesity, diabetes, dyslipidemia, and insulin resistance. We aimed to evaluate the changes in serum adiponectin, resistin and leptin concentrations related to alanine aminotransferase (ALT) elevations in Korean men with NAFLD. METHODS: We studies 38 men who were diagnosed with fatty liver by abdominal ultrasonography. None had a history of excessive alcohol consumption, autoimmune hepatitis, inherited or metabolic liver disease or viral hepatitis. The subjects were divided into two groups. One group had normal levels of ALT (n=28) and the other had increased ALT (n=10). We compared anthropometrical parameters, biochemical items and serum adipokine levels between these two groups. RESULTS: Serum adiponectin levels were lower in the increased ALT group than in the normal ALT group (3.89 +/- 1.77 vs 7.01 +/- 2.54 microgram/dL, P=0.001). But there were no significant differences in serum leptin and resistin levels between two groups (4.02 +/- 2.04 vs 3.26 +/- 1.41 ng/mL, p=0.245, 80.14 +/- 14.8 vs 80.5 +/- 11.34 ng/mL, P=0.937, respectively). Multiple linear regression analyses demonstrated that the serum adiponectin level is inversely correlated with serum ALT level and that the serum aspartate aminotransferase (AST) level is positively correlated with the serum ALT level. CONCLUSIONS: Our study shows that hypoadiponectinemia is associated with an ALT elevation in patients with NAFLD. Adiponectin may play an indirect role in the development of NAFLD.

Adiponectin↗
PubMed2006

[The role of adiponectin in increased insulin sensitivity of patients with anorexia nervosa].

The aim of the present study was to determine the relationship between plasma levels of adipocytokine adiponectin and the degree of insulin sensitivity in patients with anorexia nervosa (AN). AN is a psychiatric disorder characterized mainly by severe malnutrition and loss of body fat. We measured fasting plasma adiponectin, insulin and glucose levels in ten women with a restrictive type of AN and in twelve healthy normal-weight women. Plasma adiponectin levels were significantly increased in patients with AN compared to healthy women (p < 0.01) and were negatively related to body mass index and percent body fat in both groups. Plasma adiponectin levels were negatively related to plasma insulin levels in the AN group only. Using homeostasis model assessment of insulin resistance (HOMA-IR), we found significantly increased insulin sensitivity in patients with AN compared to control women (p < 0.05). In conclusion, hyperadiponectinemia in patients with AN might contribute to increased insulin sensitivity in these patients.

Adiponectin↗
PubMed2006

Comparison of adiponectin, leptin and blood lipid levels in normal and obese postmenopausal women.

OBJECTIVE: To determine adiponectin, leptin and blood lipid levels in normal and obese postmenopausal women and to compare them. METHODS: Eighty postmenopausal women were selected which included 40 normal controls and 40 obese women matched for age and height. Adiponectin and leptin levels were determined by ELISA. Triglycerides, cholesterol, LDL cholesterol and HDL cholesterol were determined by standard kit methods using Clinicon 4010. RESULTS: Serum adiponectin level decreased and leptin level increased significantly (P < 0.001) in obese women compared to controls. Similarly triglycerides, cholesterol and LDL cholesterol were increased significantly (P < 0.001) in obese subjects compared with controls. No significant change in HDL cholesterol was observed in both groups. Significant correlation of leptin with lipid profile was observed when both groups were combined. CONCLUSION: Serum adiponectin level decreased and leptin level increased significantly in obese women compared to controls. Significant correlation exists between leptin and lipid profile in combined group.

Adiponectin↗
PubMed2004

Expression of key genes of fatty acid oxidation, including adiponectin receptors, in skeletal muscle of Type 2 diabetic patients.

AIMS/HYPOTHESIS: Defective oxidation of long-chain fatty acids is a feature of insulin resistance and Type 2 diabetes. Our aim was to compare the expression levels of the genes encoding the major proteins and enzymes of this pathway in skeletal muscle of healthy subjects and Type 2 diabetic patients. METHODS: The basal and insulin-regulated mRNA concentration of 16 genes was quantified using real-time PCR in skeletal muscle biopsies taken before and at the end of a 3-hour hyperinsulinaemic-euglycaemic clamp in healthy lean subjects and in insulin-resistant obese patients with manifest Type 2 diabetes. RESULTS: Acetyl CoA carboxylase-2 mRNA expression was increased 2.5-fold in the muscle of the diabetic patients. The expression of carnitine palmitoyl transferase-1, of the two adiponectin receptors and of genes involved in fatty acid transport and activation was not altered in diabetic patients. Hyperinsulinaemia for 3 hours increased the expression of several genes of fatty acid oxidation, including adiponectin receptor-1 and peroxisome proliferator-activated receptor gamma coactivator-1 alpha. It also reduced pyruvate dehydrogenase 4 mRNA levels. The effects of insulin on gene expression were markedly altered in the muscle of Type 2 diabetic patients except for adiponectin receptor-1 and pyruvate dehydrogenase 4 mRNAs. CONCLUSIONS/INTERPRETATION: The expression of adiponectin receptors was not altered in the muscle of Type 2 diabetic patients. The observed overexpression of acetyl CoA carboxylase-2 is consistent with the hypothesis that increased skeletal muscle malonyl CoA concentrations in Type 2 diabetes may contribute to the inhibition of long-chain fatty acid oxidation.

Blood Glucose↗
PubMed2005

Implications of decreased serum adiponectin for type IIb hyperlipidaemia and increased cholesterol levels of very-low-density lipoprotein in type II diabetic patients.

The present study was performed to investigate the relevance of cholesterol levels of plasma lipoproteins [HDL (high-density lipoprotein), LDL (low-density lipoprotein), IDL (immediate-density lipoprotein), VLDL (very-LDL) and chylomicrons] determined by a novel HPLC method, with adiponectin, which is decreased in Type II diabetes and assumed to be involved in dysregulated metabolism and atherogenesis. Type II diabetic patients who were not treated with insulin, statins and fibrates were enrolled. Study subjects included Type II diabetic patients with normolipidaemia (DM-NL; n=15), type 4 hyperlipidaemia (DM-T4HL; n=13), Type IIa hyperlipidaemia (DM-T2aHL; n=15) and Type IIb hyperlipidaemia (DM-T2bHL; n=13). Fasting blood samples were collected. The serum adiponectin level was lower in DM-T2bHL than in any of the other groups. Cholesterol levels of each lipoprotein fraction, serum triacylglycerol (triglyceride), remnant-like particle-cholesterol, fasting plasma glucose, HbA1c (glycated haemoglobin), age, gender difference and BMI (body mass index) were incorporated into a stepwise regression analysis as independent variables. VLDL-cholesterol correlated inversely with adiponectin independently of age, BMI, gender difference and glycaemic control. Although the mechanisms remain to be explored, serum adiponectin was reduced particularly in Type II diabetics with type IIb hyperlipidaemia and correlated inversely with VLDL-cholesterol. Measuring VLDL-cholesterol may be helpful for understanding the pathological features of diabetic dyslipidaemia.

Adult↗
PubMed2006

Leptin and Adiponectin in the HIV Associated Metabolic Syndrome: Physiologic and Therapeutic Implications.

Leptin and adiponectin represent two newly discovered adipose tissue derived hormones with important roles in energy homeostasis and insulin resistance. Their interrelations with the manifestations of the HIV associated metabolic syndrome and specific somatomorphic changes i.e. fat redistribution is reviewed. A synopsis of published studies is presented and the potential role of leptin and adiponectin is discussed. We have described an association of the HIV metabolic syndrome with a state of reduced insulin sensitivity due to adiponectin deficiency. The metabolic syndrome is also accompanied by leptin deficiency in lipoatrophic subjects and possibly by a leptin resistance state in lipohypertrophic patients. Adiponectin and / or leptin therapy in a manner similar to other leptin deficiency states may assist in the future management of such patients.

Journal Article↗
PubMed2005

Regulation of adiponectin receptor 1 in human hepatocytes by agonists of nuclear receptors.

The adiponectin receptors AdipoR1 and AdipoR2 have been identified to mediate the insulin-sensitizing effects of adiponectin. Although AdipoR2 was suggested to be the main receptor for this adipokine in hepatocytes, AdipoR1 protein is highly abundant in primary human hepatocytes and hepatocytic cell lines. Nuclear receptors are main regulators of lipid metabolism and activation of peroxisome proliferator-activated receptor alpha and gamma, retinoid X receptor (RXR), and liver X receptor (LXR) by specific ligands may influence AdipoR1 abundance. AdipoR1 protein is neither altered by RXR or LXR agonists nor by pioglitazone. In contrast, fenofibric acid reduces AdipoR1 whereas hepatotoxic troglitazone upregulates AdipoR1 protein in HepG2 cells. Taken together this work shows for the first time that AdipoR1 protein is expressed in human hepatocytes but that it is not a direct target gene of nuclear receptors. Elevated AdipoR1 induced by hepatotoxic troglitazone may indicate a role of this receptor in adiponectin-mediated beneficial effects in liver damage.

Adiponectin↗
PubMed2005

Adiponectin inhibits Toll-like receptor family-induced signaling.

Recent studies have shown that adiponectin, an adipocyte-derived cytokine, acts as a potent inhibitor of inflammatory responses. It has been also demonstrated that bacterial and viral signalings in host cells are triggered via Toll-like receptor (TLR) molecules. Therefore, in the present study, we investigated whether globular adiponectin (gAd) would be able to inhibit TLR-mediated nuclear factor-kappaB (NF-kappaB) signaling in mouse macrophages (RAW264). gAd predominantly bound to the AdipoR1 receptor and suppressed TLR-mediated NF-kappaB signaling. gAd-mediated inhibition of TLR-mediated IkappaB phosphorylation and NF-kappaB activation was eliminated by the pretreatment of cycloheximide. Also their inhibitions of gAd were blocked by preincubation of the cells with an antibody against AdipoR1, but not with an antibody against AdipoR2. Taken together, these findings indicate that adiponectin negatively regulates macrophage-like cell response to TLR ligands via an unknown endogenous product(s).

3T3-L1 Cells↗