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PubMed2006

[Adiponectin, a new hormone: its role in the pathogenesis of diabetes mellitus].

Adiponectin is a hormone of adipose tissue, activating lipid metabolism and other physiological functions. Adiponectin deficiency induces obesity and decreases insulin-regulated carbohydrate metabolism, thus leading to insulin resistance. Blood level of adiponectin falls in type 2 diabetes. Adiponectin receptors--AdipoR1 and AdipoR2--are proteins with 7 transmembrane domains, which are synthesized mostly in muscles and the liver and function in a close connection with G proteins. Obesity and diabetes lower the tissue concentration of the receptors, thus impeding adiponectin regulation of lipid exchange and lowering the effectiveness of the insulin control of carbohydrate exchange. Adiponectin also influences cardiovascular functions and prevents atherosclerosis and some of the other kinds of vascular pathology.

Adiponectin↗
PubMed2004

Beyond insulin resistance in NASH: TNF-alpha or adiponectin?

Adiponectin has antilipogenic and anti-inflammatory effects, while tumor necrosis factor alpha (TNF-alpha) reduces insulin sensitivity and has proinflammatory effects. We examined (1) the extent to which hypoadiponectinemia and TNF-alpha activation are features of nonalcoholic steatohepatitis (NASH) and (2) whether serum levels of these markers correlate with the severity of histological changes in 109 subjects with nonalcoholic fatty liver disease (NAFLD), including 80 with NASH and 29 with simple steatosis. By multivariate analysis, subjects with NASH had reduced adiponectin level and increased TNF-alpha and soluble TNF receptor 2 (sTNFR2)-but not leptin levels, compared with controls matched by age, sex, and body mass index; these differences were independent of the increased insulin resistance (by homeostasis model [HOMA-IR]) in NASH. When compared with simple steatosis, NASH was associated with lower adiponectin levels and higher HOMA-IR, but there were no significant differences in the levels of TNF-alpha and sTNFR2. The majority of subjects with steatohepatitis (77%) had adiponectin levels less than 10 microg/mL and HOMA-IR greater than 3 units, but only 33% of those with pure steatosis had these findings. HOMA-IR and low serum adiponectin were also independently associated with increased grades of hepatic necroinflammation. In conclusion, hypoadiponectinemia is a feature of NASH independent of insulin resistance. Reduced adiponectin level is associated with more extensive necroinflammation and may contribute to the development of necroinflammatory forms of NAFLD.

Adiponectin↗
PubMed2005

Adipokines in NASH: postprandial lipid metabolism as a link between adiponectin and liver disease.

Circulating levels of four adipokines (adiponectin, TNF-alpha, leptin, and resistin) and the postprandial lipid and adiponectin responses to an oral fat load were assessed in 25 non-obese, non-diabetic patients with biopsy-proven nonalcoholic steatohepatitis (NASH) and correlated with metabolic indices and liver histology. Circulating adiponectin was lower in NASH compared with controls (5,476 +/- 344 vs. 11,548 +/- 836 ng/mL; P = .00001) and on multiple regression analysis correlated negatively with liver steatosis, necroinflammation (OR = 5.0; P = .009), and fibrosis (OR = 8.0; P = .003). The magnitude of postprandial lipemia was significantly higher in NASH than in controls and was related to fasting adiponectin (beta = -0.78; P = .00003). Controls showed a significant increase in serum adiponectin in response to the fat load, whereas patients with NASH showed a slight decrease. Postprandial free fatty acids response correlated inversely with adiponectin response in both groups and independently predicted the severity of liver steatosis in NASH (beta = 0.51; P = .031). In conclusion, hypoadiponectinemia is present before overt diabetes and obesity appear and correlates with the severity of liver histology in NASH. Impaired postprandial lipid metabolism may be an additional mechanism linking hypoadiponectinemia and NASH and posing a higher cardiovascular risk to these subjects. The mechanism(s) underlying these differences are unknown, but the type of dietary fat seems to play a role. These findings may have important pathogenetic and therapeutic implications in both liver and metabolic disease.

Adiponectin↗
PubMed2005

Adiponectin induces growth arrest and apoptosis of MDA-MB-231 breast cancer cell.

Recently, it was reported that reduction in serum adiponectin levels is correlated with the incidence of breast cancer. As an effort to explain this, we screened various human breast cancer cell lines to identify those in which proliferation is directly controlled by adiponectin. Among the five tested cell lines, proliferation of MDA-MB-231 cancer cell was significantly suppressed by adiponectin within the range of physiological concentration. Furthermore, prolonged adiponectin treatment caused cell growth arrest and even apoptosis of MDA-MB-231. This result is the first to show that adiponectin can directly control cancer cell growth and provides a rationale for the theory that reduction in plasma adiponectin levels could be a risk factor for breast cancer.

Adiponectin↗
PubMed2003

Globular adiponectin upregulates nitric oxide production in vascular endothelial cells.

AIMS/HYPOTHESIS: Adiponectin, also called ACRP30, is a novel adipose tissue-specific protein that has been shown to improve insulin sensitivity and to exert anti-atherogenic effects. It is known that knockout mice lacking endothelial NO synthase (eNOS) develop hypertension, insulin resistance, hyperlipidaemia, and show augmented ischaemia-reperfusion damage. Thus, we examined whether globular adiponectin activates eNOS to produce NO. METHODS: To analyze NO production in bovine aortic endothelial cells (BAE), NOx (nitrite and nitrate) was measured in the medium with an automated NO detector/high-performance liquid chromatography system. eNOS activation was assessed by phosphorylation of the enzyme and its activity was evaluated by citrulline synthesis in human umbilical vein endothelial cells (HUVEC). eNOS mRNA and protein expressions in HUVEC were evaluated by Realtime PCR and Western blot analysis. RESULTS: Gobular adiponectin increased NO production in BAE. It also caused eNOS phosphorylation and potentiated eNOS activity in HUVEC. In addition, globular adiponectin up-regulated the eNOS gene to increase protein expression in HUVEC. CONCLUSION/INTERPRETATION: Globular adiponectin increases NO production through two mechanisms, namely, by activation of eNOS enzyme activity and via an increase in eNOS expression. Activation and up-regulation of eNOS could explain some of the observed vasoprotective properties of globular adiponectin, as well as its beneficial effects on the cardiovascular system.

Adiponectin↗
PubMed2004

The prospective association between adiponectin and coronary artery disease among individuals with type 1 diabetes. The Pittsburgh Epidemiology of Diabetes Complications Study.

AIMS/HYPOTHESIS: Recent findings suggest the potential involvement of adiponectin in obesity, diabetes and cardiovascular disease. We assessed the prospective association between adiponectin concentration and coronary artery disease in individuals with type 1 diabetes. METHODS: Participants were identified from the Pittsburgh Epidemiology of Diabetes Complications cohort, a prospective follow-up study of childhood-onset type 1 diabetes. At baseline, subjects had a mean age of 28 years, and a mean diabetes duration of 19 years. Cases (determined by physician-diagnosed angina, confirmed myocardial infraction, stenosis >or=50%, ischemic ECG or revascularization) were matched to the control subjects with respect to sex, age and diabetes duration. Samples and risk factors for analyses were identified from the earliest exam prior to incidence in cases. Sera and information on all covariates were available for 28 cases and 34 control subjects. Proportional hazards models were constructed including matching variables. RESULTS: Compared with those in men, adiponectin concentrations were elevated in females (p=0.009) and among individuals with macroalbuminuria (p=0.04). In multivariable analyses (adjusting for standard risk factors as well as lipoprotein measurements determined by nuclear magnetic resonance spectroscopy, E-selectin or antioxidants), adiponectin inversely predicted the incidence of coronary artery disease (hazard ratio=0.37 per 1 SD increase, 95% CI 0.19-0.73, p=0.004). CONCLUSIONS/INTERPRETATION: The results suggest that increased adiponectin concentration is prospectively associated with a lower risk of coronary artery disease type 1 diabetes. The potential of adiponectin determination as a useful marker of, and potential therapeutic target for, coronary artery disease prevention in type 1 diabetes should be further explored.

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PubMed2006

Adiponectin and leptin: potential tools in the differential diagnosis of pediatric diabetes?

The incidence of type 1 and type 2 diabetes mellitus in the pediatric population has increased over the past decade. The practitioner is often faced with the challenge of differentiating between type 1 and type 2 diabetes at the time of initial diagnosis because of the overlap of clinical and laboratory characteristics between these two entities. Adipokines are proteins secreted by the adipose tissue. Leptin and adiponectin are two adipokines that have been extensively studied in vitro, in animal studies, and in human subjects with type 1 and type 2 diabetes. Leptin and adiponectin play a significant role in the regulation of lipid and carbohydrate metabolism. Adiponectin increases insulin sensitivity in both the liver and skeletal muscle. Leptin decreases appetite, increases energy expenditure, suppresses insulin synthesis and secretion and increases insulin sensitivity. Changes in the secretion or sensitivity to leptin and adiponectin may contribute to the development of type 1 and type 2 diabetes. Adiponectin is higher in adult and pediatric patients with type 1 diabetes compared to those with type 2 diabetes. Data regarding leptin levels are contradictory. Most studies report decreased serum leptin at the time of diagnosis in type 1 diabetes compared to type 2 diabetes subjects and non-diabetic controls. This paper will review basic research and clinical evidence supporting the role of adiponectin and leptin in the development of type 1 and type 2 diabetes and discuss their potential use as tools in the differential diagnosis of pediatric diabetes.

Adiponectin↗
PubMed2004

Decreased plasma adiponectin concentrations in women with gestational diabetes mellitus.

OBJECTIVE: Adiponectin is an adipocyte-specific protein that has been found to be associated with insulin sensitivity and obesity. Because gestational diabetes mellitus is associated with obesity and decreased insulin sensitivity, we have analyzed plasma adiponectin levels in women with gestational diabetes mellitus. STUDY DESIGN: Twenty women with gestational diabetes mellitus and 21 unaffected women were included in the study. Plasma adiponectin levels were analyzed with the use of enzyme-linked immunosorbent assay. RESULTS: Women with gestational diabetes mellitus were significantly older (34.3 years vs 29.4 years; P < .001) than unaffected women. Adiponectin plasma levels were significantly lower in women with gestational diabetes mellitus when compared with women without gestational diabetes mellitus (5827 +/- 1988 ng/mL vs 8085 +/- 3816 ng/mL; P = .02). Adiponectin plasma levels were correlated negatively with plasma glucose concentrations of the oral glucose tolerance test ( r > -0.38; P < .04) and correlated positively with gestational age ( r = 0.36; P = .03). CONCLUSION: Our data show that decreased plasma adiponectin levels were found in women with gestational diabetes mellitus compared with unaffected women.

Adiponectin↗
PubMed2005

Adiponectin, insulin resistance, and left ventricular structure in dipper and nondipper essential hypertensive patients.

BACKGROUND: Adiponectin is an adipocyte-derived protein with insulin-sensitizing and antiatherogenic properties. Failure to decrease blood pressure (BP) normally during night in hypertensive patients has been independently associated with left ventricular hypertrophy. METHODS: We examined the relationship between adiponectin levels, insulin sensitivity, and left ventricular structure in 40 newly diagnosed never-treated patients with essential hypertension, including 20 patients with a normal night-time pressure decrease (ie, dippers) and 20 patients with BP persistently elevated throughout the 24-h period (ie, nondippers). All subjects had grade 1-2 hypertension, aged 18 to 65 years, no diabetes mellitus, no obesity, no hyperlipidemia, and no cardiopulmonary, renal, or hepatic disease. RESULTS: The two groups of patients were similar for age, sex, body mass index, and had no differences for clinic, 24-h, and diurnal BP, and 24-h, diurnal, and nocturnal heart rate, as well as glucose, total cholesterol, and triglyceride levels. Plasma insulin and homeostasis model assessment (HOMA index) were higher (P < .01), and adiponectin levels were lower (P < .005) in nondippers than in dippers. Adiponectin correlated inversely with HOMA index and insulin levels (r = -0.58, and r = -0.62, respectively, P < .001) in the entire population. Nondippers showed left ventricular mass, relative wall thickness, and measure of early and late diastolic peak flow velocity ratio similar to those of dippers. CONCLUSIONS: In the absence of major cardiovascular risk factors, nondipper essential hypertensive patients show more prominent insulin resistance and lower adiponectin compared to dippers. Therapeutic modulation of adiponectin or insulin resistance might provide additional benefit to the conventional antihypertensive treatment.

Adiponectin↗
PubMed2006

Low birth weight is associated with reduced adiponectin concentration in adult.

PURPOSE: Low birth weight has been associated with metabolic and vascular diseases, but the precise mechanism is debated. Adiponectin is one of the key molecules in metabolic disease, and a decrease in level precedes the onset of type 2 diabetes and development of atherosclerosis. Our aim is to examine whether low birth weight is associated with adiponectin concentration in adult. METHODS: We conducted a population-based cross-sectional study of 2277 subjects (1661 men and 616 women) aged 35 to 66 years who had their self-reported birth weights and adiponectin concentrations measured as adults. RESULTS: After adjusting for potential confounders, including age, sex, current body mass index (BMI), smoking status, alcohol consumption, and exercise, geometric mean adiponectin levels were 6.63, 6.45, 6.86, 7.05, 6.75, and 7.22 microg/mL for subjects with birth weights less than 2500, 2500 to less than 2800, 2800 to less than 3000, 3000 to less than 3200, 3200 to less than 3500, and greater than 3500 g, respectively. A positive association was found between birth weight and adiponectin concentration (trend p = 0.002). Stratified by current BMI of 25 kg/m2, a positive association was not observed for subjects with a BMI less than 25 kg/m2, but was pronounced in those with a BMI of 25 kg/m2 or greater. CONCLUSION: This study indicates that low birth weight contributes to decreased adiponectin concentrations in adult life independently of current BMI, especially for obese subjects.

Adiponectin↗
PubMed2006

Adiponectin and its gene variants as risk factors for insulin resistance, the metabolic syndrome and cardiovascular disease.

The increasing prevalence of obesity and metabolic syndrome/insulin resistance has attracted considerable interest due to their identification as risk factors for cardiovascular disease and, hence, targets for cardiovascular disease prevention. This review focuses on adiponectin, the most profusely secreted protein from adipose tissue, which itself is being increasingly recognised as an important and very active endocrine organ, secreting a wide range of biologically active substances known as adipokines or adipocytokines. Adiponectin has been demonstrated to have insulin sensitising effects, and secretion of adiponectin is reduced as adipose tissue mass increases. Adiponectin has also been demonstrated to have anti-inflammatory and anti-atherogenic properties, and is independently associated with cardiovascular disease. The evidence that suggests adiponectin plays a role in the relationship between obesity and insulin resistance, and also insulin resistance and cardiovascular disease, is examined. Variation in the adiponectin gene is one tool to determine whether this relationship is causal. The association of identified variants with human disease, specifically obesity and its consequences, type 2 diabetes and cardiovascular disease is reviewed. This data may enable patients at greater risk of the adverse effects of obesity to be identified and, as such, benefit from more targeted therapy of its consequences.

Adiponectin↗
PubMed2006

Pravastatin improved glucose metabolism associated with increasing plasma adiponectin in patients with impaired glucose tolerance and coronary artery disease.

Reduced incidence of type-2 diabetes has been shown in patients treated with pravastatin. Adiponectin can exhibit beneficial effects on glucose metabolism. We investigated whether pravastatin could improve glucose tolerance associated with increasing adiponectin levels in patients with impaired glucose tolerance (IGT). This study consisted of 40 coronary artery disease (CAD) patients with IGT assessed by oral glucose tolerance test (OGTT). Patients were randomized to receive pravastatin (n=20) or no lipid-lowering medications (control group, n=20) for 6 months, after which OGTT was repeated and adiponectin levels were measured. Pravastatin treatment significantly decreased levels of total cholesterol (16%), low-density lipoprotein cholesterol (23%) and high-sensitivity C-reactive protein (37%) (p<0.01, respectively). At 2h in OGTT, pravastatin significantly improved hyperglycemia (-14%) and hyperinsulinemia (-23%). Pravastatin treatment significantly elevated plasma adiponectin levels (35%; p<0.001) but not in the control group. The glucose reduction at 2h post-OGTT was significantly associated with increased levels of adiponectin (r=-0.462; p=0.003). Pravastatin treatment is an independent predictor for improvement of post-loaded hyperglycemia (odds ratio; 5.7; 95% confidence interval 1.7-19.3; p=0.003) and achieved beneficial conversion from IGT to normal glucose tolerance (40%; p=0.03). Pravastatin exhibits beneficial effects on glucose metabolism especially in the postprandial state associated with increasing plasma adiponectin levels in CAD patients with IGT.

Adiponectin↗
PubMed2006

Insulin and adiponectin inhibit the TNFalpha-induced ADMA accumulation in human endothelial cells: the role of DDAH.

OBJECTIVE: Insulin and adiponectin exert important effects on the vasculature. We wanted to explore whether the eNOS inhibitor asymmetric dimethylarginine (ADMA) contribute to their effects. METHODS: Human umbilical vein endothelial cells (HUVECs) and human coronary artery endothelial cells (HCAECs) were incubated with growth medium in the presence or absence of tumor necrosis factor-alpha (TNFalpha), D-glucose, insulin or adiponectin. Further, cells exposed to TNFalpha for 24h were co-stimulated with insulin or adiponectin for additional 24h. Concentrations of ADMA in conditioned media and activity of dimethylarginine dimethylaminohydrolase (DDAH) in cell lysates were determined. RESULTS: The dose-dependent TNFalpha-induced ADMA accumulation was significantly inhibited when co-stimulated with insulin or adiponectin in both cell lines (p<0.01 for all), accompanied by significant increases in DDAH activity in all conditions. Insulin alone resulted in a significant, but inversely dose-dependent accumulation of ADMA as compared to control cells in both cell lines, accompanied by increased DDAH activity. Adiponectin alone tended, dose-dependently to decrease ADMA, but without an increase of DDAH activity. CONCLUSION: The results indicate that ADMA accumulation in human cultured endothelial cells is influenced by both insulin and adiponectin, and both mediators counteract the TNFalpha-induced accumulation of ADMA through the DDAH pathway.

Adiponectin↗
PubMed2005

Adiponectin: Identification, physiology and clinical relevance in metabolic and vascular disease.

Adiponectin is the most abundant adipose-specific protein. Its expression is reduced in obesity, insulin resistance and type 2 diabetes, and plasma concentrations are inversely related to body weight, especially visceral adiposity. Adiponectin is also inversely associated with other traditional cardiovascular risk factors, such as blood pressure, low-density lipoprotein cholesterol and triglyceride levels, and is positively related to high-density lipoprotein cholesterol (HDL-C) levels. Recent research has indicated that adiponectin has anti-inflammatory, anti-atherogenic and antidiabetic properties. The ability of adiponectin to reduce insulin resistance in conjunction with its anti-inflammatory and anti-atherogenic properties makes this novel adipocytokine a promising therapeutic target, and agents that enhance adiponectin secretion or action have potential for treatment of metabolic and vascular disease. Current management strategies that may increase endogenous adiponectin production in humans include weight loss, soy protein and therapy with peroxisome proliferator-activating receptor gamma (PPARgamma) agonists.

Adiponectin↗
PubMed2004

Adiponectin down-regulates acyl-coenzyme A:cholesterol acyltransferase-1 in cultured human monocyte-derived macrophages.

Acyl-coenzyme A:cholesterol acyltransferase-1 (ACAT-1) catalyzes the formation of cholesteryl esters (CE) and plays a significant role in formation of macrophage-derived foam cells in atherosclerotic lesions. Adiponectin was reported to play an anti-atherogenic role by inhibiting class A scavenger receptor (SR-A) expression in human macrophages. To further clarify its additional property, we examined its effect on ACAT-1 expression using human macrophages. Immunoblot analyses revealed a significant reduction of ACAT-1 protein by a low concentration (1 microg/ml) of adiponectin. The ACAT activity was also decreased in parallel by adiponectin. Northern blot analyses revealed that all four ACAT-1 mRNA transcripts (2.8, 3.6, 4.3, and 7.0 kb) were decreased almost equally by adiponectin. Furthermore, acetyl-LDL-induced CE-accumulation in these macrophages was reduced significantly by this adipocytokine. These results demonstrate the inhibitory effect of adiponectin on ACAT-1 expression, suggesting that adiponectin may play an anti-atherogenic role by down-regulating the expression of ACAT-1 as well as SR-A in human macrophages.

Adiponectin↗
PubMed2004

Adiponectin induces the anti-inflammatory cytokines IL-10 and IL-1RA in human leukocytes.

There is increasing evidence that the adipose tissue and immunologic processes are closely linked. The most abundant protein within the adipocyte is adiponectin. Our current work reports that adiponectin has potent immuno-suppressive properties, as it induces the production of the anti-inflammatory mediators IL-10 and IL-1RA in primary human monocytes, monocyte-derived macrophages, and dendritic cells. In addition, adiponectin significantly impaired the production of the pro-inflammatory cytokine IFN-gamma in human macrophages. Moreover, adiponectin-treated macrophages exhibit a reduced phagocytotic and allo-stimulatory capacity. However, we could not detect any functional deficits or phenotypic changes in adiponectin-treated monocytes and monocyte-derived DC. In summary, the presented data support the idea that adiponectin might be of critical relevance for cytokine regulation in obesity and fatty liver diseases affecting primarily macrophage functions. This might represent a fundamental link between over-nutrition and an impaired inflammatory immune response.

Adiponectin↗
PubMed2006

Hypoxia dysregulates the production of adiponectin and plasminogen activator inhibitor-1 independent of reactive oxygen species in adipocytes.

Low plasma levels of adiponectin (hypoadiponectinemia) and elevated circulating concentrations of plasminogen activator inhibitor (PAI)-1 are causally associated with obesity-related insulin resistance and cardiovascular disease. However, the mechanism that mediates the aberrant production of these two adipokines in obesity remains poorly understood. In this study, we investigated the effects of hypoxia and reactive oxygen species (ROS) on production of adiponectin and PAI-1 in 3T3-L1 adipocytes. Quantitative PCR and immunoassays showed that ambient hypoxia markedly suppressed adiponectin mRNA expression and its protein secretion, and increased PAI-1 production in mature adipocytes. Dimethyloxallyl glycine, a stabilizer of hypoxia-inducible factor 1alpha (HIF-1alpha), mimicked the hypoxia-mediated modulations of these two adipokines. Hypoxia caused a modest elevation of ROS in adipocytes. However, ablation of intracellular ROS by antioxidants failed to alleviate hypoxia-induced aberrant production of adiponectin and PAI-1. On the other hand, the antioxidants could reverse hydrogen peroxide (H2O2)-induced dysregulation of adiponectin and PAI-1 production. H2O2 treatment decreased the expression levels of peroxisome proliferator-activated receptor gamma (PPARgamma) and CCAAT/enhancer binding protein (C/EBPalpha), but had no effect on HIF-1alpha, whereas hypoxia stabilized HIF-1alpha and decreased expression of C/EBPalpha, but not PPARgamma. Taken together, these data suggest that hypoxia and ROS decrease adiponectin production and augment PAI-1 expression in adipocytes via distinct signaling pathways. These effects may contribute to hypoadiponectinemia and elevated PAI-1 levels in obesity, type 2 diabetes, and cardiovascular diseases.

3T3-L1 Cells↗
PubMed2006

Aldehyde oxidase 1 is highly abundant in hepatic steatosis and is downregulated by adiponectin and fenofibric acid in hepatocytes in vitro.

Adiponectin protects the liver from steatosis caused by obesity or alcohol and therefore the influence of adiponectin on human hepatocytes was analyzed. GeneChip experiments indicated that recombinant adiponectin downregulates aldehyde oxidase 1 (AOX1) expression and this was confirmed by real-time RT-PCR and immunoblot. AOX1 is a xenobiotic metabolizing protein and produces reactive oxygen species (ROS), that promote cell damage and fibrogenesis. Adiponectin and fenofibric acid activate peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and both suppress AOX1 protein and this is blocked by the PPAR-alpha antagonist RU486. Obesity is associated with low adiponectin, reduced hepatic PPAR-alpha activity and fatty liver, and AOX1 was found induced in the liver of rats on a high-fat diet when compared to controls. Free fatty acids and leptin, that are elevated in obesity, failed to upregulate AOX1 in vitro. The current data indicate that adiponectin reduces AOX1 by activating PPAR-alpha whereas fatty liver disease is associated with elevated hepatic AOX1. High AOX1 may be associated with higher ROS well described to induce fibrogenesis in liver tissue but may also influence drug metabolism and activity.

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