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PubMed2006

The influence of hormonal changes during menstrual cycle on serum adiponectin concentrations in healthy women.

Adiponectin is an adipocyte-derived hormone involved in the regulation of carbohydrate and lipid metabolism. Its concentrations are decreased in patients with obesity, type 2 diabetes and atherosclerosis and are higher in females than in males. Gender differences of adiponectin levels raise the possibility that sex hormones directly regulate its serum concentrations, which may in turn influence insulin sensitivity in different phases of the menstrual cycle. To test this hypothesis we measured serum adiponectin, estradiol, progesterone, luteinizing hormone and follicle-stimulating hormone concentrations daily throughout the menstrual cycle in six healthy women. Mean adiponectin levels strongly positively correlated with serum cortisol concentrations [R=0.94286; p=0.0048 (Spearman correlation test)], but were not significantly related to other anthropometric, biochemical and hormonal characteristics of the subjects (BMI, blood glucose, insulin, testosterone, prolactin, cholesterol, HDL cholesterol, LDL cholesterol, triglycerides concentrations, or atherogenic index). Furthermore, no significant changes of serum adiponectin levels were found throughout the menstrual cycle. We conclude that changes in sex hormones during the menstrual cycle do not affect total circulating adiponectin levels in healthy women. Therefore, the differences in insulin sensitivity in various phases of the menstrual cycle are not due to changes of circulating adiponectin levels.

Adiponectin↗
PubMed2005

Adiponectin as a protective factor in hepatic steatosis.

AIM: Obesity and insulin resistance (IR) are closely related to hepatic steatosis (HS), and adiponectin is a hepatic insulin sensitizer that has important effects in liver function. This study aims at investigating the relationship between serum adiponectin concentration and the presence of HS. METHODS: We carried out a cross-sectional study in a check-up unit of a University Hospital in Mexico City. We enrolled 196 subjects, comprising 98 subjects with HS (27 women, 71 men) and 98 controls (37 women and 61 men). Anthropometric, metabolic and biochemical variables were measured in the two groups. Serum adiponectin and leptin concentrations were determined, their association with grade of HS tested, and concentrations, according to quartiles, compared between cases and controls. chi(2) analysis for linear trends was used to test for a dose-response relationship and logistic regression analysis was conducted to test for a protective effect of adiponectin. RESULTS: The HS subjects were older and more obese than controls, with a central obesity pattern. In the fourth quartile of adiponectin concentrations, HS was less common and severe. In a multivariate model of the fourth quartile of the adiponectin concentrations, we observed a protective effect (OR = 0.17, 95%CI: 0.04-0.67, P = 0.01). In subjects with more severe HS, we observed higher leptin concentrations, and caloric intakes, total fat and iron consumption were higher than in controls. CONCLUSION: The results of the present study suggest that a high serum concentration of adiponectin is associated with a protective effect against HS.

Adiponectin↗
PubMed2006

[Relationship between adiponectin and beta-cell function in abdominal visceral obesity women].

OBJECTIVE: To investigate the relationship between adiponectin and beta-cell function in abdominal visceral obesity women. METHODS: Nine abdominal visceral obesity women (VO), 9 normal subjects (C) and 7 patients with type 2 diabetes mellitus (T2DM) were enrolled in the study. Beta-cell function and insulin sensitivity were determined by hyperglycemic clamp, fasting serum adiponectin was assayed by ELISA and regional body fat was measured by MRI. RESULT: The levels of first phase insulin release (FPIR), glucose disposal rates (GDR), insulin sensitivity index (ISI) and adiponectin were significantly elevated in control group compared with VO group and T2DM group. As compared with T2DM group, the levels of adiponectin, FPIR, second phase insulin release (SPIR) and maximum insulin release (INS(max)) increased significantly in VO group. Multiple stepwise regression analysis showed that age, FPIR and GDR were positively correlated to adiponectin (B=0.145, 0.194, 0.277 respectively, all P<0.05), while waist-hip ratio was negatively correlated with adiponectin (B=-7.424, P<0.05). CONCLUSION: The visceral obesity women have lower adiponectin levels, and hyperadiponectinemia may be the link with insulin secretion.

Abdominal Fat↗
PubMed2003

Adiponectin, a fat cell product, influences the earliest lymphocyte precursors in bone marrow cultures by activation of the cyclooxygenase-prostaglandin pathway in stromal cells.

Adiponectin, an adipocyte-derived hormone, is attracting considerable interest as a potential drug for diabetes and obesity. Originally cloned from human s.c. fat, the protein is also found in bone marrow fat cells and has an inhibitory effect on adipocyte differentiation. The aim of the present study is to explore possible influences on lymphohematopoiesis. Recombinant adiponectin strongly inhibited B lymphopoiesis in long-term bone marrow cultures, but only when stromal cells were present and only when cultures were initiated with the earliest category of lymphocyte precursors. Cyclooxygenase inhibitors abrogated the response of early lymphoid progenitors to adiponectin in stromal cell-containing cultures. Furthermore, PGE(2), a major product of cyclooxygenase-2 activity, had a direct inhibitory influence on purified hematopoietic cells, suggesting a possible mechanism of adiponectin action in culture. In contrast to lymphopoiesis, myelopoiesis was slightly enhanced in adiponectin-treated bone marrow cultures, and even when cultures were initiated with single lymphomyeloid progenitors. Finally, human B lymphopoiesis was also sensitive to adiponectin in stromal cell cocultures. These results suggest that adiponectin can negatively and selectively influence lymphopoiesis through induction of PG synthesis. They also indicate ways that adipocytes in bone marrow can contribute to regulation of blood cell formation.

Adipocytes↗
PubMed2003

Decreased plasma adiponectin levels in young obese males.

Plasma adiponectin levels are reduced in middle-aged obesity and in patients with type 2 diabetes and coronary artery disease. The purpose of this study was to investigate the effects of early-aged obesity on plasma adiponectin level. Twenty-six male college students (19.2 +/- 1.1 years, obese group: n = 15, [body mass index > 25, percent body fat > 25%], non-obese group: n = 11) participated in the present study. We measured anthropometric parameters and plasma adiponectin and leptin level. Plasma adiponectin levels in the obese group were significantly lower than those in the non-obese group (obese: 4.7 +/- 2.0 micro g/ml, non-obese: 6.8 +/- 2.2 micro g/ml, p < 0.05). On the other hand, plasma leptin levels in the obese group were significantly higher than those in the non-obese group (obese: 8.4 +/- 3.2 ng/ml, non-obese: 2.6 +/- 2.1 ng/ml, p < 0.001). Plasma adiponectin levels were significantly correlated with body weight (r = -0.415, p < 0.05) and percent body fat (r = -0.412, p < 0.05). Stepwise multiple regression analysis revealed that percent body fat was a significant independent predictor of plasma adiponectin level (r = 0.406, p < 0.05). These results show that obesity is associated with reduced plasma adiponectin even in young subjects.

Adiponectin↗
PubMed2005

Caribbean female patients with type 2 diabetes mellitus have lower serum levels of adiponectin than nondiabetic subjects.

BACKGROUND: Previous studies in other populations suggest that low levels of serum adiponectin may be a cardiovascular risk factor. We aimed to determine the baseline concentration of serum adiponectin and its relationship with selected biochemical risk factors for coronary artery disease (CAD) in a cross-section of Caribbean patients with type 2 diabetes. METHODS: Anthropometric indices and fasting plasma concentrations of glucose, insulin, adiponectin, triglyceride, and total and HDL cholesterol were measured in 56 type 2 diabetic patients and 33 nondiabetic subjects. Insulin resistance (IR) was determined using the homeostatic model assessment (HOMA) method. RESULTS: Consistent with previous reports, Caribbean type 2 diabetic patients had significantly lower fasting serum adiponectin levels and higher mean levels of glucose, triglyceride and IR than the nondiabetic subjects (all, p < 0.01). The nondiabetic female subjects had significantly higher serum adiponectin levels than did the female diabetics or nondiabetic males (p < 0.01). Serum adiponectin level was negatively correlated with triglyceride or LDL cholesterol and positively related with HDL cholesterol among nondiabetic subjects, and the latter relationship persisted after adjusting for the effects of age, sex and BMI (r = 0.70, p < 0.01). CONCLUSION: Similar to reports from other populations, Caribbean patients with type 2 diabetes, particularly the females, have lower levels of serum adiponectin than their nondiabetic counterparts and this is an additional CVD risk factor for the patients.

Adiponectin↗
PubMed2005

[Adiponectin as an adipose tissue hormone and its role in the metabolic syndrome and cardiovascular disease].

Adiponectin, is a novel hormone secreted by the adipose tissue. This active protein plays a role in the regulation of whole body energy homeostasis. It enhances insulin sensitivity and has antiatherogenic properties, reduces hepatic glucose production, and diminishes gluconeogenesis. Adiponectin accelerates the oxidation process of fatty acids in muscle cells, reduces triglycerides plasma concentration. In addition, plasma adiponectin levels negatively correlated with BMI and fat content. Numerous analyses have indicated that hypoadiponectinemia is a consequence of the development of obesity in childhood. The adiponectin secretion in newborn children is higher than in older, an child small for gestational age has lower plasma concentration of this protein. Clinical studies suggest that adiponectin deficiency associates with gestational diabetes in women. However, serum adiponectin levels in type 1 diabetes have not been elucidated, probably factors other than glucose and insulin play a significant role in adiponectin secretion in type 1 diabetes.

Adiponectin↗
PubMed2005

[Adipokines: adiponectin, leptin, resistin and coronary heart disease risk].

Visceral obesity is among the known risk factors of atherosclerotic cardiovascular diseases. As long as adipose tissue was considered only an inert store of excess energy, accumulated in triglycerides, explanation of the mechanisms causing increased cardiovascular risk in obesity was difficult. Finding that the adipose tissue is an active endocrine organ and that the adipokines secreted in it influence several metabolic processes, allowed better understanding of this correlation. Several disturbances in secretion, function and balance of adipokines occur in the course of obesity. Changes of adiponectin, leptin and resistin concentrations are among the reasons of accelerated atherosclerosis occurring in the visceral adiposity. Adiponectin concentrations are decreased in visceral adiposity. Adiponectin is adipokine possessing antiatherogenic properties. It's effects exerted though the specific receptors in skeletal muscles and liver include decreased insulin resistance and improved plasma lipid profile. Acting directly in the vessel wall adiponectin prevents development of atheromatic lesions by inhibiting production of adhesive molecules and formation of foam cells. It has been found that decreased adiponectin concentrations are connected not only with increased coronary risk but also with progression of atherosclerosis in coronary vessels. Moreover it was found that adiponectin plasma concentration is significantly decreased in acute coronary incidences. Leptin regulates energy metabolism and balance. The concentrations of this adipokine are increased in obesity and correlate with insulin resistance. Hiperleptinemia has been also recognized as cardiovascular diseases risk factor. Resistin is considered to be a substance increasing insulin resistance, however the exact mechanisms are not known. Resistin plasma concentrations are increased in obese subjects and correlate with the inflammatory state that underlies the initiation and progression of atherosclerotic lesions. Correlation between resistin concentration and the extent of atherosclerotic plaques in the coronary vessels has also been found. The disturbances in secretion, function and balance of adiponectin, leptin and resistin are to be considered not only a link between visceral adiposity and cardiovascular risk but also independent risk factor of coronary heart disease.

Adiponectin↗
PubMed2005

Adiponectin and some inflammatory and endothelial markers in type-2 diabetes with and without cardiovascular disease.

This study was designed to examine the association between adiponectin and C-reactive protein (CRP), interleukin-6 (IL-6) and endothelin-1, (ET-1) and their possible role in prediction of type-2 diabetes and development of diabetes and macrovascular complications. Forty subjects were studied. They were classified into four equal groups: Control, newly diagnosed type-2 diabetes, diabetics with old myocardial infarction (OMI) and acute myocardial infarction (AMI) groups. They were matched for body mass index (BMI), age, and sex. Adiponectin and IL-6 were determined by ELISA technique, CRP was determined by immunonephlometry and ET-1 was determined by radioimmunoassay. Adiponectin was found to be decreased in newly diagnosed diabetics (6.64 +/- 2.3 microg/ml), OMI (4.7 +/- 1.05 microg/ml) and AMI (4.23 +/- 0.73 microg/ml) when compared to controls (9.81 +/- 2.2 microg/ml), whereas CRP, IL- 6 and ET-1 were significantly elevated in AMI (18.6 +/- 5.3 mg/l, 12.6 +/- 4.2 pg/ml and 36.8 +/- 10.4 fmol/ml, respectively). The changes were marked in AMI group compared to other diabetic groups. Only adiponectin significantly decreased in newly diagnosed type-2 diabetics, but CRP, IL-6 and ET-1 did not significantly altered in newly diagnosed diabetics (4.9 +/- 1.6 mg/l, 6.9 +/- 2.3 pg/ml and 22.1 +/- 8.6 fmol/ml, respectively) compared to control. Adiponectin correlated negatively with CRP, IL-6 and ET-1, BMI and HbA1c, whereas inflammatory and vascular markers correlated positively with each other and with BMI and HbA1c. In conclusions, adiponectin may be implicated in the development of type-2 diabetes and macrovascular complications and can be used as an early predictor of type-2 diabetes. Whereas, none of the inflammatory and vascular markers can predict diabetes, but can be used as markers of acute vascular events and in follow up of these cases. Immunomodulation of adiponectin may help prevention and treatment of type-2 diabetes and its complications.

Adiponectin↗
PubMed2006

Relationship of body composition and circulatory adiponectin to bone mineral density in young premenopausal women.

OBJECTIVE: Adiponectin is a recently discovered hormone secreted by adipocytes. Adiponectin plays an important role in the regulation of insulin sensitivity as well as the propensity to inflammation and atherosclerosis. In the present study, the authors explore the relationship between adiponectin and bone mass in premenopausal women. The relationship of fat mass compared to lean body mass to bone mass was also investigated MATERIAL AND METHOD: Two hundred premenopausal women aged between 20 and 40 years were studied. Bone mineral density (BMD) was measured at L2-4 and femoral neck by dual-energy X-ray absorptiometry (DEXA). Serum adiponectin concentrations were measured by radioimmunoassay. RESULTS: At the lumbar spines, factors associated with BMD were age (p < 0.01) and lean body mass (p < 0.001). No independent association with fat mass was demonstrated Likewise, at the femoral neck, only lean body mass was related to BMD (p < 0. 01). In terms of the relation of serum adiponectin to BMD, no association of serum adiponectin to BMD at the lumbar spines or femoral neck was found CONCLUSION: Altogether, the present findings do not suggest the independent role of adiponectin in the accrual of bone mass in females, although such a role still cannot be excluded in men or postmenopausal women.

Adiponectin↗
PubMed2005

Relationship of lipoprotein lipase and hepatic triacylglycerol lipase activity to serum adiponectin levels in Japanese hyperlipidemic men.

OBJECTIVE: The aim of this study was to determine how lipoprotein lipase (LPL) and hepatic triacylglycerol lipase (HTGL) activity relate to serum adiponectin levels. RESEARCH DESIGN AND METHODS: Fifty-five hyperlipidemic Japanese men were recruited for this study. LPL and HTGL activity in post-heparin plasma (PHP) was measured using Triton X-100 emulsified-[14C] triolein. The remaining activity in the presence of 1M NaCl was defined as HTGL activity. Serum adiponectin levels were determined by an enzyme-linked immunosorbent assay system. RESULT: LPL activity had a positive relationship with HDL2, but had no relation with HDL3, while HTGL had positive relationship with HDL3, but had no relationship with HDL2. LPL activity showed a positive relationship [r = 0.345, p = 0.010] to serum adiponectin levels, while and HTGL activity showed an inverse relationship [r = - 0.365 p = 0.006]. Multiple regression analysis with LPL and HTGL as dependent variables and age, BMI, serum adiponectin and the homeostasis model assessment of insulin resistance (HOMA-IR) as independent variables showed LPL and HTGL's association to adiponectin did not persist after adjustments for these covariants. However, the association of LPL activity to HOMA-IR was found to persist after adjustments of age, BMI, and serum adiponectin. CONCLUSIONS: There was a co-linearity between insulin sensitivity and adiponectin as well as insulin sensitivity and LPL/HTGL activity.

Aged↗
PubMed2005

Association of adiponectin and resistin with adipose tissue compartments, insulin resistance and dyslipidaemia.

AIM: In this study, we investigated the association of plasma adiponectin and resistin concentrations with adipose tissue compartments in 41 free-living men with a wide range of body mass index (22-35 kg/m(2)). METHODS: Using enzyme immunoassays, plasma adiponectin and resistin were measured. Intraperitoneal, retroperitoneal, subcutaneous abdominal and posterior subcutaneous abdominal adipose tissue masses (IPATM, RPATM, SAATM and PSAATM, respectively) were determined using magnetic resonance imaging. Total adipose tissue mass (TATM) was measured using bioelectrical impedance. Insulin resistance was estimated with the help of homeostasis model assessment (HOMA) score. RESULTS: In univariate regression, plasma adiponectin levels were inversely related to IPATM (r = -0.389, p < 0.05), SAATM (r = -0.500, p < 0.001), PSAATM (r = -0.502, p < 0.001), anterior SAATM (r = -0.422, p < 0.01) and TATM (r = -0.421, p < 0.01). In multiple regression models, adiponectin was chiefly correlated with PSAATM. Plasma adiponectin concentrations were also inversely correlated with HOMA score (r = -0.540, p < 0.001) and triglyceride (r = -0.632, p < 0.001), and positively correlated with high-density lipoprotein cholesterol (r = 0.508, p < 0.001). There were no significant correlations between resistin levels and adipose tissue masses, insulin resistance or dyslipidaemia. CONCLUSIONS: In men, total body fat is significantly correlated with plasma adiponectin, but not with plasma resistin levels. Low plasma adiponectin levels appear to be chiefly determined by the accumulation of posterior subcutaneous abdominal fat mass, as opposed to intra-abdominal fat, and are strongly predictive of insulin resistance and dyslipidaemia.

Abdomen↗
PubMed2006

Thyroid status influence on adiponectin, acylation stimulating protein (ASP) and complement C3 in hyperthyroid and hypothyroid subjects.

BACKGROUND: Thyroid abnormalities (hyperthyroid and hypothyroid) are accompanied by changes in intermediary metabolism including alterations in body weight, insulin resistance and lipid profile. The aims of this study were to examine plasma ASP, its precursor C3 and adiponectin in hyperthyroid and hypothyroid subjects as compared to controls. METHODS: A total of 99 subjects were recruited from endocrinology/out-patient clinics: 46 hyperthyroid subjects, 23 hypothyroid subjects and 30 control subjects. Subjects were evaluated for FT4, FT3, TSH, glucose, insulin, complete lipid profile and the adipokines: adiponectin, acylation stimulating protein (ASP) and complement C3. RESULTS: Hyperthyroidism was associated with a 95% increase in adiponectin (p = 0.0002), a 47% decrease in C3 (p < 0.0001), no change in ASP and increased ASP/C3 ratio (p = 0.0012). Hypothyroidism was associated with a 31% increase in ASP (p = 0.008). Adiponectin and C3 correlated with FT3 (r = 0.383, p = 0.004 and r = -0.277, p = 0.007, respectively) and FT4 (r = 0.464, p = 0.003 and r = -0.225, p = 0.03, respectively). ASP correlated with TSH (r = 0.202, p = 0.04). Adiponectin did not correlate with either ASP or C3, only ASP and C3 correlated (r = -0.197, p = 0.05). Adiponectin was negatively correlated with BMI, total cholesterol and plasma triglyceride, while C3 was positively correlated with BMI and total cholesterol. Surprisingly, adiponectin was positively correlated with insulin (r = 0.293, p = 0.02) and HOMA-IR (r = 0.373, p = 0.003) while C3 was negatively correlated with glucose (r = -0.242, p = 0.022, insulin (r = -0.184, p = 0.05) and HOMA-IR. CONCLUSION: These changes suggest that thyroid disease may be accompanied by changes in adipokines, which may contribute to the phenotype expressed.

Journal Article↗
PubMed2006

Gene expression of leptin, resistin, and adiponectin in the white adipose tissue of obese patients with non-alcoholic fatty liver disease and insulin resistance.

BACKGROUND: Adipose tissue is an active endocrine organ that secretes a variety of metabolically important substances including adipokines. These factors affect insulin sensitivity and may represent a link between obesity, insulin resistance, type 2 diabetes (DM), and nonalcoholic fatty liver disease (NAFLD). This study uses real-time polymerase chain reaction (PCR) quantification of mRNAs encoding adiponectin, leptin, and resistin on snap-frozen samples of intra-abdominal adipose tissue of morbidly obese patients undergoing bariatric surgery. METHODS: Morbidly obese patients undergoing bariatric surgery were studied. Patients were classified into two groups: Group A (with insulin resistance) (N=11; glucose 149.84 +/- 40.56 mg/dL; serum insulin 8.28 +/- 3.52 microU/mL), and Group B (without insulin resistance) (N=10; glucose 102.2 +/- 8.43 mg/dL; serum insulin 3.431 +/- 1.162 microU/mL). RESULTS: Adiponectin mRNA in intra-abdominal adipose tissue and serum adiponectin levels were significantly lower in Group A compared to Group B patients (P<0.016 and P<0.03, respectively). Although serum resistin was higher in Group A than in Group B patients (P<0.005), resistin gene expression was not different between the two groups. Finally, for leptin, neither serum level nor gene expression was different between the two groups. Serum adiponectin level was the only predictor of nonalcoholic steatohepatitis (NASH) in this study (P=0.024). CONCLUSIONS: Obese patients with insulin resistance have decreased serum adiponectin and increased serum resistin. Additionally, adiponectin gene expression is also decreased in the adipose tissue of these patients. This low level of adiponectin expression may predispose patients to the progressive form of NAFLD or NASH.

Adult↗
PubMed2006

T cell-mediated hepatic inflammation modulates adiponectin levels in mice: role of tumor necrosis factor alpha.

Experimental T cell-mediated hepatitis induced by concanavalin A (ConA) results in the initiation of an inflammatory response and the production of cytokines. Adiponectin is an adipocytokine produced by adipose tissue that is involved in the reciprocal regulation of other cytokines, including tumor necrosis factor alpha (TNF-alpha). Concanavalin A administration to C57BL/6J mice reduced circulating levels of adiponectin, whereas leptin was markedly increased. Adiponectin messenger RNA expression in adipose tissue was also decreased; however, the expression of both the adiponectin receptors remained unchanged. Neutralization of TNF-alpha reduced ConA-induced liver damage, and this was associated with restored circulating levels of adiponectin. These findings indicate that inflammation-induced TNF-alpha is a critical mediator of adipose-tissue-derived adiponectin in vivo.

Adiponectin↗
PubMed2006

A high-fat diet has a tissue-specific effect on adiponectin and related enzyme expression.

OBJECTIVE: This study was designed to test whether adiponectin plays a role in diet-induced obesity and insulin resistance and acts as a mediator to induce or inhibit specific metabolic pathways involved in lipid metabolism RESEARCH METHODS AND PROCEDURES: Forty C57BL/6J male mice were fed either a high-fat (HF) or control diet for 4 months, and adiponectin, its receptors, and enzyme expression in liver and muscle tissue were measured. RESULTS: Mice fed the HF diet exhibited significantly greater weight gain, abnormal oral glucose tolerance test curves, and elevated homeostasis model assessment of insulin resistance (5.3 +/- 0.89 vs. 2.8 +/- 0.39). A significant reduction of adiponectin RNA expression (51%) and protein levels (15%) was observed in the adipose tissue of HF animals; however, serum adiponectin levels did not differ between groups (7.12 +/- 0.34 mug/mL vs. 6.44 +/- 0.38 microg/mL). Expression of hepatic mRNA of AdipoR1 and AdipoR2 was reduced by 15% and 25%, respectively, in animals fed the HF diet. In contrast, receptor mRNA expression of AdipoR1 and AdipoR2 increased by 25% and 30%, respectively, in muscle tissue. No effect was found on hepatic adenosine monophosphate-activated protein kinase expression; however, a significant reduction of phosphoadenosine monophosphate kinase levels in muscles was observed. Hepatic acetyl-coenzyme A carboxylase was similar between groups, but in muscles, the inactive form phosphoacetyl-coenzyme A carboxylase was significantly reduced (p < 0.05). DISCUSSION: The HF diet led to decreased insulin sensitivity accompanied by impaired activity of adiponectin-related enzymes in skeletal muscles but not in the liver. These results suggest that the HF diet has a tissue-specific effect on adiponectin and associated enzyme expression.

Acetyl-CoA Carboxylase↗
PubMed2007

Insulin-sensitizing effects of thiazolidinediones are not linked to adiponectin receptor expression in human fat or muscle.

Circulating adiponectin levels are increased by the thiazolidinedione (TZD) class of PPARgamma agonists in concert with their insulin-sensitizing effects. Two receptors for adiponectin (AdipoR1 and AdipoR2) are widely expressed in many tissues, but their physiological significance to human insulin resistance remains to be fully elucidated. We examined the expression patterns of AdipoR1 and AdipoR2 in fat and skeletal muscle of human subjects, their relationship to insulin action, and whether they are regulated by TZDs. Expression patterns of both AdipoRs were similar in subcutaneous and omental fat depots, with higher expression in adipocytes than in stromal cells and macrophages. To determine the effects of TZDs on AdipoR expression, subcutaneous fat and quadriceps muscle were biopsied in 14 insulin-resistant subjects with type 2 diabetes mellitus after 45 mg pioglitazone or placebo for 21 days. This duration of pioglitazone improved insulin's suppression of glucose production by 41% and enhanced stimulation of glucose uptake by 27% in concert with increased gene expression and plasma levels of adiponectin. Pioglitazone did not affect AdipoR expression in muscle, whole fat, or cellular adipose fractions, and receptor expression did not correlate with baseline or TZD-enhanced insulin action. In summary, both adiponectin receptors are expressed in cellular fractions of human fat, particularly adipocytes. TZD administration for sufficient duration to improve insulin action and increase adiponectin levels did not affect expression of AdipoR1 or AdipoR2. Although TZDs probably exert many of their effects via adiponectin, changes in these receptors do not appear to be necessary for their insulin-sensitizing effects.

Adiponectin↗
PubMed2006

[Adiponectin and its role in the pathogenesis of obesity, diabetes mellitus and insulin resistance].

The paper reviews the structure and role of adiponectin in the regulation of metabolic balance. Adiponectin is the most abundant adipocytokine that is produced exclusively in the fat tissue. Its high concentration protects from diabetes mellitus, atherosclerosis and insulin resistance, its low concentration increases the risk of these disorders. The adiponectin gene is one of the many candidate genes in type 2 diabetes. Adiponectin binds to two types of receptors: 1 and 2, encoded by two genes: AdipoR1, and AdipoR2, respectively. The receptors are found in all tissues, with type 1 predominant in the muscles, and type 2 in the liver. Most importantly, the role of adiponectin in the body and the results of animal model experiments suggest the possible future use of adiponectin in the treatment of diabetes, atherosclerosis and obesity.

Adiponectin↗