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PubMed2002

Adiponectin reduces atherosclerosis in apolipoprotein E-deficient mice.

BACKGROUND: Dysregulation of adipocyte-derived bioactive molecules plays an important role in the development of atherosclerosis. We previously reported that adiponectin, an adipocyte-specific plasma protein, accumulated in the injured artery from the plasma and suppressed endothelial inflammatory response and vascular smooth muscle cell proliferation, as well as macrophage-to-foam cell transformation in vitro. The current study investigated whether the increased plasma adiponectin could actually reduce atherosclerosis in vivo. METHODS AND RESULTS: Apolipoprotein E-deficient mice were treated with recombinant adenovirus expressing human adiponectin (Ad-APN) or beta-galactosidase (Ad-betagal). The plasma adiponectin levels in Ad-APN-treated mice increased 48 times as much as those in Ad-betagal treated mice. On the 14th day after injection, the lesion formation in aortic sinus was inhibited in Ad-APN-treated mice by 30% compared with Ad-betagal-treated mice (P<0.05). In the lesions of Ad-APN-treated mice, the lipid droplets became smaller compared with Ad-betagal-treated mice (P<0.01). Immunohistochemical analyses demonstrated that the adenovirus-mediated adiponectin migrate to foam cells in the fatty streak lesions. The real-time quantitative polymerase chain reaction revealed that Ad-APN treatment significantly suppressed the mRNA levels of vascular cell adhesion molecule-1 by 29% and class A scavenger receptor by 34%, and tended to reduce levels of tumor necrosis factor-alpha without affecting those of CD36 in the aortic tissue. CONCLUSIONS: These findings documented for the first time that elevated plasma adiponectin suppresses the development of atherosclerosis in vivo.

Adiponectin↗
PubMed2005

Plasma adiponectin levels and five-year survival after first-ever ischemic stroke.

BACKGROUND AND PURPOSE: This study aimed to investigate the association between plasma adiponectin levels and 5-year survival after first-ever ischemic stroke. METHODS: Plasma adiponectin measured within 24 hours after first-ever ischemic stroke was related to 5-year outcome. The Kaplan-Meier technique was applied in survival analysis, and the Cox proportional hazards model was used to evaluate the relationship between risk factors and prognosis. RESULTS: The probabilities of death were 92.8%, 52.5%, and 10.5% (P<0.001) for patients stratified according to tertiles of adiponectin (<4 microg/mL, 4 to 7 microg/mL, and >7 microg/mL, respectively). The relative risk of death was 8.1 (95% CI, 3.1, 24.5; P<0.001) for individuals with adiponectin levels in the lowest tertile compared with the upper tertile. Adiponectin <4 microg/mL (hazard ratio [HR], 5.2; 95% CI, 2.1, 18.4; P<0.001), score >15 in the National Institutes of Health Stroke Scale (HR, 3.6; 95% CI, 1.7, 15.9; P<0.001), and coronary heart disease (HR, 2.9; 95% CI, 1.5, 12.3; P<0.001) were independently associated with mortality. CONCLUSIONS: Low plasma adiponectin is related to an increased risk of 5-year mortality after first-ever ischemic stroke, independently of other adverse predictors.

Adiponectin↗
PubMed2003

Activation of the hexosamine signaling pathway in adipose tissue results in decreased serum adiponectin and skeletal muscle insulin resistance.

Overexpression of the rate-limiting enzyme for hexosamine synthesis (glutamine:fructose-6-phosphate amidotransferase) in muscle and adipose tissue of transgenic mice was previously shown to result in insulin resistance and hyperleptinemia. Explanted muscle from transgenic mice was not insulin resistant in vitro, suggesting that muscle insulin resistance could be mediated by soluble factors from fat tissue. To dissect the relative contributions of muscle and fat to hexosamine-induced insulin resistance, we overexpressed glutamine:fructose-6-phosphate amidotransferase 2.5-fold, specifically in fat under control of the aP2 promoter. Fasting glucose, insulin, and triglycerides were unchanged in the transgenic mice; leptin and beta-hydroxybutyrate levels were 91% and 29% higher, respectively. Fasted transgenic mice have mild glucose intolerance and skeletal muscle insulin resistance in vivo. In fasting transgenic mice, glucose disposal rates with hyperinsulinemia were decreased 27% in females and 10% in males. Uptake of 2-deoxy-D-glucose into muscle was diminished by 45% in female and 21% in male transgenics. Serum adiponectin was also lower in the fasted transgenics, by 37% in females and 22% in males. TNF alpha and resistin mRNA levels in adipose tissue were not altered in the fasted transgenics; levels of mRNA for leptin were increased and peroxisome proliferator-activated receptor gamma decreased. To further explore the relationship between adiponectin and insulin sensitivity, we examined mice that have been refed for 6 h after a 24-h fast. Refeeding wild-type mice resulted in decreased serum adiponectin and increased leptin. In transgenic mice, however, the regulation of these hormones by refeeding was lost for adiponectin and diminished for leptin. Refed transgenic female and male mice no longer exhibited decreased serum adiponectin in the refed state, and they were no longer insulin resistant as by lower or unchanged insulin and glucose levels. We conclude that increased hexosamine levels in fat, mimicking excess nutrient delivery, are sufficient to cause insulin resistance in skeletal muscle. Changes in serum adiponectin correlate with the insulin resistance of the transgenic animals.

3-Hydroxybutyric Acid↗
PubMed2003

Glucose-to-insulin ratio rather than sex hormone-binding globulin and adiponectin levels is the best predictor of insulin resistance in nonobese women with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS), the main androgen disorder in women, has been suggested to be associated with a high risk of developing cardiovascular disease and type 2 diabetes. In many PCOS patients, overweight or central obesity is generally associated with increases in fasting insulin levels, insulin resistance, and glucose intolerance, and has been identified as a target for new therapeutic strategy, including early change in lifestyle. Early biochemical marker(s) for identifying at-risk patients will be useful for prevention studies. The main goal of the present study was to search for such tool(s). We investigated 16 nonobese PCOS women by performing euglycemic hyperinsulinemic clamp and measuring insulin levels during fasting and oral glucose tolerance test, as well as the serum concentrations of SHBG, leptin, and adiponectin, the newly identified adipose factors. Eight of the 16 patients had a steady-state glucose disposal rate less than 8.5 mg/kg.min, the lowest normal value for nonobese control women. These insulin-resistant patients had significant higher body mass index (BMI) and waist-to-hip ratio (WHR), and lower high-density lipoprotein cholesterol and SHBG levels. As expected, glucose disposal correlated negatively with BMI (P = 0.01), WHR (P = 0.01), and fasting insulin level (P = 0.003). On stepwise regression analysis, however, the glucose-to-insulin ratio (GIR) emerged as the strongest independent parameter to appraise insulin resistance (R(2) = 0.61). SHBG level correlated positively with GIR (P < 0.001) and negatively with BMI (P = 0.003) but did not correlate with either insulin response during the glucose tolerance test or plasma leptin and/or adiponectin levels. In contrast, BMI was the only independent predictive parameter of SHBG (P = 0.003, R(2) = 0.73). Interestingly, plasma adiponectin levels were positively associated with glucose disposal rate (P = 0.043) and negatively with WHR (P = 0.024), waist circumference being the best predictor of adiponectin level (P < 0.01). Leptin level correlated only with BMI (r = 0.62, P = 0.01). This study confirmed that insulin resistance, despite the lack of obesity as such, is clearly present in many PCOS women, and demonstrated that GIR is the best predictor for insulin resistance. It was also shown that adiponectin level is a good indicator of abdominal fat mass and is associated to insulin resistance. Finally, low SHBG levels in PCOS are intimately associated with BMI, suggesting that some signal(s) from the adipose tissue, independent of adiponectin and leptin, may regulate liver production of SHBG.

Adiponectin↗
PubMed2004

Adiponectin, an adipocyte-derived protein, predicts future insulin resistance: two-year follow-up study in Japanese population.

It has been reported that the serum adiponectin level was negatively correlated with body mass index (BMI), insulin resistance index, and triglycerides and was positively correlated with high-density lipoprotein cholesterol in several cross-sectional studies. However, the causal relationship has not been elucidated. We investigated whether the baseline adiponectin level could predict subsequent changes in insulin resistance, lipid profile, or body weight in a 2-yr longitudinal study. This study included 590 male Japanese subjects, aged 30-65 yr, who received annual health checkups in both 2000 and 2002. Blood pressure, heart rate, and anthropometric and metabolic parameters, including serum insulin and adiponectin levels, were determined. The insulin resistance index was calculated based on homeostasis model assessment. Baseline adiponectin level was not correlated with the subsequent change in lipid profile or BMI in 2 yr after adjustment for each baseline value. However, the baseline adiponectin level was negatively correlated with subsequent changes in insulin and insulin resistance index based on homeostasis model assessment, even after adjustment for change in BMI (r = -0.162 and r = -0.140, respectively). These findings suggest that the serum adiponectin concentration predicts subsequent changes in insulin resistance, but not in lipid profile or body weight.

Adiponectin↗
PubMed2004

Circulating adiponectin and endometrial cancer risk.

Circulating levels of adiponectin, a hormone with insulin-sensitizing properties, are decreased in conditions related to obesity and hyperinsulinemia, which are recognized risk factors for endometrial cancer. Eighty-seven cases with incident, histologically confirmed endometrial cancer and 132 controls admitted for acute, nonneoplastic diseases were interviewed in northeastern Italy between 1999 and 2002, and blood samples were collected. Levels of adiponectin were evaluated in samples by means of a RIA. An inverse association with endometrial cancer risk emerged for plasma adiponectin levels [odds ratio (OR), 0.42; 95% confidence interval, 0.19-0.94] when comparing the highest vs. the lowest tertiles. Similar results emerged for serum adiponectin (OR, 0.30; 95% confidence interval, 0.14-0.68). The association was stronger in pre- than in postmenopausal women, but no significant heterogeneity was observed across strata of body mass index (BMI) or parity. BMI and adiponectin showed independent effects on the risk of endometrial cancer according to a multiplicative model (OR, 6.45 in the highest level of BMI and in the lowest one of adiponectin).

Adiponectin↗
PubMed2004

Adiponectin and breast cancer risk.

Adiponectin, an adipocyte-secreted hormone, is closely and inversely associated with insulin resistance and was recently found to be inversely and independently associated with endometrial cancer. Because insulin resistance in the setting of obesity has also been associated with the development of breast cancer, we have hypothesized that decreased adiponectin levels might underlie the association between breast cancer and obesity/insulin resistance. We evaluated the association of adiponectin with the occurrence of breast cancer in a case-control study comprising 174 women with newly diagnosed, histologically confirmed breast cancer and 167 controls. We found an inverse, fairly strong, and statistically significant association of serum adiponectin with breast cancer (odds ratio, 0.84; 95% confidence interval, 0.71-0.99). Importantly, despite a fairly robust inverse association of adiponectin with breast cancer risk among postmenopausal women (odds ratio, 0.82; 95% confidence interval, 0.67-1.00), no such significant association between adiponectin and breast cancer was found among premenopausal women. The observed associations were independent of possible effects of major components of the IGF system, leptin, body mass index, sociodemographic variables, and known risk factors for breast cancer. Future studies are needed to prove causality and provide further insights into both the mechanisms underlying the actions of this hormone and its potential role in breast cancer.

Adiponectin↗
PubMed2004

Adiponectin, inflammation, and the expression of the metabolic syndrome in obese individuals: the impact of rapid weight loss through caloric restriction.

Severe obesity increases the prevalence of the metabolic syndrome, and moderate acute weight loss with a very low-calorie diet in obese subjects with the metabolic syndrome leads to significant metabolic benefits. Adiponectin has been implicated in both the pathogenesis of obesity-related insulin resistance and increased inflammation. We analyzed the relationship of the adipocyte-derived hormone adiponectin with indices of inflammation, adiposity, and insulin resistance in obese subjects with (MS+, n = 40) and without (MS-, n = 40) the metabolic syndrome and examined the acute effects of rapid weight loss. MS+ subjects had significantly lower adiponectin (7.6 +/- 0.6 vs. 10.4 +/- 0.6 microg/ml; P = 0.003) and significantly higher TNF-alpha (3.3 +/- 0.2 vs. 2.8 +/- 0.3 pg/ml; P = 0.004) levels compared with MS- subjects matched for age and body mass index. Plasma adiponectin and TNF-alpha levels were inversely related to the number of metabolic syndrome factors in a stepwise manner. After 4-6 wk of weight loss, there was marked improvement in glucose, insulin, leptin, and triglycerides, whereas adiponectin and TNF-alpha concentrations did not change. Thus, increases in plasma levels of adiponectin or reductions in TNF-alpha are not required for marked improvements in glucose/insulin and lipid metabolism with acute weight loss.

Adiponectin↗
PubMed2004

Serum adiponectin is reduced in acromegaly and normalized after correction of growth hormone excess.

Adiponectin, an adipocyte-derived hormone, possesses insulin-sensitizing, antiinflammatory, and antiatherogenic properties. We hypothesized that hypoadiponectinemia was present in acromegaly, as in other conditions with increased insulin resistance and cardiovascular risk. Using an in-house RIA, serum adiponectin was determined in 35 patients with active acromegaly and 35 age-, sex-, and body mass index-matched healthy controls. Twenty-five patients were restudied after GH-lowering therapies. Serum adiponectin was significantly reduced in the acromegalic patients (4.3 +/- 1.8 vs. 6.7 +/- 1.8 microg/ml in controls; P < 0.001), but was increased after treatment with Sandostatin LAR, a long-acting somatostatin analog (5.8 +/- 2.6 vs. 3.8 +/- 1.6 microg/ml pretreatment; P < 0.001; n = 15) or transsphenoidal surgery (6.5 +/- 2.7 vs. 3.9 +/- 1.5 microg/ml preoperation; P < 0.01; n = 10). Fasting insulin was an independent determinant of serum adiponectin levels (P < 0.01) in control subjects, contributing to 11.7% of the variance in circulating adiponectin. In cultured 3T3-L1 adipocytes, adiponectin mRNA levels were decreased by insulin (1.5 microm; P < 0.005) or IGF-I (1 microg/ml; P < 0.05), but not by GH (1 microm) or somatostatin (1 microm). In conclusion, hypoadiponectinemia is present in active acromegaly, probably secondary to the inhibitory effect of high circulating insulin levels. Hypoadiponectinemia, reversible with GH-lowering therapies, may contribute to the increased insulin resistance and cardiovascular risk in patients with acromegaly.

3T3-L1 Cells↗
PubMed2004

Lack of an association between peroxisome proliferator-activated receptor-gamma gene Pro12Ala polymorphism and adiponectin levels in the polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is one of the most common endocrine metabolic diseases and is characterized by obesity in approximately 50% of those affected. Adiponectin is an adipocyte-derived protein that possesses an antiatherosclerotic action and improves insulin sensitivity. Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) regulates the transcription of several adipocyte-specific genes. The aim of this study was to investigate the putative influence of the PPAR-gamma gene Pro12Ala polymorphism on the adiponectin levels in PCOS and healthy women. One hundred twenty women with PCOS and 120 healthy women whose ages and body mass indexes matched those of the PCOS patients were investigated. The genetic analysis of PPAR-gamma gene Pro12Ala polymorphism was performed by restriction fragment of polymorphisms. Serum adiponectin levels were evaluated, and the homeostasis model assessment score was also calculated. No subject was homozygous for the Ala12 allele of the PPAR-gamma gene. No significant differences in body mass index, plasma glucose and lipid levels, and homeostasis model assessment scores were observed between and within genotype groups in PCOS and control women. No significant differences in serum adiponectin concentrations were observed between and within genotype groups in PCOS and control women. In conclusion, our results confirm that adiponectin concentrations are similar in PCOS and controls and demonstrate no effect of the PPAR-gamma gene Pro12Ala polymorphism on serum adiponectin levels.

Adiponectin↗
PubMed2005

Decreased plasma adiponectin concentrations are closely related to steatosis in hepatitis C virus-infected patients.

OBJECTIVES: The mechanisms underlying steatosis during hepatitis C virus (HCV) infection are complex and multifactorial. Obesity is a well-recognized risk factor for the development of steatosis in chronic hepatitis C infection. The aim of our study was to investigate the role of adipocytokines in HCV-related steatosis. Therefore, we hypothesized that the endocrine function of adipose tissue could be, in part, responsible for HCV-related steatosis. Seventy-one consecutive untreated chronic hepatitis C patients were studied to assess the effects of adipocytokines, body mass index (BMI), age, and HCV genotype on steatosis. We used ELISA to determine serum adiponectin, leptin, and soluble TNF receptors I and II concentrations. RESULTS: Steatosis was observed in 42 (59.1%) patients. BMI was significantly associated with leptin (r = 0.64; P = 0.0001) and was border significantly associated with adiponectin concentrations (r = -0.22; P = 0.06). In univariate analyses, age, HCV genotype 3, BMI, increased leptin level, increased insulin level, and decreased adiponectin concentration were associated with steatosis. In multivariate analysis, steatosis was significantly associated with low adiponectin concentration, age, HCV genotype 3, and aspartate aminotransferase (ASAT) level, whereas steatosis was not associated with leptin, insulin, and BMI. CONCLUSION: In chronic HCV patients, hypoadiponectinemia is significantly associated with the development of liver steatosis. The fact that the plasma levels of adiponectin inversely correlate with steatosis in HCV-infected subjects suggests that hypoadiponectinemia may contribute to hepatic steatosis progression and liver injury in this population. One practical implication is that therapy to increase circulating adiponectin concentration, such as overweight reduction or thiazolidinediones, provides the potential to improve steatosis in chronic hepatitis C infection.

Adiponectin↗
PubMed2005

Plasma adiponectin level is associated with insulin-stimulated nonoxidative glucose disposal.

CONTEXT: Impaired nonoxidative glucose disposal and decrease in mitochondrial glucose oxidation both contribute to insulin resistance in diabetic subjects. OBJECTIVE: In the present study, we investigated whether plasma adiponectin is associated with glucose oxidation and nonoxidative glucose disposal in subjects with and without type 2 diabetes. DESIGN: Euglycemic-hyperinsulinemic clamp was performed in 42 type 2 diabetic (T2DM) and 13 nondiabetic (non-DM) subjects. The whole-body glucose disposal rate (GDR) was evaluated as the mean of the glucose infusion rate during steady state of the clamp. Glucose and fat oxidation rates were assessed by indirect calorimetry, and nonoxidative glucose disposal rate was calculated by subtracting glucose oxidation rate from GDR. RESULTS: Plasma adiponectin level was significantly lower in T2DM than non-DM (2.87 +/- 1.40 vs. 3.96 +/- 2.39 microg/ml, P = 0.045). GDR (3.39 +/- 1.53 vs. 4.83 +/- 1.70 mg/kg x min, P = 0.006) and nonoxidative glucose disposal rate (1.89 +/- 1.39 vs. 3.11 +/- 1.76 mg/kg x min, P = 0.012) were significantly lower in T2DM, compared with non-DM, although no difference was found in glucose oxidation rate between the two groups. In all subjects, plasma adiponectin level was positively correlated with GDR (r = 0.351, P = 0.009) and nonoxidative glucose disposal rate (r = 0.324, P = 0.016) but not glucose oxidation rate. There was no significant correlation between plasma adiponectin level and fat oxidation, either before or during the clamp. CONCLUSIONS: In conclusion, plasma adiponectin level is associated with nonoxidative glucose disposal, which is reduced in type 2 diabetic subjects. Our results suggest that adiponectin controls insulin sensitivity by modulating the glycogen synthetic process in human skeletal muscle.

Adiponectin↗
PubMed2005

Adiponectin predicts insulin resistance but not endothelial function in young, healthy adolescents.

BACKGROUND: Adiponectin, an adipocyte-derived hormone found in lower concentration with greater adiposity, is suggested to reduce the risk of insulin resistance, atherosclerosis, and cardiovascular disease. We tested this hypothesis in a healthy, nonobese population. METHODS AND RESULTS: Brachial artery flow-mediated endothelial-dependent vasodilation and distensibility, measures of vascular function relevant to the early atherosclerotic process, were determined in 294 adolescents (aged 13-16 yr) using high-resolution vascular ultrasound. Fasting insulin concentration and the homeostasis model assessment of insulin resistance were used to estimate insulin resistance. Fat mass was measured by bioelectric impedance analysis; fasting serum adiponectin concentration by RIA; and lipid profile, fasting insulin, glucose, and C-reactive protein concentrations using standard laboratory techniques. Adiponectin concentration was associated with insulin resistance independent of potential confounding factors (e.g. -1.3% change in fasting insulin concentration per 10% increase in adiponectin concentration; 95% confidence interval, -2.4% to -0.1%; P = 0.03), but not with flow-mediated endothelial-dependent vasodilation or arterial distensibility. CONCLUSIONS: Lower adiponectin concentration was associated with lower insulin sensitivity in a healthy, nonobese population. Our study supports the hypothesis that adiponectin benefits insulin sensitivity from a young age but, in contrast to experimental models and data from older subjects, does not affect vascular changes associated with early atherosclerosis.

Adiponectin↗
PubMed2006

Serum adiponectin is a predictor of coronary heart disease: a population-based 10-year follow-up study in elderly men.

CONTEXT: Cross-sectional and nested case-control studies indicate a relationship between adiponectin, obesity, and coronary heart disease (CHD). OBJECTIVE: Our objective was to investigate whether adiponectin could predict CHD in a population-based cohort of elderly men. DESIGN AND SETTING: From 1991-1995 a baseline investigation was carried out in 832 healthy men aged 70 yr in the Uppsala Longitudinal Study of Adult Men (ULSAM study). They were followed up to 10.4 yr using Swedish national registry data. The baseline investigation included anthropometry, blood pressure, smoking, serum lipids, a euglycemic insulin clamp, and fasting serum adiponectin. MAIN OUTCOME MEASURES: Main outcome measures were defined as death or first-time hospitalization for CHD (n = 116), recorded in the Cause of Death Registry or in the Hospital-Discharge Registry of the National Board of Health and Welfare, Sweden. Associations were analyzed using Cox's proportional hazards regression, presented as hazard ratios (HR) with 95% confidence intervals (CI) for 1 sd increase in the predictor variable. RESULTS: In a multivariable analysis including total cholesterol (HR, 1.24; CI, 1.02-1.50), high-density lipoprotein cholesterol (HR, 0.72; CI, 0.58-0.89), smoking (HR, 1.39; CI, 0.91-2.14), and systolic blood pressure (HR, 1.26; CI, 1.05-1.52), serum adiponectin was associated with lower risk for CHD (HR, 0.81; CI, 0.66-0.99). The association was independent of BMI and remained significant after adjustment for insulin sensitivity index. CONCLUSIONS: In this population-based cohort of healthy men, elevated serum levels of adiponectin were associated with a lower risk for CHD. Importantly, the association between adiponectin and CHD was independent of other well-known risk factors.

Adiponectin↗
PubMed2007

Plasma adiponectin concentrations and risk of incident breast cancer.

INTRODUCTION: Previous retrospective case-control studies suggest that adiponectin, an obesity-related hormone, is inversely associated with breast cancer risk, particularly in postmenopausal women; however, no prospective studies exist. Therefore, we conducted a prospective case-control study nested within the Nurses' Health Study (NHS) and NHSII cohorts examining the association between plasma adiponectin concentrations and breast cancer risk. MATERIALS AND METHODS: Blood samples were collected from 1989 through 1990 (NHS) and 1996 through 1999 (NHSII); adiponectin was measured by RIA. The analysis included 1477 breast cancer cases diagnosed after blood collection and before June 2000 (NHS) or June 2003 (NHSII) who had one or two controls (n=2196) matched on age, menopausal status, postmenopausal hormone (PMH) use, fasting, and time of day and month of blood collection. We adjusted for body mass index at age 18, weight change from age 18 to blood draw, family history of breast cancer, history of benign breast disease, duration of PMH use, ages at menarche and first birth, and parity. RESULTS: Although we observed no association between adiponectin and breast cancer risk overall, there was a nearly significant interaction by menopausal status (P=0.08), with a relative risk, top vs. bottom quartile of 0.73 (95% confidence interval, 0.55-0.98; P trend=0.08) among postmenopausal women and 1.30 (95% confidence interval, 0.80-2.10; P trend=0.09) for premenopausal women. Among postmenopausal women, adiponectin appeared more strongly inversely associated in women who never used PMH (P heterogeneity=0.05) and women with low circulating estradiol levels (P heterogeneity=0.05). DISCUSSION: Our results suggest that adiponectin may be inversely associated with postmenopausal breast cancer risk, particularly in a low-estrogen environment.

Adiponectin↗
PubMed2006

Intra-abdominal fat adiponectin receptors expression and cardiovascular metabolic risk factors in obesity and diabetes.

BACKGROUND: The effects of adiponectin on glucose and lipid metabolism are mediated by the adiponectin receptors, adipoR1 and adipoR2, which are mainly in liver and muscle. We investigated the presence of adiponectin receptors in intra-abdominal adipose tissue (IAAT) in obesity and diabetes and their association with adiponectin expression and components of the metabolic syndrome and/or other metabolic factors associated with atherosclerotic cardiovascular disease (ASCVD). METHODS: AdipoR1 and adipoR2 gene expression was measured by quantitative real time reverse transcription polymerase chain reaction in IAAT from lean and obese patients with or without diabetes type 2. Correlation between metabolic characteristics of obese patients and expression of these receptors was studied. RESULTS: Neither obesity nor diabetes were associated with changes in IAAT-adipoR1 expression. In contrast, IAAT-adipoR2 was decreased by 39.5% in obese non-diabetics and by 52.7% in obese diabetics when compared to lean subjects. AdipoR1 and adiponectin expression was associated in lean (r=0.943, P<0.005) and obese non-diabetic patients (r=0.74, P<0.01), whereas a positive correlation between adipoR2 and adiponectin expression was only found in the presence of diabetes (r=0.883, P<0.002). AdipoR1 expression was associated with plasma free fatty acids (FFA) concentration (r=0.76, P<0.04), and adipoR2 inversely correlated with plasma levels of triglycerides (r=-0.76, P<0.04) and apolipoprotein B (r=-0.74, P<0.05). CONCLUSION: AdipoR1 expression in IAAT was not altered by obesity and/or diabetes and was related to plasma levels of FFA. IAAT-adipoR2 expression was reduced in obesity and diabetes and associated with components of metabolic processes leading to cardiovascular disease in obesity.

Abdominal Fat↗
PubMed2005

Lack of increase of serum adiponectin concentrations with a moderate weight loss during six months on a high-caloric diet in military service among a young male Finnish population.

An increase of insulin resistance and a worsening of lipid profile during 6 mo of military service in young male Finnish population has previously been shown by us. The present study demonstrates unfavorable changes of serum adiponectin concentrations and their association with weight loss in these particular circumstances. Adiponectin in a range of 4.3-21.2 microg/mL was present in the serum samples and had a significant negative correlation with weight, body mass index, waist to hip ratio, and insulin. Fasting serum lipids and plasma insulin significantly increased and serum adiponectin levels significantly decreased during the military service. Even the subjects with a 5-10% decrease in body weight showed the same result. In cases with more than 10% weight reduction and a significant decrease of fasting insulin concentration, the total and low density lipoprotein cholesterol significantly increased and adiponectin concentration tended to decreased. Only in severely obese cases (BMI >/= 30 kg/m2) with more than 10% decrease in body mass index adiponectin levels tended to increase, although not statistically significantly. This study shows that serum adiponectin concentrations decreased during a 6 mo high-caloric diet in military service, and even a moderate weight reduction induced by high-energy expenditure in exercise during service did not increase its levels.

Adiponectin↗
PubMed2005

Adiponectin levels and cardiovascular risk factors in Japanese men with type 2 diabetes.

Several cardiovascular risk factors correlate with adiponectin levels. It is not known whether total homocysteine, folate and gamma-glutamyl transferase levels correlate with adiponectin. We cross-sectionally analyzed the association between adiponectin and these cardiovascular risk factors in diabetic patients. One hundred and two male inpatients with type 2 diabetes without overt nephropathy or insulin use were studied. In a regression analysis of the quartiles of adiponectin, plasma levels of adiponectin were associated positively with HDL-cholesterol and age, and inversely with body mass index and HbA1c, but not with total homocysteine, folate or gamma-glutamyl transferase. Non-traditional cardiovascular risk factors such as homocysteine and folate levels were not associated with adiponectin levels in male type 2 diabetic patients who are not subject to insulin therapy.

Adiponectin↗