Serum Adiponectin Values Research Articles

Fasting Adiponectin is Inversely Correlated with Metabolic Syndrome in Patients with Coronary Artery Disease

Hypoadiponectemia was observed to correlate with the prevalence or extent of coronary artery disease (CAD), the relationship between metabolic syndrome and fasting serum adiponectin concentration in CAD patients are not well elucidated. Fasting blood samples were obtained from 98 CAD patients. Metabolic syndrome and its components were defined using the diagnostic criteria of the International Diabetes Federation. Adiponectin concentrations were measured using a commercial enzyme immunoassay kit. Fifty patients with CAD (51.0%) had metabolic syndrome. For this group of patients, fasting adiponectin concentrations were found to correlate inversely with metabolic syndrome (p=0.009). Fasting adiponectin values for these subjects also tended to decrease as the number of diagnostic criteria for metabolic syndrome increased (p=0.024). CAD patients with hyperlipidemia (p=0.002), obesity (p=0.030) or receiving statin therapy (p=0.005) had lower serum adiponectin values. By univariate linear regression analysis, fasting serum adiponectin values were positively correlated with age (r=0.242; p=0.017) and high density lipoprotein-cholesterol concentration (HDL-cholesterol; r=0.267; p=0.008) but were negatively correlated with triglyceride concentration (TG; r=-0.251; p=0.013). Multivariate forward stepwise linear regression analysis of the significant variables revealed that HDL-cholesterol concentration (R square=0.071, p=0.008) and age (R square=0.039, p=0.044) are the independent predictors of fasting serum adiponectin concentration for patients with CAD. Serum adiponectin concentration is inversely correlated with metabolic syndrome and the number of metabolic syndrome criteria in patients with CAD. For these patients HDL-cholesterol concentration and age are independent predictors of the serum adiponectin value.

Pre- and early post-partum adiponectin and Interleukin-1beta levels in women with and without gestational diabetes

To investigate maternal serum adiponectin and Interleukin-1beta (IL-1beta) levels during the pre- and post-partum periods in pregnant women with and without gestational diabetes mellitus (GDM). Thirty control pregnant Caucasian women without GDM and thirty body mass index (BMI) and age-matched Caucasian women with GDM examined in the outpatient clinic between the 24th and 26th week of their pregnancy and on the 3rd day postpartum underwent anthropometry and had serum blood taken. Both groups, were monitored by a dietitian and had comparable weight gain during pregnancy. Birth weight was also measured. At the 3rd day postpartum, compared to the 2nd trimester of pregnancy, women with GDM had lower serum adiponectin levels, lower serum IL-1beta levels and lower homeostasis model assessment for insulin resistance (HOMA-IR) values. At the 2nd trimester of pregnancy, women with GDM had lower serum adiponectin levels, higher IL-1beta and higher HOMA-IR values compared to women without GDM. At the 3rd day postpartum, women with GDM had lower serum adiponectin levels, higher IL-1beta and higher HOMA-IR values compared to women without GDM. Second trimester serum adiponectin values of women with GDM correlated negatively with birth weight. Gestational diabetes is a state of insulin resistance associated with altered levels of proinflammatory cytokines, increased IL-1beta and decreased adiponectin values. Both of these alterations might be attributed to placental pathology in pregnancies with GDM.

Relatively high levels of serum adiponectin in obese women, a potential indicator of anti-inflammatory dysfunction: Relation to sex hormone-binding globulin

It is unclear whether serum adiponectin concentrations diminish linearly with increasing adiposity and, if not, which factors codetermine this association. These issues were investigated cross-sectionally in 1188 men and women, representative of middle-aged and elderly Turkish adults. Serum total adiponectin was assayed by ELISA. Serum adiponectin values in men, though declining significantly in transition from the bottom to the mid tertile of body mass index (BMI) and waist circumference (WC), were similar in the two respective upper tertiles. In women, serum adiponectin concentrations were not significantly different in any tertile of these indices, were significantly correlated with BMI or WC within the low tertiles and not within the two higher tertiles. In a linear regression analysis for WC (or BMI) in a subset of the sample in which serum sex hormone-binding globulin (SHBG) was available and which additionally comprised adiponectin, fasting insulin and other confounders, only insulin and, in women SHBG, were significantly associated, but not adiponectin. In linear regression analyses for covariates of adiponectin in two models comprising 12 variables, insulin and SHBG concentrations were significantly associated in both genders though not BMI. Whereas in men HDL-cholesterol and CRP were covariates of adiponectin (both p<0.01), SHBG and apolipoprotein B positively associated in women (p<0.001), independent of BMI and fasting insulin levels. Relationship between excess adiposity and adiponectin levels is inconsistent in Turkish adults. Independently from obesity and hyperinsulinemia, serum adiponectin discloses significant relationship with inflammatory markers and HDL only in men, not in women in whom it is influenced by SHBG, with consequent attenuation of its anti-inflammatory activities.

Normal adiponectin levels despite abnormal glucose tolerance (or diabetes) and inflammation in adult patients with cystic fibrosis

Rationale Circulating adiponectin levels are negatively associated with glucose intolerance, inflammation and central adiposity. Since these conditions are common in cystic fibrosis (CF), we examined whether adiponectin values are altered in these patients. Aim To determine if CF patients have altered adiponectin levels and if these levels correlate with glucose tolerance categories (normal, impaired glucose tolerance (IGT) and cystic fibrosis-related diabetes (CFRD)), insulin resistance or inflammatory markers such as fibrinogen and C-reactive protein (CRP). Methods Oral glucose tolerance tests (OGTTs) were performed and adiponectin levels were measured in 90 CF patients not known to be diabetic and 15 healthy controls matched for age, sex and body mass index (BMI). Inflammatory markers, serum albumin concentrations and the clinical status of CF patients (i.e. pulmonary function) were also examined. Results CF pathology was characterized by a high prevalence (43.5%) of glucose tolerance abnormalities: 26.5% of IGT and 17.0% of newly diagnosed CFRD. CF patients also presented systemic inflammation as revealed by a significant increase of fibrinogen ( P = 0.029) in all patients and higher CRP levels in CFRD patients compared to the controls ( P < 0.05). On the other hand, CF and control subjects had similar albumin serum concentration. While CF patients and controls had similar serum adiponectin values, women had significantly higher hormone levels than men ( P < 0.001). Adiponectin levels did not correlate with glucose tolerance, inflammatory markers or insulin resistance. On the other hand, they correlated positively with both total and HDL–cholesterol ( P < 0.001). Conclusion CF patients did not show any alterations in adiponectin levels despite insulin resistance, glucose intolerance and sub clinical chronic inflammation. Thus, CF appears to be one of the rare conditions in which discordance between adiponectin values and insulin resistance or inflammation is evident.

Lack of association between serum adiponectin levels and the Pro12Ala polymorphism in Asian Indians

The aim of the study was to investigate the association of serum adiponectin levels with the Pro12Ala polymorphism of the peroxisome proliferator activated receptor-gamma (PPARG) gene in Asian Indians. We selected 400 diabetic subjects, 200 with the Pro12Pro genotype (100 male and 100 female) and 200 with the Pro12Ala genotype (100 male and 100 female) and 400 age- and sex-matched normal glucose tolerance subjects with similar genotype profiles from the Chennai Urban Rural Epidemiology Study. Fasting serum adiponection levels were measured using radioimmunoassay. The Pro12Ala polymorphism was genotyped by PCR-restriction fragment length polymorphism using BstUI. All clinical and biochemical parameters were similar in the subjects with the Pro12Pro and Pro12Ala genotypes. There was no significant difference in serum adiponectin values between subjects with the Pro12Pro and Pro12Ala genotypes (males 5.4 vs. 5.8 microg/ml, P = 0.546; females 6.9 vs. 7.2 microg/ml, P = 0.748). Adiponectin values did not differ among these two genotypes even when categorized based on their diabetes status (normal glucose tolerance Pro12Pro 7.9 vs. Pro12Ala 7.7 microg/ml, P = 0.994; diabetes Pro12Pro 4.7 vs. Pro12Ala 5.4 microg/ml, P = 0.622). The Pro12Ala polymorphism of the PPARG gene is not associated with serum adiponectin levels in Asian Indians.

Hypoadiponectinemia Plays a Crucial Role in the Development of Nonalcoholic Fatty Liver Disease in Patients With Type 2 Diabetes Mellitus Independent of Visceral Adipose Tissue

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver injury. The spectrum of NAFLD is broad, extending from simple steatosis through nonalcoholic steatohepatitis (NASH). Insulin resistance has been found to increase the risk of NASH, and obesity, and decreased levels of adiponectin are important factors in determining the severity of insulin resistance. Recent evidence has indicated that hypoadiponectinemia is involved in hepatic steatosis and NASH. To investigate whether hypoadiponectinemia causes hepatic steatosis in type 2 diabetes mellitus (DM) patients independently of visceral adipose tissue, we measured the plasma adiponectin concentration, hepatic fat content based on the liver-to-spleen ratio (L/S ratio) according to computed tomography (CT) attenuation values, and the amount of visceral adipose tissue and subcutaneous adipose tissue by CT in 248 type 2 DM patients. We also investigated the relationship between the serum level of adiponectin and hepatic fibrosis. Significant correlations were observed between the L/S ratios and aspartate aminotransferase, alanine aminotransferase, visceral adipose tissue, subcutaneous adipose tissue, and serum adiponectin values (r=0.300, p=0.0007), and there was a highly significant inverse correlation between the visceral adipose tissue values and the serum adiponectin levels (r=-0.327, p<0.0002). The subcutaneous adipose tissue values, however, were not correlated with the serum adiponectin levels. Multiple regression analysis was used to quantify the impact of measured variables on the L/S ratio. After adjustment for age, gender, and visceral adipose tissue, the serum adiponectin levels were still significantly correlated with the L/S ratios (p=0.0064). And there was a stepwise decrease in the serum adiponectin in parallel to the severity of hepatic fibrosis. Hypoadiponectinemia is concluded to be involved in the etiology of hepatic steatosis independently of visceral adipose tissue content, and is considered to be an important factor in the progression of fibrosis; further studies will be necessary to elucidate the exact physiological role of adiponectin and its contribution to the progression of NASH.

Effect of DHEA-sulfate on adiponectin gene expression in adipose tissue from different fat depots in morbidly obese humans

A growing body of studies has demonstrated the inverse relationship between DHEA-sulfate (DHEA-S) and the pathological alterations associated with the metabolic syndrome. However, the mechanism by which DHEA-S treatment operates has not been elucidated completely. Adiponectin, an adipose-specific protein, is thought to have anti-diabetic and anti-atherosclerotic properties. Because fat depots differ in the impact of their relationship with the undesirable consequences of obesity, the aim of the present study was to investigate the effect of DHEA-S on adiponectin expression in both s.c. and visceral tissues in a morbidly obese population. We studied the in vitro expression of the adiponectin gene from paired biopsies of human visceral and s.c. adipose tissue, obtained from men and women (body mass index = 48.68+/- 7.43 kg/m2). Adipocytes were incubated for 24 h with or without DHEA-S. Adiponectin mRNA was measured by reverse transcription-quantitative PCR. In this population, DHEA-S plasma values were 141 +/- 105 microg/100 ml. Serum adiponectin values were under normal ranges. In basal conditions, s.c. tissue expressed higher amounts (58%) of adiponectin mRNA than visceral tissue (P = 0.027). Adiponectin expression was differentially regulated in the two depots by DHEA-S. There was a significant increase in adiponectin expression specifically in the visceral tissue (P = 0.020), but no significant effect of DHEA-S on the s.c. tissue (P = 0.738). In the present study, for the first time in humans, we have shown that DHEA-S treatment is a strong upregulator of adiponectin gene expression in omental adipocytes, suggesting that the positive effects observed by DHEA-S treatment in humans suffering from metabolic syndrome could be exerted through overexpression of adiponectin in the visceral depot.