Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Adiponectin”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources
PubMed2004

Adiponectin is related to CD146, a novel marker of endothelial cell activation/injury in chronic renal failure and peritoneally dialyzed patients.

Adiponectin has antiatherogenic properties and attenuates endothelial inflammatory responses. CD146 is a novel cell adhesion molecule localized at the endothelial junction. In renal failure, endothelial dysfunction and atherosclerosis are almost universal. We studied possible correlations between adiponectin, CD146, and other markers of endothelial cell injury in patients with chronic renal failure (CRF) on conservative treatment and patients with and without diabetic nephropathy maintained on chronic ambulatory peritoneal dialysis (CAPD). We assessed adiponectin, tissue factor pathway inhibitor (TFPI), plasminogen activator inhibitor (PAI-1), thrombin-activatable fibrinolysis inhibitor, and endothelial function/injury markers: von Willebrand factor, thrombomodulin, vascular cell adhesion molecule (VCAM), intercellular adhesion molecule, and CD146. Adiponectin was elevated in patients with CRF and on CAPD. It correlated significantly, with PAI-1, thrombin-activatable fibrinolysis inhibitor, intercellular adhesion molecule, VCAM, and CD146 in nondiabetics on CAPD. In diabetics, CAPD adiponectin correlated positively with C146 and VCAM and negatively with PAI and TFPI. In multivariate regression analysis, only CD146 remained a positive predictor of adiponectin in all CAPD patients. In CRF, adiponectin correlated with CD146. In healthy volunteers, adiponectin correlated with TFPI and CD146. Elevated adiponectin related to CD146 may be the expression of a counterregulatory response aimed at mitigating the consequences in endothelial damage and increased cardiovascular risk in renal failure.

Adiponectin↗
PubMed2005

Plasma adiponectin in nonalcoholic fatty liver is related to hepatic insulin resistance and hepatic fat content, not to liver disease severity.

Plasma levels of adiponectin are decreased in patients with nonalcoholic fatty liver disease (NAFLD), but the relationship among plasma adiponectin, insulin sensitivity, and histological features is unclear. In 174 NAFLD patients and 42 controls, we examined plasma adiponectin concentrations in relation to 1) lipid profile, indices of insulin resistance, and features of the metabolic syndrome (n = 174); 2) hepatic insulin resistance (clamp technique with tracer infusion) (10 patients); and 3) histological features at liver biopsy (n = 116). When the data from all subjects were combined, plasma adiponectin levels were positively associated with increased age, female gender, and plasma high-density lipoprotein levels, and negatively associated with waist circumference, body mass index, triglycerides, indices of insulin resistance, and aminotransferase levels, and also predicted the presence of the metabolic syndrome. In step-wise regression, increased age, female gender, waist circumference, triglyceride levels, and homeostasis model assessment independently associated with adiponectin (adjusted R(2), 0.329). In NAFLD, adiponectin was only associated with increased age, female gender, and triglycerides (adjusted R(2), 0.245). When the measured histological parameters were included in the model, plasma adiponectin levels were also inversely proportional to the percentage of hepatic fat content (adjusted R(2), 0.221), whereas necroinflammation and fibrosis did not fit in the model. Adiponectin was negatively correlated with insulin-suppressed endogenous glucose production during the clamp (P = 0.011). The results demonstrate that decreased levels of circulating adiponectin in NAFLD are related to hepatic insulin sensitivity and to the amount of hepatic fat content. Hypoadiponectinemia in NAFLD is part of a metabolic disturbance characterized by ectopic fat accumulation in the central compartment.

Adiponectin↗
PubMed2005

The relationships of adiponectin with insulin and lipids are strengthened with increasing adiposity.

CONTEXT: Adipose tissue inflammation has been implicated in the pathogenesis of obesity-related comorbidities. Adiponectin, an antiinflammatory protein, improves insulin sensitivity and lipid levels systemically. Because adiponectin is secreted by adipocytes, it may also act locally to counteract insulin resistance and dyslipidemia worsened by inflammation. OBJECTIVE: The aim of this study was to determine whether associations between adiponectin and insulin sensitivity and lipids are stronger with increasing adiposity. DESIGN: This cross-sectional study involved participants in The Princeton School District Study. SETTING: The study was conducted in the Princeton City schools (Cincinnati, OH) during the 2001-2002 school year. PARTICIPANTS: A total of 1196 non-Hispanic White and Black students in grades 5-12 participated. MAIN OUTCOME MEASURE: The relationships between adiponectin and high-density lipoprotein, triglycerides, and insulin were measured. To test our hypothesis, we: 1) compared correlation and regression coefficients of lean and nonlean individuals, and 2) incorporated an adiponectin by adiposity interaction in regression models. RESULTS: For high-density lipoprotein and triglycerides, the relationship with adiponectin, although present among lean adolescents, strengthened with increasing adiposity. However, with insulin, a relationship with adiponectin was only present among nonlean adolescents. CONCLUSIONS: These analyses suggest that adiponectin's relationship with insulin and lipids strengthens with increasing adiposity, such that heavier adolescents have a greater benefit from high levels of adiponectin than their lean counterparts.

Adiponectin↗
PubMed2005

Plasma adiponectin levels are associated with insulin resistance, but do not predict future risk of coronary heart disease in women.

CONTEXT: Low adiponectin levels predict type 2 diabetes, and one prospective study in men reported its independent prediction of vascular events. Many observers thus already consider adiponectin to be a major part of the "common soil" underpinning diabetes and vascular disease. OBJECTIVE: The objective of this study was to assess the association between adiponectin and incident coronary heart disease (CHD) risk in the British Women's Heart and Health Study. DESIGN: This was a prospective (4 yr) case (n = 167) control (n = 334) study nested within the 4286 women in British Women's Heart and Health Study. SETTING: The study was performed in a primary care setting. PARTICIPANTS: The study consisted of women (n = 4286) randomly selected from 23 British towns between 1999 and 2001, who were 60-79 yr of age at baseline. MAIN OUTCOME MEASURES: Association of adiponectin with CHD risk factors and incident CHD events were the main outcome measures. RESULTS: Among both cases and controls, adiponectin positively correlated with age and high-density lipoprotein cholesterol and inversely correlated with waist to hip ratio, fasting insulin, fasting glucose, homeostasis model assessment of insulin resistance scores, C-reactive protein, and triglycerides. However, despite adequate power and these associations with CHD risk factors, adiponectin did not predict CHD events in unadjusted or adjusted analyses. The relative risk ratio for a doubling of adiponectin was 0.93 (95% confidence interval, 0.78, 1.11). CONCLUSIONS: It is premature to consider adiponectin as a root for vascular disease in women despite its association with insulin resistance and diabetes. Additional prospective studies are required to determine whether there is a true sex difference in the effect of adiponectin on CHD.

Adiponectin↗
PubMed2001

Weight reduction increases plasma levels of an adipose-derived anti-inflammatory protein, adiponectin.

Adiponectin, an adipose tissue-specific plasma protein, was recently revealed to have anti-inflammatory effects on the cellular components of vascular wall. Its plasma levels were significantly lower in men than in women and lower in human subjects with obesity, type 2 diabetes mellitus, or coronary artery disease. Therefore, it may provide a biological link between obesity and obesity-related disorders such as atherosclerosis, against which it may confer protection. In this study, we observed the changes of plasma adiponectin levels with body weight reduction among 22 obese patients who received gastric partition surgery. A 46% increase of mean plasma adiponectin level was accompanied by a 21% reduction in mean body mass index. The change in plasma adiponectin levels was significantly correlated with the changes in body mass index (r = -0.5, P = 0.01), waist (r = -0.4, P = 0.04) and hip (r = -0.6, P = 0.0007) circumferences, and steady state plasma glucose levels (r = -0.5, P = 0.04). In multivariate linear regression models, the increase in adiponectin as a dependent variable was significantly related to the decrease in hip circumference (beta = -0.16, P = 0.028), after adjusting body mass index and waist circumference. The change in steady state plasma glucose levels as a dependent variable was related to the increase of adiponectin with a marginal significance (beta = -0.92, P = 0.053), after adjusting body mass index and waist and hip circumferences. In conclusion, body weight reduction increased the plasma levels of a protective adipocytokine, adiponectin. In addition, the increase in plasma adiponectin despite the reduction of the only tissue of its own synthesis suggests that the expression of adiponectin is under feedback inhibition in obesity.

Adiponectin↗
PubMed2002

Decreased plasma adiponectin concentrations in women with dyslipidemia.

Adiponectin, the gene product of the adipose most abundant gene transcript 1, is a novel adipocyte-derived peptide that has been considered to have antiinflammatory and antiatherogenic effects. To characterize the relationship between adiponectin and lipids metabolism, we measured fasting plasma adiponectin concentration by ELISA, serum total cholesterol, high-density lipoprotein cholesterol (HDL-C), triglyceride (TG), and apolipoprotein (apo) levels in 352 nondiabetic women, 16-86 yr old, with a wide range of body weight [body mass index (BMI), 14.8-36.3 kg/m(2)]. Plasma adiponectin concentrations in women with the highest tertile of TG (1.69 mM < or approximately) were decreased, compared with the middle (1.13 < or = approximately < 1.69) or lowest tertile of TG (approximately < 1.13) (5.9 +/- 0.5 vs. 7.5 +/- 0.3, 9.2 +/- 0.2 microg/ml; P < 0.005, 0.001). Plasma adiponectin with the lowest tertile of HDL-C (approximately < 1.16 mM) was decreased, compared with the middle (1.16 < or = approximately < 1.81) or highest tertile of HDL-C (1.81 < or approximately ) (5.7 +/- 0.5 vs. 7.8 +/- 0.2, 10.1 +/- 0.4 microg/ml; both P < 0.001). These relationships had similar tendencies after adjustment for BMI, body fat mass, age, or diastolic blood pressure. Adiponectin was negatively correlated with serum TG (r = -0.33, P < 0.0001), atherogenic index [(total cholesterol - HDL-C)/HDL-C] (r = -0.34, P < 0.0001), apo B (r = -0.45, P < 0.0001), or apo E (r = -0.29, P < 0.05), and positively correlated with serum HDL-C (r = 0.39, P < 0.0001) or apo A-I levels (r = 0.42, P < 0.002). Those negative relationships became stronger after adjusting for BMI or body fat mass. The slightly positive correlation between adiponectin and age, blood urea nitrogen, or creatinine levels was also observed (all P < 0.001). These results indicate that high-TGnemia and low-HDL-Cnemia are associated with low plasma adiponectin concentrations in nondiabetic women. Further efforts must now be targeted to determine whether adiponectin causes these lipid abnormalities and thus whether it is partly responsible for the atherogenic risk seen in the metabolic syndrome.

Adiponectin↗
PubMed2006

Serum adiponectin concentration: its correlation with diabetes-related traits and quantitative trait loci analysis in mouse SMXA recombinant inbred strains.

Adiponectin is thought to be an important mediator of insulin sensitivity and atherosclerosis. Using mouse 19 SMXA recombinant inbred (RI) strains, a powerful tool for analyzing multifactorial genetic traits, we found relationships between serum adiponectin levels and diabetes-related traits, body mass index, and serum lipid levels, and also determined the loci controlling serum adiponectin levels by quantitative trait loci (QTL) analysis. RI strains exhibited widely ranging serum adiponectin concentration distribution patterns and diabetes-related traits. The serum adiponectin concentration showed the strongest negative correlation with fasting serum insulin concentration, but negative correlations were also observed with serum triglycerides, cholesterol, and liver weight. In contrast, neither the body mass index nor the blood glucose concentration correlated with serum adiponectin levels. These results suggest that hypoadiponectinemia might be used as a predictor of insulin resistance. In addition, two suggestive QTLs for serum adiponectin concentration were detected on Chromosome (Chr) 7, and an A/J allele at these loci was associated with elevated serum adiponectin concentrations. Identification of genes responsible for regulating the serum adiponectin concentration might lead to the development of novel treatments for patients with diabetes concomitant with hypoadiponectinemia.

Adiponectin↗
PubMed2005

Usefulness of serum adiponectin level as a diagnostic marker of metabolic syndrome in obese Japanese children.

This study aimed 1) to investigate the relationship between serum adiponectin levels and metabolic disorders and 2) to clarify the usefulness of serum adiponectin level as a diagnostic marker of metabolic syndrome in obese Japanese children. One hundred obese boys aged 8 to 13 years were examined. Serum adiponectin levels were measured by radioimmunoassay using a commercial kit. Abdominal fat thickness (maximum preperitoneal fat thickness: P(max); minimum subcutaneous fat thickness: S(min)) was measured by ultrasonography. The relationships between adiponectin and clinical characteristics were analyzed by simple regression. The relationships between anthropometric measurements and metabolic disorders were analyzed among three groups divided according to adiponectin percentile. The prevalence of metabolic syndrome was also analyzed, with metabolic syndrome defined as the presence of three or more complications of obesity. The criteria for metabolic syndrome by adiponectin were subjected to a receiver operating characteristic (ROC) analysis. Body weight, waist circumference, P(max), alanine aminotransferase and fasting serum insulin were all inversely correlated with adiponectin. There were significant differences in the prevalence of severe obesity, the accumulation of visceral adipose tissue, hyperinsulinemia, high serum low density lipoprotein-cholesterol, the number of complications of obesity and the prevalence of metabolic syndrome among the three groups. The area under the ROC curve for adiponectin was 0.672 +/- 0.055 and the cut-off value was 6.65 microg/ml. Hypoadiponectinemia was associated with visceral fat accumulation and metabolic syndrome in obese Japanese boys. Evaluation of adiponectin might contribute to an early intervention for obese children with metabolic syndrome.

Adiponectin↗
PubMed2006

Impact of gastric banding on plasma adiponectin levels.

BACKGROUND: Several endocrine abnormalities are reported in obesity. In an earlier study, we found that the changes in BMI following laparoscopic adjustable gastric banding (LAGB) were associated with changes in hormone profiles such as insulin and proinsulin. In the current study, we explored the changes in plasma adiponectin levels in morbidly obese subjects who lost abundant weight following LAGB. METHODS: 23 adult morbidly obese patients (15 females), aged 21-56 years, were studied. Blood samples were collected before, and 6 and 14 months after LAGB. The plasma adiponectin levels were determined by commercial kit (B-Bridge International, Inc). Statistical analysis was based on one-way repeated measures ANOVA, followed by Student-Newman-Keuls post-hoc test. Regression model was used to look for predictors of adiponectin change after LAGB. RESULTS: Mean BMI before surgery was 46.04+/-4.44 kg/m2, and decreased significantly by 18% 6 months after surgery to 37.67+/-4.47 kg/m2. BMI further decreased by 32% 14 months after surgery to a mean of 31.30+/-4.65 kg/m2 (P=.000). The mean adiponectin level before surgery was 3997+/-1766 microg/ml, and increased significantly by 16% to 4763+/-1776 microg/ml 6 months after surgery, and to 6336+/-3292 microg/ml (37%) 14 months after surgery. Although BMI persistently decreased, while adiponectin persistently increased, BMI did not correlate with adiponectin. CONCLUSION: In morbidly obese patients who underwent LAGB, adiponectin levels persistently increased, probably due to the reduction of visceral fat mass. Adiponectin plasma increase was correlated with proinsulin levels prior to the surgery. The interaction between adiponectin, proinsulin and BMI change in morbid obesity merits further investigation.

Adiponectin↗
PubMed2005

Effects of antidiabetic treatment with metformin and insulin on serum and adipose tissue adiponectin levels in db/db mice.

Decreased circulating levels of adiponectin, a novel adipose-derived adipocytokine, in obesity possibly contribute to the development of insulin resistance which is a major factor in the pathogenesis of type 2 diabetes. The present study was conducted to examine whether circulating and adipose tissue adiponectin levels are modulated by chronic treatment with metformin and intensive treatment with insulin in murine models of obesity and type 2 diabetes, db/db mice with a C57BL/KsJ genetic background. Nine-week-old male db/db mice were treated with metformin, insulin, and vehicle for 4 weeks. Expectedly, metformin treatment led to inhibition of weight gain and improvement of hyperinsulinemia. Insulin treatment lowered fasting blood glucose levels to normal values, although it sustained hyperinsulinemic state. However, after 4 weeks of treatment, serum adiponectin levels were not significantly elevated in either metformin-treated or insulin-treated db/db mouse group (14.2 +/- 0.7 and 16.7 +/- 1.0 microg/ml, respectively) compared to vehicle-treated group (14.9 +/- 0.6 microg/ml). Similarly, adipose tissue adiponectin levels determined by Western blot analysis were not increased in either metformin-treated or insulin-treated group relative to vehicle-treated group. Recent studies have shown that adiponectin possibly has the same physiological effects on lipid and glucose metabolism that metformin has. Therefore, an elevation in blood concentration of metformin following the treatment might lead to suppression in adiponectin synthesis in adipose tissue, independent of inhibition in weight gain and improvement in hyperinsulinemia by metformin treatment. The present results indicate that adiponectin is not involved in the mechanism by which metformin treatment enhances insulin sensitivity. Moreover, our results suggest that adiponectin synthesis in adipose tissue may be suppressed under hyperinsulinemic state sustained by insulin treatment, even though hyperglycemia is markedly reduced. We conclude that antidiabetic treatment with metformin and insulin does not affect circulating and adipose tissue adiponectin levels.

Adiponectin↗
PubMed2006

Hypoadiponectinemia in lean lactating women: Prolactin inhibits adiponectin secretion from human adipocytes.

Adiponectin is an adipocyte-derived hormone involved in glucose, lipid and energy metabolism. A low plasma adiponectin concentration is associated with insulin resistance, obesity and atherosclerosis. In women, energy homeostasis is remarkably changed during gestation and lactation in order to supply sufficient nutrition for a fetus or newborn. In this study we aimed to elucidate the physiological impact of gestation and lactation on the plasma adiponectin levels and the influence of reproduction-related hormones on adiponectin secretion. We studied the longitudinal changes in plasma adiponectin concentration during pregnancy (1st, 2nd and 3rd trimester) and lactation (3 days and 1 month after the delivery) in lean healthy women (n = 22). The plasma adiponectin level declined slightly as the pregnancy advanced and reached its lowest level during lactation (12.25 +/- 0.182 microg/ml at early pregnancy vs. 6.88 +/- 0.375 microg/ml at 3 days postpartum, p < 0.001). In order to investigate the role of the lactogenic hormone prolactin in the decrease of plasma adiponectin levels during lactation, we further performed in vitro experiments using human primary cultured adipocytes. Western blotting of the adipocyte lysate and ELISA of the culture medium revealed that exogenous prolactin inhibited both production and secretion of adiponectin in a dose-dependent manner. Our results thus suggests that prolactin affects the regulation of maternal metabolism through suppression of adiponectin.

Adipocytes↗
PubMed2003

Decreased plasma adiponectin concentrations in nondiabetic women with elevated homeostasis model assessment ratios.

OBJECTIVE: Whether the adipocyte-derived protein adiponectin is associated with insulin resistance independently of the effects of adiposity and the diabetic state is an important question. We explored, in a cross-sectional study of 486 Japanese nondiabetic women, the relationship between the calculated insulin resistance (homeostasis model assessment ratio (HOMA-R)) and adiponectin levels determined using a validated sandwich ELISA. DESIGN AND METHODS: All participants were stratified into tertiles for HOMA-R (approximately <1.5, 1.5< or = approximately <3.0, 3.0< or = approximately ) and the differences across tertiles of continuous variables were tested with ANOVA. Two-way ANOVA was used to determine possible relationships for plasma adiponectin between tertiles of HOMA-R and several stratified parameters. Multiple regression analyses were performed with HOMA-R or fasting serum insulin as dependent variable, and diastolic blood pressure (BP), body mass index (BMI), serum triglyceride (TG), leptin and adiponectin as independent determinants. RESULTS: Mean plasma adiponectin in the high HOMA-R group decreased compared with that in the low HOMA-R group both before (mean+/-s.e.m. 6.2+/-0.6 vs 9.2+/-0.3 microg/ml, P<0.001) and after adjustment for body fat mass (BFM) as kg or percent (0.31+/-0.04 vs 0.69+/-0.03, 0.18+/-0.02 vs 0.34+/-0.01, both P<0.001). HOMA-R was inversely associated with adiponectin levels both before (r=-0.37, P<0.001) and after adjustment for BFM (r=-0.49, -0.46, both P<0.001). After covariate adjustment for age, diastolic BP, BMI and serum TG, HOMA-R retained a significant correlation with adiponectin/BFM (kg). Both adiponectin and leptin were the significant determinants of HOMA-R or fasting insulin in multiple regression models. CONCLUSIONS: Adiponectin was inversely associated with insulin resistance in nondiabetic subjects, independently from age, BP, adiposity and serum lipids. Because adiponectin is thought to have an anti-atherogenic action, the presence of hypoadiponectinemia may predispose subjects to atherosclerosis, and may progress the atherogenesis in insulin resistance.

Adiponectin↗
PubMed2004

The associations between plasma adiponectin, ghrelin levels and cardiovascular risk factors.

OBJECTIVE: Ghrelin is a recently discovered peptide, which is produced primarily in the stomach. This orexigenic peptide participates not only in the induction of mealtime hunger but also in long-term body weight regulation and energy homeostasis. Adiponectin is a protein secreted by adipocytes, and has been proposed to mediate obesity-related insulin resistance. Moreover, concentrations of adiponectin are reduced in individuals with obesity, insulin resistance and cardiovascular disease. However, human data are sparse about the direct relationship between adiponectin, ghrelin and cardiovascular risk factors including insulin resistance. DESIGN: Three hundred and thirty-eight elderly Korean women (mean age+/-s.d., 72.3+/-5.5 years) were included in the present study. METHODS: Plasma ghrelin and adiponectin levels were measured by RIA. Anthropometric measurements were taken and a 75 g oral glucose tolerance test performed. Fasting insulin and lipid profile were measured and insulin resistance was determined using the homeostasis model assessment insulin resistance index (HOMA-R) and the quantitative insulin sensitivity check index. RESULTS: Plasma adiponectin levels were negatively correlated with central obesity indices such as waist circumference (r=-0.27, P<0.001) and waist-to-hip ratio (WHR) (r=-0.32, P<0.001), and with insulin resistance indices such as fasting insulin (r=-0.17, P=0.004) and HOMA-R (r=-0.13, P=0.035). Plasma ghrelin levels were negatively correlated with WHR (r=-0.12, P=0.03), but plasma adiponectin and ghrelin levels were not correlated (r=0.03, P=0.66). Multiple regression analysis showed that adiponectin was associated with WHR, fasting insulin and fasting glucose levels. When ghrelin was used as a dependent variable, only WHR remained in the final fitted model. CONCLUSION: Fasting plasma adiponectin and ghrelin levels were found to be associated with central obesity or insulin resistance. However, plasma adiponectin and ghrelin concentrations were not associated with each other in elderly Korean women.

Adiponectin↗
PubMed2004

Adiponectin may play a part in the pathogenesis of diabetic retinopathy.

OBJECTIVES: To measure plasma adiponectin concentrations in patients with type 2 diabetes and to investigate any association with the severity of diabetic retinopathy, because adiponectin seems to be an important modulator for metabolic and vascular diseases. METHODS: Seventy-four patients (mean age 46.8+/-5.1 years; body mass index (BMI), 26.8+/-2.10 kg/m(2)) and 54 healthy volunteers (mean age 46.8+/-5.4 years; BMI 26.47+/-2.33 kg/m(2)) were included. RESULTS: Adiponectin concentrations in the patients were significantly lower than those in controls (4.71+/-2.11 microg/ml for patients, n=74; 15.95+/-3.72 microg/ml for controls, n=54; P<0.001). In the patients group there was a significant negative correlation between adiponectin and homeostasis model assessment index (r=-0.318, P=0.006 respectively). Plasma adiponectin concentrations in patients with proliferative diabetic retinopathy (n=20; 3.16+/-1.83 microg/ml) or non-proliferative diabetic retinopathy (n=24; 3.97+/-1.47 microg/ml, P=0.014) were significantly lower than those in patients without diabetic retinopathy (n=30; 6.30+/-1.57 microg/ml, P=0.001). When the presence of diabetes was defined as the final variable in the conditional logistic regression model with the adiponectin concentration as the continuous variable, adiponectin was significantly involved in the model. CONCLUSION: The results show that adiponectin concentrations are lower in patients with type 2 diabetes and that the concentrations are associated with the severity of diabetic retinopathy. Our findings suggest that adiponectin may take part in the pathogenesis of diabetic retinopathy.

Adiponectin↗
PubMed2004

Plasma adiponectin and serum advanced glycated end-products increase and plasma lipid concentrations decrease with increasing duration of type 2 diabetes.

OBJECTIVE: To prospectively follow the concentrations of plasma adiponectin (p-adiponectin) and serum advanced glycation end-products (s-AGE) in relation to plasma lipids and retinopathy over 3 years in type 2 diabetic patients. DESIGN AND METHODS: P-adiponectin, s-AGE, plasma lipids and diabetic retinopathy were prospectively evaluated in 61 type 2 diabetic patients at baseline and at follow up 3 years later. RESULTS: Mean p-adiponectin (from 8.84+/-5.14 to 11.05+/-6.16 microg/ml; P=0.006) and s-AGE (from 637+/-242 to 781+/-173 ng/ml; P<0.0001) concentrations had increased at follow up. In addition, HbA1c (7.7+/-1.7 to 7.4+/-1.4%; P=0.0045) and fasting C-peptide (1.00+/-0.38 to 0.81+/-0.35 nM; P=0.019) had decreased and all lipid variables had significantly improved at follow up. P-adiponectin correlated inversely with fasting C-peptide (r(s)=-0.273; P=0.045) and low-density lipoprotein (LDL)/high-density lipoprotein (HDL) ratio (r(s)=-0.362; P=0.011), and directly with plasma HDL cholesterol (r(s)=0.381; P=0.005) at follow up. Analysis of variance with adiponectin and s-AGE as dependent variables and fasting C-peptide, plasma HDL and plasma LDL cholesterol as covariates demonstrated that the increase in s-AGE was independent (P=0.001) and the increase in p-adiponectin dependent on covariate changes (P=0.862). There was a slight correlation between s-AGE at baseline versus the degree of retinopathy at follow up (r(s)=0.281; P=0.0499). CONCLUSION: Both p-adiponectin and s-AGE increased during the 3 years. The increase in p-adiponectin was explained by improvements in insulin sensitivity and dyslipidaemia, whereas the increase in s-AGE was independent of changes in metabolic covariates. s-AGE increase when the duration of type 2 diabetes increases.

Adiponectin↗
PubMed2006

Adiponectin and the development of diabetes in patients with coronary artery disease and impaired fasting glucose.

OBJECTIVES: Adiponectin has insulin-sensitizing properties, and high adiponectin levels have been shown to be associated with reduced risk of developing diabetes. Patients with coronary artery disease (CAD) have relatively low adiponectin levels and high prevalence of glucose intolerance. The role of adiponectin in predicting the development of diabetes in this high-risk group has not been determined. The study aimed to determine whether baseline adiponectin levels predict the development of diabetes in a group of patients with CAD and impaired fasting glucose (IFG). METHODS: A total of 588 patients who participated in the Bezafibrate Infarction Prevention (BIP) study and who had at baseline fasting glucose of 100-125 mg/dl were included and followed for 6.2+/-1.3 years. Adiponectin was determined in frozen plasma samples taken at baseline. RESULTS: Of the patients with IFG at baseline, 256 (44%) developed diabetes during follow-up. The patients who developed diabetes had at baseline higher body-mass index, fasting glucose, C-reactive protein, triglycerides, homeostatic assessment of insulin resistance (HOMA-IR) and diastolic blood pressure than patients who did not develop diabetes. Adiponectin levels at baseline were significantly lower in patients who developed diabetes than in patients who did not develop diabetes (P = 0.009, nonparametric Kruskall-Wallis test). An increase of 1 unit of natural logarithm of adiponectin level was associated with a hazard ratio of 0.77 (95% CI, 0.61-0.96) for diabetes development. CONCLUSION: Patients with CAD and IFG have a very high rate of conversion to type 2 diabetes. Even in this high-risk group, high adiponectin levels are associated with reduced risk of developing diabetes.

Adiponectin↗
PubMed2004

Cloning and expression of porcine adiponectin, and its relationship to adiposity, lipogenesis and the acute phase response.

Adiponectin is an adipocyte-derived hormone that has been implicated recently in the regulation of inflammation in immunocytes, and in lipid metabolism and glucose homeostasis in liver, skeletal muscle and adipocytes. However, information in non-rodent models is limited. We have cloned and sequenced the porcine adiponectin open reading frame and evaluated the regulation of adiponectin in vivo following lipopolysaccharide (LPS) or E. coli administration. The porcine sequence shares approximately 88, 86, 85 and 83% homology with the dog, human, cow and mouse adiponectin respectively, and 79-83% similarity with dog, human, cow and mouse proteins at the amino acid level, based on the translated porcine sequence and GenBank submissions for the other species. Relative serum adiponectin concentrations were not altered in pigs infused with E. coli, and mRNA expression in adipose tissue was not responsive to LPS. However, analysis of serum from very lean vs a substantially fatter genotype of pig indicated that relative circulating adiponectin concentrations are higher (P<0.01) in the lean pigs than in the fatter genotype, and that the difference is established relatively early in the growth curve. Also, incubating pig adipocytes for 6 h with recombinant pig adiponectin resulted in an approximately 30% reduction (P<0.05) in lipogenesis compared with adipocytes under basal conditions and with those incubated in the presence of insulin. This is the first report in any species that adiponectin antagonizes the incorporation of glucose carbon into lipid in the adipocyte, and provides additional evidence that adiponectin acts as an autocrine regulatory factor to regulate energy metabolism.

Acute-Phase Reaction↗
PubMed2006

Measurement of the high-molecular weight form of adiponectin in plasma is useful for the prediction of insulin resistance and metabolic syndrome.

OBJECTIVE: The high-molecular weight (HMW) form of adiponectin, an adipocyte-derived insulin-sensitizing hormone, has been reported to be the most active form of this hormone. We investigated whether measurement of plasma HMW adiponectin levels, using our newly developed enzyme-linked immunosorbent assay system for selective measurement of human HMW adiponectin level, may be useful for the prediction of insulin resistance and metabolic syndrome. RESEARCH DESIGN AND METHODS: A total of 298 patients admitted for diabetes treatment or coronary angiography served as study subjects. Receiver operator characteristic (ROC) curves for the HMW ratio (HMWR; ratio of plasma level of HMW adiponectin to that of total adiponectin) and plasma total adiponectin levels were plotted to predict the presence of insulin resistance and metabolic syndrome. RESULTS: The area under the ROC curve (AUC) of the HMWR values to predict the presence of insulin resistance was significantly larger than that of plasma total adiponectin level in total subjects (0.713 [95% CI 0.620-0.805] vs. 0.615 [0.522-0.708], P = 0.0160). The AUC for the HMWR values to predict the presence of metabolic syndrome was significantly larger than that for plasma total adiponectin levels in men (0.806 [0.747-0.865] vs. 0.730 [0.660-0.800], P = 0.0025) and in women (0.743 [0.659-0.828] vs. 0.637 [0.532-0.742], P = 0.0458). CONCLUSIONS: The HMWR value has better predictive power for the prediction of insulin resistance and metabolic syndrome than plasma total adiponectin level.

Adiponectin↗