Adiponectin Resistance Research Articles

Variations of Adipokines and Insulin Resistance in Primary Hypothyroidism.

Hypothyroidism is a common concern in endocrinology practice, which plays a significant role in metabolic and development processes. Obesity, hyperlipidaemia and hypertension may complicate hypothyroidism. Recent studies have shown that cytokines like leptin and adiponectin, secreted by adipose tissue and exert their endocrinal functions by modulating appetite, obesity and insulin sensitivity in conjunction with thyroid hormones. Interrelation between thyroid hormone, insulin resistance and adipokines are not yet clear. To estimate serum leptin, adiponectin and insulin resistance in patients with hypothyroidism and to compare with control subjects and measure the relation between the mean value of one variable with others. Forty primary hypothyroidism patients and forty age and sex matched controls were selected for the study with informed consent. Fasting serum Thyroid Stimulating Hormone (TSH), leptin, adiponectin, glucose and insulin were estimated. Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) was evaluated from fasting plasma glucose and serum insulin levels. Statistical analysis was carried out using SPSS version 17.0. Unpaired t-test and regression analysis were used to compare and determine the dependence, p<0.05 was considered significant. Serum TSH, leptin, adiponectin HOMA-IR were significantly higher (p<0.05) in patients with hypothyroidism (10.37±4.10, 10.97±0.60, 31.09±4.07, 3.64±0.40) than controls (2.41±2.09, 10.37±0.12, 33.32±1.44, 2.36±0.35). Regression analysis showed that leptin was significantly (p=0.054) dependent on adiponectin but not on others. Increased oxidative stress by hypothyroid mediated leptin secretion and increased insulin resistance can down-regulate the adiponectin secretion and future complications. Serum estimation and correction of imbalance of adipokines in hypothyroidism can prevent severe consequences.

Aqueous seed extract of Hunteria umbellata (K. Schum.) Hallier f. (Apocynaceae) palliates hyperglycemia, insulin resistance, dyslipidemia, inflammation and oxidative stress in high-fructose diet-induced metabolic syndrome in rats

Ethnopharmacological relevanceHunteria umbellata is used in the management and treatment of diabetes and obesity in Nigeria. This study evaluates the effect of aqueous seed extract of Hunteria umbellata on insulin resistance, dyslipidemia, inflammation and oxidative stress in high-fructose diet-induced metabolic syndrome Materials and methodsRats were randomized into seven groups (A-G). Control (group A) and group C rats received control diet for nine weeks while rats in groups B, D – G were placed on high-fructose diet for 9 weeks. In addition to the diets, groups C – F rats orally received 400, 100, 200 and 400mg/kg body weight aqueous seed extract of Hunteria umbellata for 3 weeks starting from 6th – 9th week. ResultsHigh-fructose diet (when compared to control rats) mediated a significant (p<0.05) increase in body weight, body mass index and abdominal circumference. Similarly, levels of blood glucose, insulin, leptin, adiponectin and insulin resistance were increased. It also caused a significant increase in the levels of cholesterol, triglycerides, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, atherogenic index, cardiac index and coronary artery index while high-density lipoprotein cholesterol was decreased significantly. Levels of proinflammatory factor, tumour necrosis factor-α, interleukin-6 and 8 were also increased by the high fructose diet. Moreover, it mediated decrease in activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glucose 6-phosphate dehydrogenase and level of glutathione reduced. Conversely, levels of malondialdehyde, conjugated dienes, lipid hydroperoxides, protein carbonyl and fragmented DNA were elevated. Aqueous seed extract of Hunteria umbellata significantly ameliorated the high fructose diet-mediated alterations. ConclusionsFrom this study, it is concluded that aqueous seed extract of Hunteria umbellata possesses hypoglycemic, hypolipidemic and antioxidants abilities as evident from its capability to extenuate insulin resistance, dyslipidemia, inflammation and oxidative stress in high-fructose diet-induced metabolic syndrome rats.

Downregulation of AdipoR1 is Associated with Increased Circulating Adiponectin Levels in Serbian Chronic Kidney Disease Patients

SummaryBackgroundSince the rise in plasma adiponectin levels in chronic kidney disease (CKD) patients has not yet been elucidated, we sought to investigate if patients on hemodialysis (HD) have altered expression of adiponectin receptors in peripheral blood mononuclear cells (PBMCs) compared to healthy subjects.MethodsThis study included 31 patients with chronic kidney disease on HD and 33 healthy subjects (CG). Circulating adiponectin levels were measured by ELISA while AdipoR1 and AdipoR2 mRNA levels in PBMCs were determined by real-time PCR.ResultsPlasma adiponectin levels were significantly higher in patients compared to control group (P=0.036). After adjustment for age, BMI and creatinine, this difference became even more significant (P=0.004). In both groups adiponectin correlated with creatinine (CG: r=-0.472, P=0.006; HD: r=-0.375, P=0.038), triglycerides (CG: r=- 0.490, P=0.004; HD: r=-0.488, P=0.005), insulin (CG: r=-0.386, P=0.038; HD: r=-0.506, P=0.012) and high density lipoprotein cholesterol (HDL-C) (CG: r=-0.672, P<0.001; HD: r=-0.584, P=0.001). Significantly lower expression of PBMCs AdipoR1 mRNA was found in patients compared to CG (P=0.034), while AdipoR2 mRNA levels were similarly expressed in PBMCs in both groups.ConclusionsComplex pathological processes in CKD cause downregulation of AdipoR1 which could ultimately influence AdipoR1 protein levels leading to a state of ≫adiponectin resistance≪.

The impact of rapid weight loss (4%) on leptin, adiponectin, and insulin resistance in elite adult free style wrestlers.

The effect of rapid weight loss program on adipocytokines is not yet clear. Therefore the aim of the present study was the effect of rapid weight loss (4%) on leptin, adiponectin, and insulin resistance in elite free style wrestlers. For this purpose, fifteen young freestyle wrestlers (weight 67.6±0.8, BMI 22.5±0.21 kg/m², body fat percent 6.12±0.18, waist to hip circumference ratio 0.82±0.08) in two weight categories (60 and 66 kg) were randomly selected. Caloric intake (mean 7 days measured by Food analyzer software) measured at 1 week before weight loss program by standard methods. Wrestlers performed a week rapid weight loss (average of 4% of body weight loss) protocol by caloric and water restriction by 60% (600-700 kcal per day), under the supervision of their coach. Anthropometric characteristics, leptin, adiponectin and insulin resistance were measured before and 12 and 36 hours after rapid weight loss program. Rapid weight loss program with 4% of weight loss had a significantly reduced impact on anthropometric factors; leptin level, insulin resistance, and increased beta cell function, while the changes of adiponectin were not significant after rapid weight loss. Findings of this study shows that rapid weight loss program significantly decreased leptin, L/A ratio and HOMA-IR, without significant changes on adiponectin levels. These changes may have harmful physiological effects on wrestlers' bodies but they can be useful to regulate of fatty acid, glucose metabolism, and insulin resistance.

Four months of combined and compound morning training improves testosterone/cortisol ratio, adiponectin and insulin resistance in male students

Purpose The aim of the study was to assess whether combined and compound morning training (CCMT) can improve hormonal and metabolic profiles in healthy male students.

Changes in profile of lipids and adipokines in patients with newly diagnosed hypothyroidism and hyperthyroidism.

Changes in profile of lipids and adipokines have been reported in patients with thyroid dysfunction. But the evidence is controversial. The present study aimed to explore the relationships between thyroid function and the profile of lipids and adipokines. A cross-sectional study was conducted in 197 newly diagnosed hypothyroid patients, 230 newly diagnosed hyperthyroid patients and 355 control subjects. Hypothyroid patients presented with significantly higher serum levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDLC), fasting insulin, resistin and leptin than control (p < 0.05). Hyperthyroid patients presented with significantly lower serum levels of high-density lipoprotein cholesterol, LDLC and leptin, as well as higher levels of fasting insulin, resistin, adiponectin and homeostasis model insulin resistance index (HOMA-IR) than control (p < 0.05). Nonlinear regression and multivariable linear regression models all showed significant associations of resistin or adiponectin with free thyroxine and association of leptin with thyroid-stimulating hormone (p < 0.001). Furthermore, significant correlation between resistin and HOMA-IR was observed in the patients (p < 0.001). Thus, thyroid dysfunction affects the profile of lipids and adipokines. Resistin may serve as a link between thyroid dysfunction and insulin resistance.

The role of adipose tissue and adipokines in the manifestation of type 2 diabetes in the long-term period following myocardial infarction.

BackgroundThis study aimed to evaluate the markers of insulin resistance and adipokine status in patients with visceral obesity during hospitalization following myocardial infarction (MI) and assess the disturbances of carbohydrate metabolism present 1 year after MI onset.Methods94 male patients with MI were recruited. The exclusion criteria were as follows: age less than 50 or greater than 80 years, the presence of type 2 diabetes mellitus (T2DM), and a prior history of pronounced renal failure.Obesity types were defined according to body mass index (BMI), waist circumference (WC) and visceral adipose tissue (VAT) area. Glucose, insulin, adiponectin, leptin, and insulin resistance (IR) index were measured on days 1 and 12 after the onset of MI. New-onset type 2 diabetes was assessed 1 year after MI onset.ResultsAccording to computed tomography assessments of all study patients, 69 % of patients with MI suffered from visceral obesity. The VAT area was more closely associated with the risk of developing type 2 diabetes compared with the obesity parameters, BMI and WC. Patients with a VAT area greater than 130 cm2 had a 3.6-fold higher risk of developing type 2 diabetes. The presence of IR and hyperleptinemia increased the risk of developing diabetes in the post-MI period 3.5 and 3.7 times, respectively, in patients with visceral obesity compared with patients without visceral obesity.ConclusionVisceral obesity is associated with IR, a 5.7-fold increase in leptin levels and a high risk of developing type 2 diabetes 1 year after MI onset.

Tumor necrosis factor-α impairs adiponectin signalling, mitochondrial biogenesis, and myogenesis in primary human myotubes cultures.

Skeletal muscle metabolic changes are common in patients with chronic heart failure (HF). Previously, we demonstrated a functional skeletal muscle adiponectin resistance in HF patients with reduced left ventricular ejection fraction (HFrEF). We aimed to examine the impact of adiponectin receptor 1 (AdipoR1) deficiency and TNF-α treatment on adiponectin signaling, proliferative capacity, myogenic differentiation, and mitochondrial biogenesis in primary human skeletal muscle cells. Primary cultures of myoblasts and myotubes were initiated from the musculus vastus lateralis of 10 HFrEF patients (left ventricular ejection fraction; 31.30 ± 2.89%) and 10 age- and gender-matched healthy controls. Healthy control cultures were transfected with siAdipoR1 and/or exposed to TNF-α (10 ng/ml; 72 h). Primary cultures from HFrEF patients preserved the features of adiponectin resistance in vivo. AdipoR1 mRNA was negatively correlated with time to reach maximal cell index (r = -0.7319, P = 0.003). SiRNA-mediated AdipoR1 silencing reduced pAMPK (P < 0.01), AMPK activation (P = 0.046), and myoblast proliferation rate (xCELLigence Real-Time Cellular Analysis; P < 0.0001). Moreover, TNF-α decreased the mRNA expression of genes involved in glucose (APPL1, P = 0.0002; AMPK, P = 0.021), lipid (PPARα, P = 0.025; ACADM, P = 0.003), and mitochondrial (FOXO3, P = 0.018) metabolism, impaired myogenesis (MyoD1, P = 0.053; myogenin, P = 0.048) and polarized cytokine secretion toward a growth-promoting phenotype (IL-10, IL-1β, IFN-γ, P < 0.05 for all; Meso Scale Discovery Technology). Major features of adiponectin resistance are retained in primary cultures from the skeletal muscle of HFrEF patients. In addition, our results suggest that an increased inflammatory constitution contributes to adiponectin resistance and confers alterations in skeletal muscle differentiation, growth, and function.

Abstract 13094: High Glucose/High Lipids Impair Vascular Adiponectin Function via Inhibition of Caveolin-1/AdipoR1 Signalsome Formation

Background and Aims: Reduced levels of adiponectin (APN) contribute to cardiovascular injury in the diabetic population. Recent studies demonstrate elevated circulating APN levels are associated with endothelial dysfunction during pre-diabetes, suggesting the development of APN resistance. However, mechanisms leading to, and the role of, vascular APN resistance in endothelial dysfunction remain unidentified. The current study determined whether diabetes cause endothelial APN resistance, and by what mechanisms. Methods and Results: In HUVECs cultured under normal condition (control), APN caused eNOS, AMPK and Akt phosphorylation, increased nitric oxide (NO) production, and inhibited TNF-induced adhesion molecule expression. Under high glucose/high lipids (HG/HL), APN-stimulated nitric oxide production was decreased, phosphorylation of eNOS, AMPK, and Akt was attenuated (P&lt;0.01 vs. control), and APN’s anti-TNFα effect was blunted (P&lt;0.01). APN receptor expression remained normal, whereas Cav1 expression was reduced in HG/HL cells (P&lt;0.01). The AdipoR1/Cav1 signaling complex was dissociated in HG/HL cells. Knock-down of Cav1 inhibited APN’s anti-oxidative and anti-inflammatory actions. Conversely, preventing HG/HL-induced Cav1 downregulation by Cav1 overexpression preserved APN signaling in HG/HL cells. Knock-in of a wild type Cav1 in Cav1 knock-down cells restored caveolae structure and rescued APN signaling. In contrast, knock-in of a mutated Cav1 scaffolding domain restored caveolae structure, but failed to rescue APN signaling in Cav1 knock-down cells. Finally, AdipoR1/Cav1 interaction was significantly reduced, and the vasorelaxative response to APN was impaired in vascular segments from diabetic animals. Conclusion: The current study demonstrates for the first time that the interaction between AdipoR1 and Cav1 is critical for adiponectin-mediated vascular signaling. The AdipoR1/Cav1 interaction is adversely affected by HG/HL, due largely to reduced Cav1 expression, supporting a potential mechanism for the development of APN resistance, contributing to diabetic endothelial dysfunction.

Adiponectin resistance in skeletal muscle: pathophysiological implications in chronic heart failure.

Skeletal muscle wasting is a common complication of chronic heart failure (CHF) and linked to poor patient prognosis. In recent years, adiponectin was postulated to be centrally involved in CHF‐associated metabolic failure and muscle wasting. This review discusses current knowledge on the role of adiponectin in CHF. Particular emphasis will be given to the complex interaction mechanisms and the intracellular pathways underlying adiponectin resistance in skeletal muscle of CHF patients. In this review, we propose that the resistance process is multifactorial, integrating abnormalities emanating from insulin signalling, mitochondrial biogenesis, and ceramide metabolism.

Issue Highlights

Issue Highlights

High glucose/High Lipids impair vascular adiponectin function via inhibition of caveolin-1/AdipoR1 signalsome formation

Reduced levels of adiponectin (APN) contribute to cardiovascular injury in the diabetic population. Recent studies demonstrate elevated circulating APN levels are associated with endothelial dysfunction during pre-diabetes, suggesting the development of APN resistance. However, mechanisms leading to, and the role of, vascular APN resistance in endothelial dysfunction remain unidentified. The current study determined whether diabetes cause endothelial APN resistance, and by what mechanisms. Under high glucose/high lipids (HG/HL), APN-stimulated nitric oxide production by HUVEC was decreased, phosphorylation of eNOS, AMPK, and Akt was attenuated (P<0.01), and APN's anti-TNFα effect was blunted (P<0.01). APN receptor expression remained normal, whereas Cav1 expression was reduced in HG/HL cells (P<0.01). The AdipoR1/Cav1 signaling complex was dissociated in HG/HL cells. Knock-down of Cav1 inhibited APN's anti-oxidative and anti-inflammatory actions. Conversely, preventing HG/HL-induced Cav1 downregulation by Cav1 overexpression preserved APN signaling in HG/HL cells. Knock-in of a wild type Cav1 in Cav1 knock-down cells restored caveolae structure and rescued APN signaling. In contrast, knock-in of a mutated Cav1 scaffolding domain restored caveolae structure, but failed to rescue APN signaling in Cav1 knock-down cells. Finally, AdipoR1/Cav1 interaction was significantly reduced in diabetic vascular tissue, and the vasorelaxative response to APN was impaired in diabetic animals. The current study demonstrates for the first time the interaction between AdipoR1 and Cav1 is critical for adiponectin-mediated vascular signaling. The AdipoR1/Cav1 interaction is adversely affected by HG/HL, due largely to reduced Cav1 expression, supporting a potential mechanism for the development of APN resistance, contributing to diabetic endothelial dysfunction.

Reply to comment on: Effects of ezetimibe/simvastatin combination on metabolic parameters by Prof. Moses S Elisaf

Article history: Received 17 August 2015 Accepted 20 August 2015 Available online 25 August 2015 statin dose-dependently worsen insulin sensitivity by reducing plasma levels of adiponectin and increased the risk of type 2 diabetes in humans [6,7]. Andwefirst reported that losartan compensated theuntoward effect of simvastatin on insulin sensitivity when combined [3]. In addition to lowering LDL cholesterol further, ezetimibe reduced visceral fat with beneficial effects on adiponectin and insulin resistance. Indeed, experimental studies demonstrated that ezetimibe improves

Globular adiponectin ameliorates metabolic insulin resistance via AMPK‐mediated restoration of microvascular insulin responses

Adiponectin is an adipokine with anti-inflammatory and anti-diabetic properties. Hypoadiponectinaemia is closely associated with endothelial dysfunction and insulin resistance in obesity and diabetes. Insulin resistance is present in muscle microvasculature and this may contribute to decreased insulin delivery to, and action in, muscle. In this study we examined whether adiponectin ameliorates metabolic insulin resistance by affecting muscle microvascular recruitment. We demonstrated that a high-fat diet induces vascular adiponectin and insulin resistance but globular adiponectin administration can restore vascular insulin responses and improve insulin's metabolic action via an AMPK- and nitric oxide-dependent mechanism. This suggests that globular adiponectin might have a therapeutic potential for improving insulin resistance and preventing cardiovascular complications in patients with diabetes via modulation of microvascular insulin responses. Hypoadiponectinaemia is closely associated with endothelial dysfunction and insulin resistance, and microvasculature plays a critical role in the regulation of insulin action in muscle. Here we tested whether adiponectin replenishment could improve metabolic insulin sensitivity in male rats fed a high-fat diet (HFD) via the modulation of microvascular insulin responses. Male Sprague-Dawley rats were fed either a HFD or low-fat diet (LFD) for 4 weeks. Small resistance artery myograph changes in tension, muscle microvascular recruitment and metabolic response to insulin were determined. Compared with rats fed a LFD, HFD feeding abolished the vasodilatory actions of globular adiponectin (gAd) and insulin on pre-constricted distal saphenous arteries. Pretreatment with gAd improved insulin responses in arterioles isolated from HFD rats, which was blocked by AMP-activated protein kinase (AMPK) inhibition. Similarly, HFD abolished microvascular responses to either gAd or insulin and decreased insulin-stimulated glucose disposal by ∼60%. However, supplementing gAd fully rescued insulin's microvascular action and significantly improved the metabolic responses to insulin in HFD male rats and these actions were abolished by inhibition of either AMPK or nitric oxide production. We conclude that HFD induces vascular adiponectin and insulin resistance but gAd administration can restore vascular insulin responses and improve insulin's metabolic action via an AMPK- and nitric oxide-dependent mechanism in male rats.

Combined Adiponectin Deficiency and Resistance in Obese Patients: Can It Solve Part of the Puzzle in Nonalcoholic Steatohepatitis.

BACKGROUND:Nonalcoholic fatty liver disease (NAFLD) has become the most prevalent cause of liver disease, nonalcoholic steatohepatitis (NASH) and fibrosis in obese patients identifies the risk group with increased incidence of liver-related deaths.AIM:To clarify the role of serum adiponectin and its receptor liver gene expression in the progression of liver damage in NAFLD.METHODS:Fifty four (54) obese patients with NAFLD preliminary diagnosed by liver ultra-sound were recruited. Full medical history, anthropometric measurement, biochemical studies, serum adiponectin level, liver biopsy for histological examination and NAS score to identify NASH patients, and assessment of adiponectin receptor gene expression by RT-PCR, were conducted for each patients. Fifteen ages matched average weight healthy adult had been chosen as a control for serum adiponectin level.RESULTS:According to NAS score, patients were divided into non- NASH (8 patients), and NASH (46 patients). Serum adiponectin level was significantly lower in NAFLD patients compared to normal participants (p < 0.004). Serum adiponectin level was lower in NASH patients (4.437 ± 2.569 ng/dl in NASH vs. 5.138 ± 2.841 ng/dl in non-NASH). Adiponectin receptor liver gene expression was lower in NASH patients (0.8459 ± 0.4671 vs. 1.0688 ± 0.3965 in non-NASH).CONCLUSION:Both adiponectin deficiency and resistance had a role in progression of simple liver steatosis to severe injury in obese patients.

Association of adipokines with metabolic disorders in patients with schizophrenia: Results of comparative study with mental healthy cohort

AimThe role of adipose tissue hormones, adipokines, in formation of metabolic disorders in schizophrenia is not fully understood. The aim was to investigate the association of leptin and adiponectin plasma levels with metabolic parameters in antipsychotic treated patients with schizophrenia and in the group of age, gender and body mass index matched mental healthy persons. MethodsOne hundred patients with diagnosis of schizophrenia, who took antipsychotic medication, and equal number of control subjects, were enrolled for cross-sectional evaluation. Fasting blood plasma levels of glucose, lipids, insulin, adiponectin, leptin concentrations and insulin resistance HOMA index were determined. ResultsIn both groups plasma leptin concentration positively correlated with body mass index, insulin plasma level and HOMA index, while adiponectin level had negative correlations with adiposity measures and positive associations with high density lipoprotein cholesterol content. At the same time, in schizophrenia group, but not in control subjects, leptin level positively associated with cholesterol and triglycerides concentrations and adiponectin negatively correlated with plasma insulin content, HOMA index and triglycerides levels. After controlling for confounders significant correlations remained for leptin concentration with HOMA index and plasma triglycerides level in schizophrenic patients and for adiponectin concentration with plasma high density lipoprotein cholesterol concentrations in both studied groups. ConclusionsBoth adipokines associate with metabolic parameters in antipsychotic treated patients with schizophrenia. Leptin can play more specific role in pathogenesis of metabolic syndrome in schizophrenic persons than in mental healthy subjects.

Effect of Zhenggan Tang decoction on the serum levels of leptin, adiponectin and insulin resistance on HBV-induced cirrhotic patients

To evaluate the effect of Zhenggan Tang decoction on serum levels of leptin, adiponectin and insulin resistance on liver cirrhosis induced by chronic hepatitis B. Sixty-six patients were recruited and randomly assigned either to a control group or to an intervention group, with 35 cases in the treatment and 31 in the control group respectively. Patients in the control group received inosine tablets and vitamin C treatment while patients in the treatment group were given Zhenggan Tang decoction additionally. After 3 months of treatment, the serum levels of leptin and adiponectin were detected and the index of insulin resistance calculated. There were no significant difference between the serum levels of leptin, adiponectin and the index of insulin resistance seen in the control group before and after the treatment. Serum levels of leptin and adiponectin and the index of insulin resistance in treatment group were reduced significantly after the treatment (P < 0.05). There were significant difference in the serum levels of leptin and adiponectin between treat group and control group (P < 0.05). Zhenggan Tang decoction seemed to have reduced the serum levels of leptin, adiponectin and the index of insulin resistance among cirrhotic patients that induced by chronic hepatitis B.

Are decreased AdipoR1 mRNA levels associated with adiponectin resistance in coronary artery disease patients?

The aim of the present study was to investigate if circulating adiponectin levels and the expression of AdipoR1 and AdipoR2 in peripheral blood mononuclear cells (PBMC) are altered in coronary artery disease (CAD) patients, with and without significant stenosis, compared to healthy patients. The present study included 69 patients with presenting symptoms of CAD (26 patients with significant stenosis and 43 patients without significant stenosis). The control group (CG) consisted of 33 healthy patients. Circulating adiponectin levels were measured by enzyme-linked immunosorbent assay, whereas AdipoR1 and AdipoR2 mRNA levels in PBMC were determined by real-time polymerase chain reaction. Adiponectin levels were significantly higher in patients with and without significant stenosis compared to the CG (P < 0.001 vs P = 0.006, respectively). Both patient groups had lower AdipoR1 levels compared to the CG (P < 0.001 vs P < 0.001, respectively). There were no significant differences in these parameters between the two patient groups. Adiponectin negatively correlated with body mass index, triglycerides, insulin and homeostasis model assessment of insulin resistance index (HOMA IR), and positively with high-denisty lipoprotein cholesterol in the CG. Glucose, insulin, and the HOMA IR index negatively correlated with adiponectin in patients. A positive correlation between adiponectin receptors was found in patients and the CG. Decreased AdipoR1 mRNA levels and increased circulating adiponectin in advanced stages of CAD, as well as in patients without significant stenosis, compared to the CG, implies that CAD could be related to 'adiponectin resistance'. Despite increased adiponectin, its protective effects could be diminished even in early stages of atherosclerosis.

The Impact of 4% Rapid Weight Loss on Leptin, Adiponectin, and Insulin Resistance Among Elite Adult Freestyle Wrestlers

ABSTRACT.Rapid weight reduction techniques that emphasize severe restrictions of food intake and water consumption during a short period of time are commonly employed by wrestlers before weigh-in. Along with the negative effects of rapid weight loss on a wrestler's physiological functions, we investigated leptin and adiponectin levels and insulin resistance in young wrestlers during their rapid weight loss program. Fifteen freestyle wrestlers were randomly selected as the subjects. They had a mean of age 23±1y and anthropometric characteristics of: weight 67.6±0.8, BMI 22.5±0.21 kg/m2, body fat percentage 6.12±0.18, waist-to-hip circumference ratio 0.82±0.08. Caloric intake (mean 7 days measured by food analyzer software) and anthropometric characteristics were measured by standard methods. The concentrations of the leptin and adiponectin hormones and insulin resistance index were measured with a sandwich ELISA kit method and (HOMA) from fasting glucose and insulin levels, respectively. Rapid weight loss ...

Osteocalcin is inversely associated with adiposity and leptin in adolescent boys.

Recently, osteocalcin (OC), an osteoblast-derived hormone, has been found to correlate with adiposity, adipocytokines and insulin resistance in adults, but few studies have investigated this in children. The aim of this study was to investigate these associations in adolescent boys, for whom it is a time of significant bone mineral accrual, taking into account possible confounders related to adipose and bone tissues. Participants were 141 adolescent boys (mean age 13.9±0.7 years), who were divided into tertiles according to OC levels. Across these groups, differences in total body fat mass (FM), body fat distribution, adiponectin, leptin and insulin resistance values were examined with relation to age, pubertal stage, daily energy and calcium intakes, and physical activity. Mean body mass index (BMI), FM, body fat% and leptin differed significantly between subjects in the three OC tertiles after adjustment for age, pubertal stage, energy and calcium intakes, and physical activity. There were no differences in fat free mass (FFM), bone mineral content, energy and calcium intakes, physical activity, adiponectin and insulin resistance values between study groups. For the entire cohort, mean serum OC was 130.2±45.2 ng/mL and was related to body mass, BMI, FM, body fat distribution and leptin. Circulating OC was not associated with FFM, daily energy and calcium intakes, physical activity, adiponectin or insulin resistance (insulin, glucose, homeostasis model assessment-insulin resistance) values. In male adolescents, OC is inversely related to body adiposity and leptin values, even after consideration of several factors that may affect bone and adipose tissues.