Diet-induced weight loss and exercise alone and in combination enhance the expression of adiponectin receptors in adipose tissue and skeletal muscle, but only diet-induced weight loss enhanced circulating adiponectin. Effects of different hypocaloric diets on protein secretion from adipose tissue of obese women. Effect of marked weight loss on adiponectin gene expression and plasma concentrations. Effects of an in-patient treatment program based on regular exercise and a balanced diet on high molecular weight adiponectin, resistin levels, and insulin resistance in adolescents with severe obesity. Addition of Exercise Increases Plasma Adiponectin and Release from Adipose Tissue. Increased Adiponectin Secretion by Highly Purified Eicosapentaenoic Acid in Rodent Models of Obesity and Human Obese Subjects Epidemiologic Evidence on Serum Adiponectin Level and Lipid Profile Circulating cytokines as determinants of weight loss-induced improvements in insulin sensitivity The effect of thiazolidinediones on plasma adiponectin levels in normal, obese, and type 2 diabetic subjects. Effects of long-term exercise and diet intervention on plasma adipokine concentrations. Circulating concentrations of the adipocyte protein adiponectin are decreased in parallel with reduced insulin sensitivity during the progression to type 2 diabetes in rhesus monkeys. The influence of very-low-calorie-diet on serum leptin, soluble leptin receptor, adiponectin and resistin levels in obese women. [Impact of weight loss on adipocytokines, C-reactive protein and insulin sensitivity in hypertensive women with central obesity]. Plasma adiponectin concentration is associated with skeletal muscle insulin receptor tyrosine phosphorylation, and low plasma concentration precedes a decrease in whole-body insulin sensitivity in humans. Enhanced adiponectin multimer ratio and skeletal muscle adiponectin receptor expression following exercise training and diet in older insulin-resistant adults. The effect of a very low calorie diet on insulin sensitivity, beta cell function, insulin clearance, incretin hormone secretion, androgen levels and body composition in obese young women Consuming a hypocaloric high fat low carbohydrate diet for 12 weeks lowers C-reactive protein, and raises serum adiponectin and high density lipoprotein-cholesterol in obese subjects.
OBJECTIVE The aim of the study was to investigate the effect of weight loss and exercise independently and in combination on circulating levels of adiponectin including low molecular weight , medium molecular weight , and high molecular weight adiponectin and expression of adiponectin and adiponectin receptors ( AdipoR ) in adipose tissue ( AT ) and skeletal muscle ( SM ) . DESIGN AND METHODS Seventy-nine obese males and females were r and omized into the following : 1 ) exercise only ( 12 wk of exercise without diet restriction ) ; 2 ) hypocaloric diet [ 8 wk of very low energy diet ( 600 kcal/d ) followed by 4 wk with a weight maintenance diet ] ; and 3 ) hypocaloric diet and exercise ( DEX ; 8 wk very low energy diet 800 kcal/d followed by 4 wk weight maintenance diet combined with exercise throughout the 12 wk ) . Blood sample s and biopsies from sc abdominal AT and SM were collected at baseline and after 12 wk . The molecular subforms of adiponectin in serum were determined by Western blot . RESULTS The mRNA expression of AdipoR1 and -2 in SM was increased significantly in the exercise-only and DEX groups ( both P < 0.05 ) . The mRNA expression of adiponectin and AdipoRs in AT was increased significantly in all three groups ( all P < 0.01 ) , whereas serum total circulating adiponectin was significantly increased only in the DEX and hypocaloric diet groups ( both P < 0.01 ) . All the adiponectin subforms changed in a similar manner as total adiponectin , indicating no specific regulation of any of the subforms by the intervention . CONCLUSION Exercise alone and in combination with a diet-induced weight loss enhance the mRNA expression of adiponectin receptors in AT and in SM but only a pronounced hypocaloric-induced weight-loss increases circulating adiponectin in obese subjects Little is known about common factors ( e.g. , macronutrients and energy supply ) regulating the protein secretory function of adipose tissue . We therefore compared the effects of r and omly assigned 10-week hypoenergetic ( -600 kcal/day ) diets with moderate-fat/moderate-carbohydrate or low-fat/high-carbohydrate content on circulating levels and production of proteins ( using radioimmunoassays and enzyme-linked immunosorbent assays ) from subcutaneous adipose tissue in 40 obese but otherwise healthy women . Similar results were obtained by the two diets .  Body weight decreased by approximately 7.5 % . The secretion rate of leptin decreased by approximately 40 % , as did that of tumor necrosis factor-alpha ( TNF-alpha ) , and interleukin (IL)-6 and -8 decreased by 25 - 30 % , whereas the secretion of plasminogen activator inhibitor 1 ( PAI-1 ) and adiponectin did not show any changes . Regarding mRNA expression ( by real-time PCR ) , only that of leptin and IL-6 decreased significantly . Circulating levels of leptin and PAI-1 decreased by 30 and 40 % , respectively , but there were only minor changes in circulating TNF-alpha , IL-6 , or adiponectin . In conclusion , moderate caloric restriction but not macronutrient composition influences the production and secretion of adipose tissue-derived proteins during weight reduction , leptin being the most sensitive and adiponectin and PAI-1 the least sensitive OBJECTIVE Adiponectin is the most abundant protein secreted by adipose tissue and is inversely associated with adiposity and insulin resistance . The aim of this study was to evaluate the hypothesis that marked weight loss , induced by gastric bypass surgery ( GBS ) , would increase adiponectin gene expression in both upper and lower subcutaneous body fat and increase plasma adiponectin concentration . RESEARCH METHODS AND PROCEDURES Adiponectin subcutaneous abdominal and femoral adipose tissue gene expression , determined by using quantitative reverse transcriptase-polymerase chain reaction , and adiponectin plasma concentrations , determined by using enzyme-linked immunosorbent assay , were evaluated in six extremely obese women ( BMI = 57.1 + /- 4.1 kg/m2 ) before and 1 year after GBS . RESULTS After GBS , subjects lost 36 + /- 5 % of their initial body weight and showed increased insulin sensitivity , manifested by a marked decrease in homeostasis model assessment of insulin resistance from 10.7 + /- 4.1 to 1.4 + /- 0.3 ( p < 0.05 ) . Adiponectin gene expression increased 8- to 15-fold in subcutaneous abdominal and femoral adipose tissues ( p < 0.05 ) . Plasma adiponectin concentrations increased from 5.2 + /- 0.9 to 8.4 + /- 1.2 mug/mL ( p < 0.05 ) . DISCUSSION These data show that marked weight loss induced by GBS increases adiponectin gene expression in both upper- and lower-body subcutaneous fat . The increase in adipose tissue adiponectin production result ed in an increase in plasma adiponectin concentrations , which likely contributed to the decrease in insulin resistance observed after weight loss Adiponectin , the most abundant hormone produced by adipose tissue , circulates in 3 isoforms , including high molecular weight ( HMW ) adiponectin . The latter has been suggested to be a better predictor of metabolic disturbances and insulin resistance associated with obesity . This study investigated changes in total and HMW adiponectin , resistin , and homeostasis model assessment ( HOMA ) during a 9-month in-patient treatment program based on physical exercise and a balanced diet in 32 severely obese adolescents .  Total and HMW adiponectin , resistin , and HOMA were measured at baseline ( month 0 ) and during the program ( months 3 , 6 , 9 ) . In addition , a control group of 15 teenagers served as a reference for the baseline assessment s. At baseline , HMW adiponectin was more markedly decreased in obese adolescents than total adiponectin , and both were lower than in controls . Conversely , resistin and HOMA were higher in obese adolescents . During the program , there was a significant change in body composition and improved insulin sensitivity among obese teenagers . In addition , HMW adiponectin and the ratio of HMW-to-total adiponectin increased throughout the study , whereas total adiponectin only increased up until the sixth month . On the contrary , resistin did not show any significant change . In obese adolescents , a long-term combination of aerobic exercise and a balanced diet , inducing change in body composition and improved insulin sensitivity , markedly increased HMW adiponectin compared with total adiponectin , without any change in resistin concentrations . Our results thus suggest that the determination of HMW adiponectin could be more useful than measurement of total adiponectin in clinical setting INTRODUCTION Adiponectin is an adipose tissue-derived anti-inflammatory protein that is down-regulated in obesity . The effects of caloric restriction and exercise-induced weight loss on adiponectin are not clear . PURPOSE To determine whether addition of aerobic exercise training to caloric restriction has additive effects over caloric restriction alone on circulating adiponectin concentrations and adiponectin release from abdominal and gluteal adipose tissue . METHODS Overweight or obese ( body mass index , 25 - 40 kg·m(-2 ) ; waist > 88 cm ) postmenopausal women were r and omized to 20-wk caloric restriction with and without aerobic exercise ( CR + EX , n = 48 ; and CR , n = 22 ) . Blood sample s were collected for measuring plasma adiponectin concentration , and abdominal and gluteal subcutaneous adipose tissue biopsies were performed in a subgroup to determine in vitro adiponectin release , before and after the interventions . RESULTS The interventions elicited similar amounts of weight loss ( CR + EX , -11.3 ± 4.6 kg ; CR,-11.2 ± 3.4 kg ) and fat loss ( CR + EX , -8.0 ± 3.5 kg ; CR , -7.4 ± 2.7 kg ) . The two groups had differential changes in plasma adiponectin concentrations ( for interaction , P = 0.014 ) ; CR + EX increased ( 6.9 ± 3.9 to 8.5 ± 4.9 μg·mL(-1 ) ; P = 0.0001 ) , whereas CR did not alter ( 6.4 ± 4.4 to 6.5 ± 4.5 μg·mL(-1 ) ; P = 0.42 ) plasma adiponectin . Likewise , adiponectin release from abdominal and gluteal subcutaneous adipose tissue increased with CR + EX ( P = 0.0076 and P = 0.089 , respectively ) but did not change with CR ( P = 0.13 and P = 0.95 , respectively ) . CONCLUSION Despite similar reductions in body weight and fat mass , the addition of aerobic exercise to caloric restriction increased plasma adiponectin concentrations , which may be partly explained by increased adiponectin release from abdominal and gluteal subcutaneous adipose tissue Objectives —Fish oil rich in n-3 polyunsaturated fatty acids ( PUFAs ) or n-3 PUFAs have been shown to reduce the incidence of coronary heart disease . Here we investigated the effect of highly purified eicosapentaenoic acid ( EPA ) on production of adiponectin , the only established antiatherogenic and antiinflammatory adipocytokine , in rodent models of obesity and human obese subjects . Methods and Results —We demonstrated that EPA increases adiponectin secretion in genetically obese ob/ob mice and high-fat diet – induced obese mice . In the in vitro coculture of adipocytes and macrophages , EPA reversed the coculture-induced decrease in adiponectin secretion at least in part through downregulation of tumor necrosis factor-&agr ; in macrophages . We also showed significant increase in plasma adiponectin concentrations in human obese subjects after a 3-month treatment with EPA ( 1.8 g daily ) . Multivariate regression analysis revealed that EPA treatment is the only independent determinant of plasma adiponectin concentrations . Conclusion —This study demonstrates that EPA increases adiponectin secretion in rodent models of obesity and human obese subjects , possibly through the improvement of the inflammatory changes in obese adipose tissue . Because EPA has reduced the risk of major coronary events in a large-scale , prospect i ve , r and omized clinical trial , this study provides important insight into its therapeutic implication in obesity-related metabolic sequelae The concentration of adiponectin , a hormone which is secreted from adipose tissue , is inversely correlated with body fat mass . This hormone has anti inflammatory and anti atherogenic properties . Its concentration reduces in metabolic syndrome and cardiovascular diseases . This study review s the evidence on the relationship between serum  adiponectin concentration and lipid profile .  In this study former clinical trials , cross sectional and prospect i ve studies have been review ed . The PubMed search engine has been used to find related research for the topic by considering dyslipidemia , total cholesterol ( TC ) , high and low density protein ( HDL and LDL ) , triglyceride ( TG ) , lipid profile ( LP ) and adiponectin as the key words . Finally , 25 articles were recruited to review in the present article . Serum adiponectin level was positively correlated with plasma HDL cholestrol concentrations . There was a significant inverse relationship between plasma triglyceride and serum adiponectin . An inverse correlation between very low density lipoprotein ( VLDL ) and LDL levels and adiponectin was reported from the studies . So , Adiponectin has an important role in the metabolism of lipid profile including HDLc Dietary calorie restriction and exercise promote weight loss and may have additive effects for improving insulin sensitivity , independent of weight loss . It is not known if these effects are attributable to changes in circulating cytokines . We evaluated the hypothesis that modest , matched weight loss induced by calorie restriction and exercise have additive effects on circulating cytokines and these changes correlate with improvements in insulin sensitivity . Overweight and sedentary women and men ( n = 52 , 45–65 years ) were r and omized to undergo 7 % weight loss by using 3–6 months of calorie restriction , exercise , or a combination of both calorie restriction and exercise . Concentrations of cytokines and hormones were measured in fasting and oral glucose tolerance test blood sample s. Insulin sensitivity was estimated based on oral glucose tolerance test for glucose and insulin . With all groups combined , fasting leptin ( p < 0.0001 ) and high molecular weight adiponectin ( p = 0.04 ) decreased and pentraxin-3 increased ( p < 0.0001 ) , in a manner that correlated with improvements in insulin sensitivity ( all p ≤ 0.0002 ) . These changes , combined with decreases in glucose-dependent insulinotropic polypeptide from the oral glucose tolerance test , explained 63 % of the variance ( p < 0.0001 ) in insulin sensitivity improvements . Exercise and calorie restriction had additive effects on leptin , with a similar trend for high molecular weight adiponectin . Monocyte chemoattractant protein-1 and C-reactive protein concentrations did not change . Calorie restriction and exercise had opposite effects on soluble tumor necrosis factor receptor-1 .  Modest weight loss in overweight adults  decreases serum leptin and high molecular weight adiponectin , and increases pentraxin-3 concentrations in a manner that correlates with increased insulin sensitivity . Exercise has additive effects to those induced by calorie restriction for reductions in leptin and possibly adiponectin . These changes may contribute to the additive effects of calorie restriction and exercise for improving insulin sensitivity The insulin-sensitizing effects of thiazolidinediones are thought to be mediated through peroxisome proliferator-activated receptor-gamma , a nuclear receptor that is highly abundant in adipose tissue . It has been reported that adipocytes secrete a variety of proteins , including tumor necrosis factor-alpha , resistin , plasminogen activator inhibitor-1 , and adiponectin . Adiponectin is a fat cell-secreted protein that has been reported to increase fat oxidation and improve insulin sensitivity . Our aim was to study the effects of troglitazone on adiponectin levels in lean , obese , and diabetic subjects . Ten diabetic and 17 nondiabetic subjects ( 8 lean , BMI < 27 kg/m(2 ) and 9 obese , BMI > 27 kg/m(2 ) ) participated in the study . All subjects underwent an 80 mU. m(-2 ) . min(-1 ) hyperinsulinemic-euglycemic glucose clamp before and after 3 months ' treatment with the thiazolidinedione ( TZD ) troglitazone ( 600 mg/day ) . Fasting plasma glucose significantly decreased in the diabetic group after 12 weeks of treatment compared with baseline ( 9.1 + /- 0.9 vs. 11.1 + /- 0.9 mmol/l , P < 0.005 ) but was unchanged in the lean and obese subjects . Fasting insulin for the entire group was significantly lower than baseline ( P = 0.02 ) after treatment . At baseline , glucose disposal rate ( R(d ) ) was lower in the diabetic subjects ( 3.4 + /- 0.5 mg . kg(-1 ) . min(-1 ) ) than in the lean ( 12.3 + /- 0.4 ) or obese subjects ( 6.7 + /- 0.7 ) ( P < 0.001 for both ) and was significantly improved in the diabetic and obese groups ( P < 0.05 ) after treatment , and it remained unchanged in the lean subjects . Baseline adiponectin levels were significantly lower in the diabetic than the lean subjects ( 9.0 + /- 1.7 vs. 16.7 + /- 2.7 micro g/ml , P = 0.03 ) and rose uniformly in all subjects ( 12.2 + /- 2.3 vs. 25.7 + /- 2.6 micro g/ml , P < 10(-4 ) ) after treatment , with no significant difference detected among the three groups . During the glucose clamps , adiponectin levels were suppressed below basal levels in all groups ( 10.2 + /- 2.3 vs. 12.2 + /- 2.3 micro g/ml , P < 0.01 ) . Adiponectin levels correlated with R(d ) ( r = 0.46 , P = 0.016 ) and HDL cholesterol levels ( r = 0.59 , P < 0.001 ) and negatively correlated with fasting insulin ( r = -0.39 , P = 0.042 ) and plasma triglyceride ( r = -0.61 , P < 0.001 ) . Our findings show that TZD treatment increased adiponectin levels in all subjects , including normal subjects in which no other effects of TZDs are observed . Insulin also appears to suppress adiponectin levels . We have confirmed these results in normal rats . These findings suggest that adiponectin can be regulated by obesity , diabetes , TZDs , and insulin , and it may play a physiologic role in enhancing insulin sensitivity BACKGROUND In a r and omized , controlled , 2 x 2 factorial trial on the effect of long-term changes in diet and exercise , a significant reduction in body weight and fat mass was observed . Alterations in leptin and plasminogen activator inhibitor-1 concentrations were previously reported from this study . OBJECTIVE We examined the separate and combined effects of a 1-y exercise and diet intervention on several adipokines ; adiponectin , interleukin-6 and -8 , tumor necrosis factor-alpha , monocyte chemoattractant protein-1 , hepatocyte growth factor , nerve growth factor , C-reactive protein , and resistin . DESIGN One hundred eighty-eight men with several risk factors for diabetes and cardiovascular disease were r and omly allocated to 4 groups : diet , exercise , combined diet and exercise , and control . RESULTS Plasma adiponectin concentrations remained unchanged , whereas body mass index and fat mass decreased after dietary changes and an increase in physical activity . In the control group , adiponectin concentrations were reduced . Analyzed according to the factorial design , only diet intervention had a significant ( P = 0.03 ) positive effect on plasma adiponectin relative to control , and this effect was largely explained by changes in fat mass . After adjustment for change in percentage body fat , there were significant positive effects on tumor necrosis factor-alpha in all 3 intervention groups ( P = 0.01 for the diet group , 0.03 for the exercise group , and 0.05 for the combined diet and exercise group ) . Minor changes were observed for the other adipokines . Neither baseline concentrations of nor changes in adiponectin and plasminogen activator inhibitor-1 were significantly correlated to the other adipokines , whereas concentrations of and changes in the other adipokines were significantly correlated . CONCLUSION Diet intervention had a significant positive effect on adiponectin concentrations , which is largely explained by a reduction in fat mass Adiponectin is an adipose-specific plasma protein whose plasma concentrations are decreased in obese subjects and type 2 diabetic patients . This protein possesses putative antiatherogenic and anti-inflammatory properties . In the current study , we have analyzed the relationship between adiponectin and insulin resistance in rhesus monkeys ( Macaca mulatta ) , which spontaneously develop obesity and which subsequently frequently progress to overt type 2 diabetes . The plasma levels of adiponectin were decreased in obese and diabetic monkeys as in humans . Prospect i ve longitudinal studies revealed that the plasma levels of adiponectin declined at an early phase of obesity and remained decreased after the development of type 2 diabetes . Hyperinsulinemic-euglycemic clamp studies revealed that the obese monkeys with lower plasma adiponectin showed significantly lower insulin-stimulated peripheral glucose uptake ( M rate ) . The plasma levels of adiponectin were significantly correlated to M rate ( r = 0.66 , P < 0.001 ) . Longitudinally , the plasma adiponectin decreased in parallel to the progression of insulin resistance . No clear association was found between the plasma levels of adiponectin and its mRNA levels in adipose tissue . These results suggest that reduction in circulating adiponectin may be related to the development of insulin resistance The aim of our study was to determine whether adipocyte-derived hormones leptin , adiponectin and resistin contribute to the improvement of insulin sensitivity after very-low calorie diet ( VLCD ) . Therefore , serum levels of these hormones were measured in fourteen obese females before and after three weeks VLCD and in seventeen age- and sex-matched healthy controls .  Body mass index , HOMA index , serum insulin and leptin levels in obese women before VLCD were significantly higher than in control group ( BMI 48.01+/-2.02 vs. 21.38+/-0.42 kg/m(2 ) , HOMA 10.72+/-2.03 vs. 4.69+/-0.42 , insulin 38.63+/-5.10 vs. 18.76+/-1.90 microIU/ml , leptin 77.87+/-8.98 vs. 8.82+/-1.52 ng/ml ) . In contrast , serum adiponectin and soluble leptin receptors levels were significantly lower in obese women before VLCD than in the control group . No differences were found in serum glucose and resistin levels between the obese group before VLCD and the control group . VLCD significantly decreased BMI , HOMA index , serum glucose , insulin and leptin levels and increased soluble leptin receptor levels . The changes in serum adiponectin and resistin levels in obese women after VLCD did not reach statistical significance . We conclude that leptin and soluble leptin receptor levels were affected by VLCD while adiponectin and resistin concentrations were not . Therefore , other mechanisms rather than changes in the endocrine function of the adipose tissue are probably involved in the VLCD-induced improvement of insulin sensitivity OBJECTIVE To assess the impact of weight reduction on serum adipocytokines , C-reactive protein ( CRP ) , and insulin sensitivity in hypertensive female patients with central obesity . METHODS This study was performed using the data base and stored serum sample s of female patients who had participated in an intervention study focused on weight loss . Thirty hypertensive women aged 18 to 65 , body mass index ( BMI ) > 27 kg/m2 , and central obesity were selected . They were r and omly assigned to receive either a low-calorie diet plus orlistat 120 mg three times daily or a low-calorie diet alone for 16 weeks . Patients who experienced weight loss greater than 5 % ( n = 24 ) were assessed for blood pressure , anthropometric parameters , visceral fat , insulin resistance ( HOMA-R - homeostasis model assessment of insulin resistance ) and sensitivity ( ISI - Insulin Sensitivity Index ) indices , plus serum lipids , adipocytokines ( adiponectin , leptin , IL-6 , and TNF-alpha ) and CRP levels . RESULTS After BMI had been reduced by approximately 5 % in both groups , visceral fat , fasting glucose , triglycerides , and TNF-alpha decreased . Only the orlistat group , which was more insulin resistant at baseline , showed a significant reduction in blood glucose after oral glucose load , in addition to increased insulin sensitivity . CONCLUSION This study 's findings indicate that a weight loss greater than 5 % is associated with improved inflammatory status and decreased insulin resistance , regardless of changes in adiponectin and TNF-a levels . The greatest improvements in insulin sensitivity experienced by the orlistat-treated patients could not be attributed to the use of this drug because of the higher number of insulin-resistant subjects in this group Adiponectin , the most abundant adipose-specific protein , has been found to be negatively associated with degree of adiposity and positively associated with insulin sensitivity in Pima Indians and other population s. Moreover , adiponectin administration to rodents has been shown to increase insulin-induced tyrosine phosphorylation of the insulin receptor ( IR ) and also increase whole-body insulin sensitivity . To further characterize the relationship between plasma adiponectin concentration and insulin sensitivity in humans , we examined 1 ) the cross-sectional association between plasma adiponectin concentration and skeletal muscle IR tyrosine phosphorylation and 2 ) the prospect i ve effect of plasma adiponectin concentration at baseline on change in insulin sensitivity . Fasting plasma adiponectin concentration , body composition ( hydrodensitometry or dual energy X-ray absorptiometry ) , insulin sensitivity ( insulin-stimulated glucose disposal , hyperinsulinemic clamp ) , and glucose tolerance ( 75-g oral glucose tolerance test ) were measured in 55 Pima Indians ( 47 men and 8 women , aged 31 + /- 8 years , body fat 29 + /- 8 % [ mean + /- SD ] ; 50 with normal glucose tolerance , 3 with impaired glucose tolerance , and 2 with diabetes ) . Group 1 ( 19 subjects ) underwent skeletal muscle biopsies for the measurement of basal and insulin-stimulated tyrosine phosphorylation of the IR ( stimulated by 100 nmol/l insulin ) . The fold increase after insulin stimulation was calculated as the ratio between maximal and basal phosphorylation . Group 2 ( 38 subjects ) had follow-up measurements of insulin-stimulated glucose disposal .  Cross-sectionally , plasma adiponectin concentration was positively associated with insulin-stimulated glucose disposal ( r = 0.58 , P < 0.0001 ) and negatively associated with percent body fat ( r = -0.62 , P < 0.0001 ) in the whole group . In group 1 plasma adiponectin was negatively associated with the basal ( r = -0.65 , P = 0.003 ) and positively associated with the fold increase in IR tyrosine phosphorylation ( r = 0.69 , P = 0.001 ) before and after the adjustment for percent body fat ( r = -0.58 , P = 0.01 and r = 0.54 , P = 0.02 , respectively ) . Longitudinally , after adjustment for age , sex , and percent body fat , low plasma adiponectin concentration at baseline was associated with a decrease in insulin sensitivity ( P = 0.04 ) . In conclusion , our cross-sectional data suggest a role of physiological concentration of fasting plasma adiponectin in the regulation of skeletal muscle IR tyrosine phosphorylation . Prospect ively , low plasma adiponectin concentration at baseline precedes a decrease in insulin sensitivity . Our data indicate that adiponectin plays an important role in regulation of insulin sensitivity in humans Circulating adiponectin is reduced in disorders associated with insulin resistance . This study was conducted to determine whether an exercise/diet intervention would alter adiponectin multimer distribution and adiponectin receptor expression in skeletal muscle . Impaired glucose-tolerant older ( > 60 yr ) obese ( BMI 30 - 40 kg/m(2 ) ) men ( n = 7 ) and women ( n = 14 ) were r and omly assigned to 12 wk of supervised aerobic exercise combined with either a hypocaloric ( ExHypo , approximately 500 kcal reduction , n = 11 ) or eucaloric diet ( ExEu , n = 10 ) . Insulin sensitivity was determined by the euglycemic ( 5.0 mM ) hyperinsulinemic ( 40 mU x m(-2 ) x min(-1 ) ) clamp . Adiponectin multimers [ high ( HMW ) , middle ( MMW ) , and low molecular weight ( LMW ) ] were measured by nondenaturing Western blot analysis . Relative quantification of adiponectin receptor expression through RT-PCR was determined from skeletal muscle biopsy sample s. Greater weight loss occurred in ExHypo compared with ExEu subjects ( 8.0 + /- 0.6 vs. 3.2 + /- 0.6 % , P < 0.0001 ) . Insulin sensitivity improved postintervention in both groups ( ExHypo : 2.5 + /- 0.3 vs. 4.4 + /- 0.5 mg x kg FFM(-1 ) x min(-1 ) , and ExEu : 2.9 + /- 0.4 vs. 4.1 + /- 0.4 mg x kg FFM(-1 ) x min(-1 ) , P < 0.0001 ) . Comparison of multimer isoforms revealed a decreased percentage in MMW relative to HMW and LMW ( P < 0.03 ) . The adiponectin SA ratio ( HMW/total ) was increased following both interventions ( P < 0.05 ) and correlated with the percent change in insulin sensitivity ( P < 0.03 ) . Postintervention adiponectin receptor mRNA expression was also significantly increased ( AdipoR1 P < 0.03 , AdipoR2 P < 0.02 ) . These data suggest that part of the improvement in insulin sensitivity following exercise and diet may be due to changes in the adiponectin oligomeric distribution and enhanced membrane receptor expression Abstract Objective . Evaluation of the effect of an 8-week very low calorie diet ( VLCD , 500–600 kcal daily ) on weight , body fat distribution , glucose , insulin and lipid metabolism , and rogen levels and incretin secretion in obese women . Methods . Seventeen overweight women ( BMI > 28 ) were recruited to the study . Glucose , insulin and lipid metabolism were evaluated by euglycemic clamp technique , indirect calorimetry and an oral glucose tolerance test ( OGTT ) . Insulin sensitivity was calculated as glucose disposal rate ( GDR ) and insulin sensitivity index ( ISI ) , and also by HOMA-IR . Insulin secretion rate ( ISR ) was calculated from plasma C-peptide measurements . Secretion of glucagon-like peptide-1 ( GLP-1 ) and glucose-dependent insulinotropic peptide ( GIP ) was measured during an oral glucose tolerance test . Abdominal fat distribution was assessed by dual x-ray absorptiometry scan and computed tomography . Results . Ten women completed the intervention . The subjects lost an average 11 % of their baseline weight . There was a significant loss of subcutaneous abdominal fatty tissue ( p < 0.01 ) and intra-abdominal fatty tissue ( p = 0.05 ) . Whole body ( HOMA-IR ) ( p < 0.05 ) insulin sensitivity increased significantly , but peripheral ( ISI ) insulin sensitivity was unaltered after weight loss . GIP increased ( p < 0.05 ) and GLP-1 was unaltered after the dietary intervention . Insulin responses did not differ before and after dietary intervention , however , a significant increase in insulin clearance ( p < 0.05 ) was observed . The weight loss result ed in a significant decrease in free testosterone . Conclusion . A VLCD is an effective weight loss treatment , which results in an immediate improvement in several metabolic parameters OBJECTIVE High fat , low carbohydrate ( HFLC ) diets have become popular tools for weight management . We sought to determine the effects of a HFLC diet compared to a low fat high carbohydrate ( LFHC ) diet on the change in weight loss , cardiovascular risk factors and inflammation in subjects with obesity . METHODS Obese subjects ( 29.0 - 44.6 kg/m2 ) recruited from Boston Medical Center were r and omized to a hypocaloric LFHC ( n=26 ) or HFLC ( n=29 ) diet for 12 weeks . RESULTS The age range of subjects was 21 - 62 years . As a percentage of daily calories , the HFLC group consumed 33.5 % protein , 56.0 % fat and 9.6 % carbohydrate and the LFHC group consumed 22.0 % protein , 25.0 % fat and 55.7 % carbohydrate . The change in percent body weight , lean and fat mass , blood pressure , flow mediated dilation , hip : waist ratio , hemoglobin A1C , fasting insulin and glucose , and glucose and insulin response to a 2h oral glucose tolerance test did not differ ( P>0.05 ) between diets after 12 weeks . The HFLC group had greater mean decreases in serum triglyceride ( P=0.07 ) , and hs-CRP ( P=0.03 ) , and greater mean increases in HDL cholesterol ( P=0.004 ) , and total adiponectin ( P=0.045 ) relative to the LFHC . Secreted adipose tissue adiponectin or TNF-α did not differ after weight loss for either diet . CONCLUSIONS Relative to the LFHC group , the HFLC group had greater improvements in blood lipids and systemic inflammation with similar changes in body weight and composition . This small-scale study suggests that HFLC diets may be more beneficial to cardiovascular health and inflammation in free-living obese adults compared to LFHC diets
Weight loss diet beneficially affects blood adiponectin concentrations .
Adiponectin secreted from adipose tissue is proposed to be inversely related to the body fat mass .
However , the magnitude of the effect of low calorie diet on adiponectin concentrations remains unknown .
The present study was aim ed to conduct a systematic review and meta- analysis on clinical trials that access the effect of low calorie diet on adiponectin concentration .