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PubMed2006

Adiponectin is regulated differently by chronic exercise than by weight-matched food restriction in hyperphagic and obese OLETF rats.

This study was intended to investigate the effects of chronic exercise on blood adiponectin level. Male Otsuka Long Evans Tokushima Fatty (OLETF) rats (26 weeks old) were divided to undergo either regular 12-week wheel running exercise (EX) or to have food restriction (FR) that resulted in body weight reduction similar to that in EX. Both EX and FR induced similar reductions in body weight, abdominal fat volume and plasma leptin concentration compared with ad libitum control. At the end of the study, although plasma adiponectin level was increased in FR, the adiponectin level did not change in EX. Plasma testosterone level was higher in EX than in either of the other two groups. A significant inverse relationship existed between plasma levels of adiponectin and testosterone for all groups. Our results suggested that 12-week voluntary wheel running exercise induces different effects on plasma adiponectin level than does food restriction, despite similar reduction in body weight, fat tissue mass and plasma leptin concentration. We speculate that the elevated plasma testosterone concentration might offset any hyperadiponectinemic effect of body weight and fat volume reduction in exercising rats.

Adipocytes↗
PubMed2004

Effects of rosglitazone on plasma adiponectin, insulin sensitivity, and insulin secretion in high-risk African Americans with impaired glucose tolerance test and type 2 diabetes.

We examined the metabolic effects of rosiglitazone therapy on glucose control, insulin sensitivity, insulin secretion, and adiponectin in first-degree relatives of African Americans with type 2 diabetes (DM) with impaired glucose tolerance (IGT) and DM for 3 months. The study was comprised of 12 first-degree relatives with IGT, 17 newly diagnosed DM, and 19 healthy relatives with normal glucose tolerance (NGT). Oral glucose tolerance test (OGTT) was performed before and after 3 months of rosiglitazone therapy (4 to 8 mg/d) in patients with IGT and DM. Serum glucose, insulin, C-peptide, and adiponectin levels were measured before and 2 hours during OGTT in the NGT and patients with IGT and DM. Insulin resistance index (HOMA-IR) and beta-cell function (HOMA-%B) were calculated in each subject using homeostasis model assessment (HOMA). Rosglitazone improved the overall glycemic control in the IGT and DM groups. Following rosiglitazone, the beta-cell secretion remained unchanged, while HOMR-IR was reduced in DM by 30% (4.12 +/- 1.95 v 6.33 +/- 3.54, P < .05) and the IGT group (3.78 +/- 2.45 v 4.81 +/- 3.49, P = not significant [NS]). Mean plasma adiponectin levels were significantly (P < .05) lower in the DM (6.74 +/- 1.95 microg/mL) when compared with the NGT group(9.61 +/- 5.09). Rosiglitazone significantly (P < .001) increased adiponectin levels by 2-fold in patients with IGT (22.2 +/- 10.97 microg/mL) and 2.5-fold greater in DM (15.68 +/- 8.23 microg/mL) at 3 months when compared with the 0 month. We conclude that adiponectin could play a significant role (1) in the pathogenesis of IGT and DM and (2) the beneficial metabolic effects of thiazolidinediones (TZDs) in high-risk African American patients.

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PubMed2005

Correlation between the adiponectin-leptin ratio and parameters of insulin resistance in patients with type 2 diabetes.

We studied the correlation between the adiponectin-leptin (A/L) ratio and parameters of insulin resistance in 220 Japanese patients with type 2 diabetes (138 men and 82 women). Body mass index (BMI), triglycerides (TGs), HDL cholesterol (HDL), and preheparin serum lipoprotein lipase (LPL mass) were examined as laboratory parameters of the insulin resistance. The correlations between these laboratory parameters and adiponectin, leptin, or A/L ratio were studied. Adiponectin levels correlated significantly with BMI (r = -0.298, P = .0003), TGs (r = -0.221, P = .0092), HDL (r = 0.31, P = .0002), and LPL mass (r = 0.26, P = .0021) in men, and with TGs (r = -0.29, P = .0093), HDL (r = 0.239, P = .0338), and LPL mass (r = 0.499, P < .0001) in women. Leptin levels correlated significantly with only BMI (r = 0.31, P = .0002) in men, and with BMI (r = 0.71, P < .0001) and TGs (r = 0.26, P = .0201) in women. Adiponectin and leptin levels tended to correlate with these parameters in an opposite manner. On the other hand, A/L ratio significantly correlated with BMI (r = -0.4, P < .0001), TG (r = -0.199, P = .0192), HDL (r = 0.235, P = .0054), and LPL mass (r = 0.244, P = .0390) in men, and with BMI (r = -0.482, P < .0001), TG (r = -0.402, P = .0002), HDL (r = 0.358, P = .0011), and LPL mass (r = 0.487, P < .0001) in women. Next, the patients were divided into 3 groups classified by their fasting plasma glucose (FPG) level, and the correlations between the parameters and A/L ratio or homeostasis model assessment (HOMA-R), and the correlation between A/L ratio and HOMA-R were investigated in each group. Significant correlations between the parameters and A/L ratio were tended to be observed as the FPG level rose; however, the significant correlations between the parameters and HOMA-R were no longer seen as FPG level elevated. The results suggested that the A/L ratio was effective in relevance as a parameter of insulin resistance to adiponectin or leptin alone, and a more sensitive and reliable marker of insulin resistance than HOMA-R as the FPG level elevated, in patients with type 2 diabetes.

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PubMed2005

Exercise training is not associated with improved levels of C-reactive protein or adiponectin.

The purpose of this study was to determine the effect of exercise training on the levels of C-reactive protein (CRP) and adiponectin, and to assess whether exercise-induced changes in insulin resistance could be explained in part by changes in these inflammation markers. Study participants included 51 middle-aged (45.3+/-8.3 years; mean+/-SD), overweight (33.7+/-4.8 BMI), insulin-resistant, nondiabetic individuals. Subjects had their insulin sensitivity, body fat, CRP, and adiponectin levels measured, and their predicted maximal fitness calculated before and after 16 weeks of moderate, intense, or no exercise training. Modest improvements in fitness, body composition, and insulin sensitivity were observed, but these changes were not associated with decreased CRP or increased adiponectin levels, even when subjects were stratified by their change in fitness or obesity. Regression analysis demonstrated that the change in percentage of body fat was significantly related to changes in insulin sensitivity, whereas changes in VO2 MAX, CRP, and adiponectin were not. Participation in moderate to intense exercise was not associated with improved measures of chronic inflammation markers, as measured by CRP and adiponectin. Moreover, improvements in insulin sensitivity resulting from exercise or modest weight loss did not appear to be related to changes in these markers.

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PubMed2005

Elevation of serum adiponectin levels in Basedow disease.

The present study was undertaken to determine whether thyroid hormone affects serum adiponectin levels in the patients with Basedow disease. Sixty-four patients with Basedow disease were examined; 32 patients had hyperthyroid state and 32 patients had euthyroid state who had been treated with antithyroid drugs. In addition, 30 age- and sex-matched subjects served as a control. Serum adiponectin, free T4, free T3, thyroid-stimulating hormone, and thyroid-stimulating hormone receptor antibody (TRAb) were measured. Serum adiponectin levels were 12.9+/-1.6 microg/mL in the hyperthyroid state, a value significantly greater than that of 8.2 +/- 0.5 microg/mL in the euthyroid state (P<.05) and that of 8.6+/-0.7 microg/mL in the control subjects (P<.05). Serum adiponectin levels had positive correlations with either of serum free T4 (r=0.453, P<.001), free T3 (r=0.47, P< .001), or TRAb (r= 0.491, P<.001), but not with body mass index. Multiple regression analysis showed TRAb had the strongest contribution to serum adiponectin concentration in the patients with Basedow disease. The present findings indicate that hyper-adiponectinemia is closely associated with increases in serum thyroid hormone levels and TRAb in Basedow disease.

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PubMed2006

Adiponectin and stress hormone responses to maximal sculling after volume-extended training season in elite rowers.

The purpose of this study was to investigate the resting and short-duration exercise-induced hormone responses of male rowers as a result of 6 months of volume-extended training season. Body composition, maximal aerobic capacity, and on-water 2000-m sculling performance were assessed before and after a 24-week training in elite rowers (n = 11; 193.1 +/- 5.2 cm; 91.6 +/- 5.8 kg; maximum oxygen consumption [VO2max], 6.2 +/- 0.5 L x min(-1)). Six rowers were selected (SEL; 192.0 +/- 6.3 cm; 93.5 +/- 7.1 kg; VO2max, 6.4 +/- 0.4 L x min(-1)) and 5 were not selected (N-SEL; 194.8 +/- 4.1 cm; 89.6 +/- 4.0 kg; VO2max, 6.0 +/- 0.5 L x min(-1)) for the national team. Resting adiponectin did not change as a result of prolonged training. Adiponectin did not change after 2000-m rowing at baseline either. No responses were also observed 24 weeks later in SEL rowers, whereas a significant decrease (P < .05) was observed in N-SEL rowers. At the same time, leptin also decreased after the first 30 minutes of recovery in N-SEL rowers. After the training period, immediate postexercise increases in growth hormone and testosterone were significantly higher in the whole group of rowers. No differences in cortisol responses were observed before and after the training period in SEL and N-SEL rowers. In conclusion, it appears that resting adiponectin does not change as a result of prolonged training. Training may modify adiponectin response to an short-duration exercise depending on the performance level of athletes. Decreased postexercise adiponectin and leptin values in rowers with lower performance capacity may be indicative of the inadequate recovery of these athletes.

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PubMed2007

Circulating leptin and adiponectin levels in patients with primary hyperparathyroidism.

Primary hyperparathyroidism (PHPT) has been associated with high cardiovascular morbidity and mortality; its pathogenesis is not fully understood. Moreover, many metabolic abnormalities are frequently present in patients with PHPT. Several substances (such as leptin and adiponectin) are secreted from adipocytes, which may contribute to regulate energy homeostasis and the development of cardiovascular diseases. We examined the relationship between leptin and adiponectin levels and metabolic disorders in 67 newly diagnosed never-treated patients with PHPT and in 46 healthy subjects (HS). Twenty (29.8%) patients with PHPT presented a metabolic syndrome (as defined by Adult Treatment Panel III criteria). Serum leptin and adiponectin levels in HS were 6.28 +/- 3.3 ng/mL (range, 1.7-19.2 ng/mL) and 6.65 +/- 1.7 microg/mL (range, 3.72-10.86 microg/mL), respectively. In all patients with PHPT, the mean leptin levels (34.28 +/- 20.4 ng/mL) were significantly higher than those of HS (P < .01) and, in particular, in PHPT patients with metabolic syndrome (52.63 +/- 31.2 ng/mL) and positively correlated with body mass index, waist circumference, and cholesterol. The mean adiponectin level was significantly lower (4.34 +/- 3.5 mug/mL) only in PHPT patients with metabolic syndrome (P < .005) and negatively correlated with waist circumference and fasting glucose. We concluded that increased serum level of leptin and decreased serum level of adiponectin coexist in patients with PHPT and may represent a pathogenetic factor for cardiovascular disease in this condition.

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PubMed2006

The cannabinoid CB1 receptor inverse agonist, rimonabant, modifies body weight and adiponectin function in diet-induced obese rats as a consequence of reduced food intake.

The cannabinoid CB1 receptor inverse agonist rimonabant induces hypophagia and body weight loss. Reduced body weight may potentially be due to decreased food intake or to direct metabolic effects of drug administration on energy expenditure. This study uses a paired-feeding protocol to quantify the contributions of energy intake to rimonabant-induced body weight loss. Diet-induced obese (DIO) rats were dosed with rimonabant (3, 10 mg/kg PO once daily) and matched with pair-fed controls. Food intake and body weight were measured daily. Blood samples and adipose tissue were collected on day 15 for measurement of plasma adiponectin and adiponectin mRNA levels. DIO rats treated with rimonabant and pair-fed controls showed very similar changes in body weight. Although tolerance developed to the anorectic effect of rimonabant, total food intake was significantly decreased over the 14-day study period and fully accounted for the observed reductions in body weight. Adiponectin mRNA and plasma adiponectin were elevated in vehicle-treated chow-fed animals compared to obese controls, and did not differ between rimonabant-treated and pair-fed animals. The similarities between rimonabant-treated and pair-fed animals in body weight loss and the absence of differences in measures of adiponectin activity between drug-treated and pair-fed animals suggest that the outcomes of this experiment were solely mediated by the drug-induced reduction in food intake.

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PubMed2006

Plasma levels of adiponectin and tumor necrosis factor-alpha in patients with remitted major depression receiving long-term maintenance antidepressant therapy.

Adiponectin, an adipose tissue-specific plasma protein, is involved in insulin sensitization and has anti-atherosclerotic properties, whereas tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory protein, plays important roles in inflammatory endothelial injury and atherosclerotic changes. It has been reported that adiponectin and TNF-alpha inhibit each other's expression and production in adipocytes. Several in vitro studies indicated that antidepressant medications decreased the production of pro-inflammatory cytokines including TNF-alpha, but the effect of antidepressants on the expression of adiponectin is still unknown. We examined the plasma levels of TNF-alpha and adiponectin in patients with remitted depression receiving maintenance antidepressant therapy for longer than half a year, and compared the levels with those in healthy controls. The plasma levels of TNF-alpha and adiponectin in the remitted depression group were significantly lower and higher than those in the control group, respectively. This preliminary cross-sectional study suggests the possibility that maintenance antidepressant therapy may have anti-inflammatory effects and prevent the development of atherosclerosis.

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PubMed2005

Effect of low doses of atorvastatin on adiponectin, glucose homeostasis, and clinical inflammatory markers in kidney transplant recipients.

INTRODUCTION: Various studies describe the pleiotropic antiinflammatory and antioxidant effects of atorvastatin, in addition to its hypolipemic effects. It has been suggested that statins modify glucose homeostasis via their antiinflammatory effects. A further hypothesis suggests that the incidence of posttransplantation diabetes is lower in statin-treated patients. This study sought to ascertain whether atorvastatin modifies glucose homeostasis, adiponectin, and inflammatory markers in kidney transplant recipients. PATIENTS AND METHODS: Sixty-eight kidney transplant recipients (41 men, 27 women; mean age, 53 +/- 12 years) with stable renal function and dyslipidemia were treated with atorvastatin (10 mg/d) for 12 weeks. Glucose, insulin, homeostasis model assessment (HOMA-IR) index, adiponectin, tumor necrosis factor (TNF)-alpha, and serum C-reactive protein (CRP) concentrations were determined at baseline and at 3 months. The lipid profile, renal function parameters (creatinine, creatinine clearance, and proteinuria), as well as GOT, GPT, and CK were determined at baseline and at 3 months. RESULTS: Treatment with atorvastatin achieved a statistically significant decrease in lipid profile. After 3 months of treatment, 74.6% of patients had total cholesterol and 78.7% low-density lipoprotein (LDL) cholesterol concentrations within reference range (<5.2 and 3.3 mmol/L, respectively). Furthermore, 47.5% of patients attained an LDL concentration <2.59 mmol/L. A greater reduction in total cholesterol (P = .05) and LDL cholesterol (P = .04) was achieved in patients with creatinine clearance <60 mL/min. Atorvastatin did not modify glucose homeostasis parameters, adiponectin, TNF-alpha, or CRP. At baseline and after 3 months of treatment, an inverse correlation was found between adiponectin and glucose, insulin, HOMA- IR index, and creatinine clearance, and a positive correlation was found between adiponectin and high-density lipoprotein (HDL) cholesterol. CONCLUSION: Atorvastatin at a dose of 10 mg/d in kidney transplant recipients does not modify glucose homeostasis or alter inflammatory markers, despite its hypolipemic effects. Its efficacy to reduce total cholesterol and LDL cholesterol was greater in patients with worse renal function.

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PubMed2002

Brown adipocytes are novel sites of expression and regulation of adiponectin and resistin.

Adiponectin and resistin, two recently identified adipocyte-specific secretory factors, are able to modulate insulin actions in target tissues. To investigate their expression and hormonal regulation in brown adipocytes, we used the brown adipocyte cell line T37i, which, beside uncoupling protein expression, secretes leptin. Adiponectin and resistin mRNA were detected as a function of cell differentiation. Both transcripts were expressed at relatively high levels in differentiated T37i cells, reaching maximal levels on day 7, while resistin expression drastically fell afterwards. These stable transcripts (t(1/2)>8 h) were differentially regulated by factors involved in insulin responsiveness. Insulin and thiazolidinedione, a peroxisome proliferator-activated receptor gamma agonist, stimulated resistin expression two- to four-fold in differentiated T37i cells, whereas adiponectin mRNA levels increased 1.5-2-fold. In contrast, dexamethasone and isoproterenol reduced by two-fold the level of adiponectin and resistin transcripts in differentiated T37i cells. This study provides the first direct evidence that differentiated brown adipocytes are endocrine cells capable of expressing adiponectin and resistin. The complex hormonal regulation of their expression in brown adipocytes clearly differs from that reported in white adipose tissue, pointing to differential physiological and pathophysiological implications of brown fat in energy homeostasis.

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PubMed2003

Fat depot-specific expression of adiponectin is impaired in Zucker fatty rats.

Adiposity, particularly increased intra-abdominal fat, is a predisposing factor for the development of insulin resistance in obesity and type 2 diabetes. Visceral fat seems to differ from subcutaneous adipose tissue in adipocytokine production. This fat depot-related difference has been viewed as an important mechanism by which adipose tissue exerts its paracrine/autocrine effects on peripheral tissue in modulating insulin sensitivity. We have studied the relative expression of adiponectin in visceral versus subcutaneous fat in Zucker fatty versus lean rats. Visceral fat, as opposed to subcutaneous fat, exhibited relatively higher levels of adiponectin production in lean animals. However, in Zucker fatty rats, adiponectin expression in visceral fat was suppressed to basal levels, which correlated with significantly reduced plasma adiponectin concentrations and increased insulin resistance. These results suggest that an impaired depot-specific expression of adiponectin is a contributing factor for the development of insulin resistance in Zucker fatty rats.

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PubMed2003

Adiponectin and protection against type 2 diabetes mellitus.

Adiponectin is an adipocyte-derived peptide, which has anti-inflammatory and insulin-sensitising properties. We designed a nested case-control study to assess whether baseline adiponectin concentrations in plasma are independently associated with risk of type 2 diabetes. We found that adiponectin concentrations in plasma were lower among individuals who later developed type 2 diabetes than among controls (mean 5.34 microg/mL [SD 3.49] vs 6.87 microg/mL [4.58], p<0.0001). High concentrations of adiponectin were associated with a substantially reduced relative risk of type 2 diabetes after adjustment for age, sex, waist-to-hip ratio, body-mass index, smoking, exercise, alcohol consumption, education, and glycosylated haemoglobin A(1c) (odds ratio 4th vs 1st quartile 0.3 [95% CI 0.2-0.7], p=0.0051). We conclude that adiponectin is independently associated with a reduced risk of type 2 diabetes in apparently healthy individuals.

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PubMed2003

Decreased plasma adiponectin concentration in patients with essential hypertension.

Adipocytes secrete several biologically active substances that are presumed to be involved in obesity-related hypertension. There are no reports that deal with the relationship between plasma adiponectin concentration and blood pressure (BP). To evaluate the role of adiponectin in essential hypertension 33 patients with essential hypertensive (EHP) (12 women, 21 men) and 33 body mass index-matched normotensive healthy subjects (NHS) (13 women, 20 men) were studied. In EHP plasma adiponectin concentration was significantly lower than in NHS (9.1 +/- 4.5 v 13.7 +/- 5.2 microg/mL, respectively). In all subjects a significant negative correlation was found between plasma adiponectin concentration and mean, systolic, and diastolic BP, suggesting that adiponectin contributes to the clinical course of essential hypertension.

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PubMed2003

Plasma adiponectin increases postprandially in obese, but not in lean, subjects.

OBJECTIVE: We investigated the acute responses of plasma adiponectin levels to a test meal in lean and obese subjects. RESEARCH METHODS AND PROCEDURES: We studied 13 lean and 11 obese subjects after a 10-hour overnight fast. Glucose, insulin, and adiponectin concentrations were measured at baseline and 15, 30, 60, 120, and 180 minutes after a fixed breakfast. RESULTS: At baseline, fasting adiponectin concentrations were lower in the obese group vs. the lean group [mean (95% confidence interval): 2.9 (2.1 to 4.1) microg/mL vs. 8.6 (6.5 to 11.3) microg/mL], but rose 4-fold postprandially in the obese group, reaching a peak at 60 minutes [baseline: 2.9 (2.1 to 4.1) microg/mL vs. 60 minutes: 12.1 (8.5 to 17.4) microg/mL; p< 0.0001] and remaining elevated for the remainder of the study. There were no postprandial changes in plasma adiponectin concentrations in lean subjects. DISCUSSION: This increase of adiponectin concentrations in obese individuals might have important beneficial effects on postprandial glucose and lipid metabolism and might be viewed as a mechanism for maintaining normal glucose tolerance in those who are obese and insulin resistant.

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PubMed2004

Adiponectin but not resistin is associated with insulin resistance-related phenotypes in baboons.

OBJECTIVE: The hormones adiponectin and resistin have been associated with insulin resistance. This paper analyzed the potential relationship between adiponectin and resistin and insulin resistance-related phenotypes in baboons. RESEARCH METHODS AND PROCEDURES: One hundred eight adult baboons (84 female and 24 male) were studied. Weight was measured, and a blood sample was collected under fasting conditions for plasma and monocyte isolation. Fasting glucose, insulin, C-peptide, and adiponectin levels in plasma were measured by standard methods. Insulin resistance was calculated by the homeostasis model assessment index. Resistin mRNA abundance in monocytes was determined by real-time quantitative reverse transcription-polymerase chain reaction. Data were clustered by weight tertiles for statistical analysis. RESULTS: As observed in humans, the insulin resistance-related phenotypes were related to weight, plasma levels of adiponectin, and C-peptide. No significant relationship between resistin circulating levels or expression in monocytes and insulin resistance-related phenotypes was found in baboons. DISCUSSION: These findings suggest that resistin is not associated with insulin resistance. However, previous observations of relationships among weight, adiponectin, and insulin resistance are confirmed.

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PubMed2006

Adiponectin in relation to childhood myeloblastic leukaemia.

Adiponectin, an adipocyte-specific secretory protein known to induce apoptosis, has been reported to be inversely related to breast and endometrial cancers and recently found to inhibit proliferation of myeloid but not lymphoid cell lines. We hypothesised that adiponectin may be inversely associated with acute myeloblastic leukaemia (AML), but not with acute lymphoblastic leukaemia of B (ALL-B) or T (ALL-T) cell origin in children. Blood samples and clinical information were collected over the period 1996-2000 from 201 children (0-14 years old) with leukaemia (22 AML, 161 ALL-B and 18 ALL-T cases) through a national network of childhood Hematology-Oncology units in Greece and from 201 controls hospitalised for minor pediatric ailments. Serum adiponectin levels were measured under code, at the Beth Israel Deaconess Medical Center, Boston, MA, USA using a radioimmunoassay procedure. Each of the three leukaemia groups was compared with the control group through multiple logistic regression. Odds ratios (OR) and 95% confidence intervals (95% CI) for an increase of adiponectin equal to 1 s.d. among controls were estimated controlling for gender, age, as well as for height and weight, expressed in age-gender-specific centiles of Greek growth curves. Adiponectin was inversely associated with AML (OR=0.56; 95% CI, 0.34-0.94), whereas it was not significantly associated with either ALL-B (OR=0.88; 95% CI, 0.71-1.10) or ALL-T (OR=1.08; 95% CI, 0.67-1.72). Biological plausibility and empirical evidence point to the importance of this hormone in the pathogenesis of childhood AML.

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PubMed2003

Adiponectin levels do not change with moderate dietary induced weight loss and exercise in obese postmenopausal women.

OBJECTIVE: The purpose of this study was to determine changes in adiponectin levels with moderate weight loss, weight loss plus aerobic exercise, or weight loss plus resistive exercise in overweight and obese, sedentary postmenopausal women. DESIGN: Longitudinal, clinical intervention study of 6-month (3 x /week) program of either weight loss (WL, n=15), weight loss + aerobic exercise (WL+AEX, n=16), or weight loss + resistive exercise (WL+RT, n=9) SUBJECTS: We studied 40 sedentary, overweight and obese (body mass index, BMI=32+/-1 kg/m(2), X+/-s.e.m.) postmenopausal (57+/-1y) women. MEASUREMENTS: Fat mass and fat-free mass (FFM) by dual-energy X-ray absorptiometry, plasma insulin, leptin, and adiponectin by radioimmunoassay. RESULTS: Age, body weight, BMI, waist and hip circumferences, waist-to-hip ratio, VO(2)max, percent fat, total body fat mass, FFM, and fasting plasma glucose, insulin, leptin, and adiponectin concentrations were similar among WL, WL+AEX, and WL+RT groups before the interventions. In all women combined, body weight, BMI, and waist and hip circumferences decreased (P < 0.001). There was a significant absolute decrease in percent body fat from 47 to 44%, representing a 13% decrease in total fat mass and a -1.6% change in FFM. Fasting concentrations of plasma adiponectin did not change (40+/-16%, P=NS), whereas fasting plasma glucose, insulin, and leptin all decreased (P<0.001). CONCLUSIONS: Plasma adiponectin levels do not change with a 6-month moderate weight reduction program even when accompanied by aerobic or resistive exercise training in overweight and obese postmenopausal women.

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