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Journal ArticleDOI

Gender differences in the association of visceral and subcutaneous adiposity with adiponectin in African Americans: the Jackson Heart Study

TL;DR: The statistically significant inverse association of VAT and adiponectin persisted after additionally adjusting for SAT, body mass index (BMI) and waist circumference (WC), suggesting that VAT provides significant information above and beyond BMI and WC.
Abstract: Adiponectin, paradoxically reduced in obesity and with lower levels in African Americans (AA), modulates several cardiometabolic risk factors. Because abdominal visceral adipose tissue (VAT), known to be reduced in AA, and subcutaneous adipose tissue (SAT) compartments may confer differential metabolic risk profiles, we investigated the associations of VAT and SAT with serum adiponectin, separately by gender, with the hypothesis that VAT is more strongly inversely associated with adiponectin than SAT. Participants from the Jackson Heart Study, an ongoing cohort of AA (n = 2,799; 64% women; mean age, 55 ± 11 years) underwent computer tomography assessment of SAT and VAT volumes, and had stored serum specimens analyzed for adiponectin levels. These levels were examined by gender in relation to increments of VAT and SAT. Compared to women, men had significantly lower mean levels of adiponectin (3.9 ± 3.0 μg/mL vs. 6.0 ± 4.4 μg/mL; p < 0.01) and mean volume of SAT (1,721 ± 803 cm3 vs. 2,668 ± 968 cm3; p < 0.01) but significantly higher mean volume of VAT (884 ± 416 cm3 vs. 801 ± 363 cm3; p < 0.01). Among women, a one standard deviation increment in VAT was inversely associated with adiponectin (β = − 0.13; p < 0.0001) after controlling for age, systolic blood pressure, fasting plasma glucose, high-density lipoprotein cholesterol, triglycerides, education, pack-years of smoking and daily intake of alcohol. The statistically significant inverse association of VAT and adiponectin persisted after additionally adjusting for SAT, body mass index (BMI) and waist circumference (WC), suggesting that VAT provides significant information above and beyond BMI and WC. Among men, after the same multivariable adjustment, there was a direct association of SAT and adiponectin (β = 0.18; p = 0.002) that persisted when controlling for BMI and WC, supporting a beneficial effect of SAT. Insulin resistance mediated the association of SAT with adiponectin in women. In African Americans, abdominal visceral adipose tissue had an inverse association with serum adiponectin concentrations only among women. Abdominal subcutaneous adipose tissue appeared as a protective fat depot in men.

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Journal ArticleDOI
TL;DR: The role of adiponectin in liver diseases in the presence and absence of surgery reported in the literature in the last ten years is described and potential targets that might be useful for the treatment of liver disease are evaluated.
Abstract: The review describes the role of adiponectin in liver diseases in the presence and absence of surgery reported in the literature in the last ten years. The most updated therapeutic strategies based on the regulation of adiponectin including pharmacological and surgical interventions and adiponectin knockout rodents, as well as some of the scientific controversies in this field, are described. Whether adiponectin could be a potential therapeutic target for the treatment of liver diseases and patients submitted to hepatic resection or liver transplantation are discussed. Furthermore, preclinical and clinical data on the mechanism of action of adiponectin in different liver diseases (nonalcoholic fatty disease, alcoholic liver disease, nonalcoholic steatohepatitis, liver cirrhosis and hepatocellular carcinoma) in the absence or presence of surgery are evaluated in order to establish potential targets that might be useful for the treatment of liver disease as well as in the practice of liver surgery associated with the hepatic resections of tumors and liver transplantation.

12 citations

Journal ArticleDOI
TL;DR: There was a J shaped association between BF% andFM and all-cause mortality risk, with the lowest risk at BF% of 25% and FM of 20 kg, and the observed positive associations were more pronounced in studies which had a longer duration, excluded participants with prevalent cardiovascular disease and cancer at baseline, and less pronounced in Studies which adjusted for potential intermediates.

12 citations

Journal ArticleDOI
TL;DR: Type 2 diabetics do not have lower adiponectin levels and may be associated with reduced risk of atherosclerosis through its effects on HDL cholesterol metabolism, according to this case control study.
Abstract: Background: Adiponectin has been associated with insulin resistance and dyslipidemia in Type 2 diabetes, though the mechanism of association is still uncertain. The adiponectin levels and lipid profile in relation to glycemic control were investigated in type 2 diabetics. Methods: Forty two diabetic subjects (35-64 years) and 33 age-matched non-diabetic subjects were recruited into this case control study. Socio-demographic characteristics, anthropometric indices and blood pressure were obtained. Total cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL), high density lipoprotein, (HDL), fasting plasma glucose (FPG), and glycated hemoglobin (HbA1c) were estimated using colorimetric methods, atherogenic index (AI) was calculated, while serum adiponectin was determined by ELISA method. Results: Adiponectin levels of type 2 diabetics were not significantly different from the non-diabetics studied (p>0.05). Higher TG levels were observed in diabetics with poor glycemic control compared with those with good glycemic control (p 0.05). Conclusion: Type 2 diabetics do not have lower adiponectin levels. Gender, duration of diabetes and glycemic control does not seem to exert any influence on adiponectin levels in type 2 diabetes. Adiponectin may be associated with reduced risk of atherosclerosis through its effects on HDL cholesterol metabolism.

10 citations

Journal ArticleDOI
TL;DR: The association of abdominal adiposity with hypertension differs qualitatively by sex and WC may be an important determinant of hypertension and may be used for risk stratification for hypertension among Chinese individuals.
Abstract: There are inconsistent interpretations of the interrelationship of adiposity, anthropometric indices, and blood pressure (BP) in hypertensive patients. Additionally, whether these relationships differ between sexes is unknown. We aimed to elucidate the associations of adiposity indices measured using quantitative computed tomography (QCT) with BP and hypertension and to determine the effect of sex on the interrelationship of these parameters in a Chinese population. Abdominal adipose fat, including the visceral adipose tissue (VAT) area and subcutaneous adipose tissue (SAT) area, was measured by QCT in 1488 patients (514 men, 974 women). Body mass index (BMI), waist circumference (WC), hip circumference (HC), and systolic (SBP) and diastolic BP (DBP) were measured. Pearson correlation coefficients, multivariate analyses, and receiver operating characteristic (ROC) curves were used to assess the relationship and potential of adiposity indices to BP and risk of hypertension within sex groups. Men had significantly greater VAT area but less SAT area than women in hypertensive group. VAT, SAT, and WC were more highly correlated with SBP in men than in women. After controlling for body weight, height, and age, VAT area and WC were positively associated with SBP (VAT: β = 0.309, p < 0.001; WC: β = 0.148, p = 0.001) and DBP (VAT: β = 0.099, p = 0.034; WC: β = 0.198, p = 0.001) in women. VAT area was positively associated with SBP (β = 0.444, p < 0.001) and DBP (β = 0.146, p = 0.021) in men. WC had a significant correlation with an increased risk of hypertension in women but a borderline association in men (p = 0.059) when adjusted for VAT area and SAT area. The association of abdominal adiposity with hypertension differs qualitatively by sex. WC may be an important determinant of hypertension and may be used for risk stratification for hypertension among Chinese individuals.

8 citations

Journal ArticleDOI
TL;DR: The data confirm previous descriptions of leptin but suggest that variations in factors determining serum adiponectin levels observed between ethnicities could also be seen between populations from the same ethnicity.
Abstract: Factors associated with plasma levels of adiponectin and leptin were studied in adult subjects without diabetes from Cotonou in Benin (West-Africa). Seventy (70) men and 45 women were included in the study. Anthropometric variables were measured and a venous blood sample was drawn from each subject, after an overnight fasting period, for measurement of plasma glucose, insulin, leptin, and adiponectin levels. HOMA-IR was determined to assess insulin resistance. Adiponectin and leptin levels were higher in women than in men (with adiponectin 18.48 ± 12.77 vs.7.8 ± 10.39 μg/mL, P < 0.0001, and leptin 30.77 ± 19.16 vs. 8.66 ± 8.24 ng/mL, P < 0.0001). Fasting insulin level and HOMA-IR were also higher in the females. Hyperleptinemia was observed in 66,96% of subjects and hypoadiponectinemia was present in 44.35% of subjects. In both men and women, leptin correlated with age (r = 0.2; P = 0.02), BMI (r = 0.572; P < 0.0001), waist circumference (r = 0.534; P < 0.0001), fasting insulin (r = 0.461; P < 0.001), and HOMA-IR (r = 0.430; P < 0.0001). No significant correlation was observed for adiponectin levels with these variables. Only in women, adiponectin was inversely correlated with fasting glucose (r = -0.423; P < 0.004). These data confirm previous descriptions of leptin but suggest that variations in factors determining serum adiponectin levels observed between ethnicities could also been seen between populations from the same ethnicity.

8 citations


Cites result from "Gender differences in the associati..."

  • ...While these data conflict with some of the data previously reported for studies in Caucasians, African Americans, and sub-Saharans (Schutte et al. 2007; Meilleur et al. 2010; Bidulescu et al. 2013; Ayina et al. 2016), they are consistent with other published data....

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  • ...These data are consistent with data previously reported on either sub-Saharan and African American subjects and for data obtained in studying other ethnicities (Ruige et al. 1999; Meilleur et al. 2010; Oshodi et al. 2012; Bidulescu et al. 2013; Zuo et al. 2013; Ayina et al. 2016)....

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References
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Journal ArticleDOI
TL;DR: The correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
Abstract: The steady-state basal plasma glucose and insulin concentrations are determined by their interaction in a feedback loop. A computer-solved model has been used to predict the homeostatic concentrations which arise from varying degrees beta-cell deficiency and insulin resistance. Comparison of a patient's fasting values with the model's predictions allows a quantitative assessment of the contributions of insulin resistance and deficient beta-cell function to the fasting hyperglycaemia (homeostasis model assessment, HOMA). The accuracy and precision of the estimate have been determined by comparison with independent measures of insulin resistance and beta-cell function using hyperglycaemic and euglycaemic clamps and an intravenous glucose tolerance test. The estimate of insulin resistance obtained by homeostasis model assessment correlated with estimates obtained by use of the euglycaemic clamp (Rs = 0.88, p less than 0.0001), the fasting insulin concentration (Rs = 0.81, p less than 0.0001), and the hyperglycaemic clamp, (Rs = 0.69, p less than 0.01). There was no correlation with any aspect of insulin-receptor binding. The estimate of deficient beta-cell function obtained by homeostasis model assessment correlated with that derived using the hyperglycaemic clamp (Rs = 0.61, p less than 0.01) and with the estimate from the intravenous glucose tolerance test (Rs = 0.64, p less than 0.05). The low precision of the estimates from the model (coefficients of variation: 31% for insulin resistance and 32% for beta-cell deficit) limits its use, but the correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.

29,217 citations

Journal ArticleDOI
01 Dec 1994-Nature
TL;DR: The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot.
Abstract: The mechanisms that balance food intake and energy expenditure determine who will be obese and who will be lean. One of the molecules that regulates energy balance in the mouse is the obese (ob) gene. Mutation of ob results in profound obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot.

12,394 citations


"Gender differences in the associati..." refers background in this paper

  • ..., leptin [42], adiponectin [43], tumor necrosis factor-α (TNF-α) [44], plasminogenactivator inhibitor type-1 (PAI-1) [45] and resistin [46]....

    [...]

Journal ArticleDOI
01 Jan 1993-Science
TL;DR: A role for TNF-alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity is indicated.
Abstract: Tumor necrosis factor-alpha (TNF-alpha) has been shown to have certain catabolic effects on fat cells and whole animals. An induction of TNF-alpha messenger RNA expression was observed in adipose tissue from four different rodent models of obesity and diabetes. TNF-alpha protein was also elevated locally and systemically. Neutralization of TNF-alpha in obese fa/fa rats caused a significant increase in the peripheral uptake of glucose in response to insulin. These results indicate a role for TNF-alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity.

7,347 citations


Additional excerpts

  • ...Several studies have demonstrated that adipose tissue actively produces a variety of locally and systemically functioning bioactive molecules that interact in various obesity-related diseases, e.g., leptin [42], adiponectin [43], tumor necrosis factor-α (TNF-α) [44], plasminogenactivator inhibitor type-1 (PAI-1) [45] and resistin [46]....

    [...]

  • ..., leptin [42], adiponectin [43], tumor necrosis factor-α (TNF-α) [44], plasminogen-activator inhibitor type-1 (PAI-1) [45] and resistin [46]....

    [...]

Journal ArticleDOI
TL;DR: Plasma concentrations of adiponectin in obese subjects were significantly lower than those in non-obese subjects, although adip onectin is secreted only from adipose tissue.

4,882 citations

Journal ArticleDOI
18 Jan 2001-Nature
TL;DR: It is shown that adipocytes secrete a unique signalling molecule, which is named resistin (for resistance to insulin), which circulating resistin levels are decreased by the anti-diabetic drug rosiglitazone, and increased in diet-induced and genetic forms of obesity.
Abstract: Diabetes mellitus is a chronic disease that leads to complications including heart disease, stroke, kidney failure, blindness and nerve damage. Type 2 diabetes, characterized by target-tissue resistance to insulin, is epidemic in industrialized societies and is strongly associated with obesity; however, the mechanism by which increased adiposity causes insulin resistance is unclear. Here we show that adipocytes secrete a unique signalling molecule, which we have named resistin (for resistance to insulin). Circulating resistin levels are decreased by the anti-diabetic drug rosiglitazone, and increased in diet-induced and genetic forms of obesity. Administration of anti-resistin antibody improves blood sugar and insulin action in mice with diet-induced obesity. Moreover, treatment of normal mice with recombinant resistin impairs glucose tolerance and insulin action. Insulin-stimulated glucose uptake by adipocytes is enhanced by neutralization of resistin and is reduced by resistin treatment. Resistin is thus a hormone that potentially links obesity to diabetes.

4,557 citations


Additional excerpts

  • ..., leptin [42], adiponectin [43], tumor necrosis factor-α (TNF-α) [44], plasminogen-activator inhibitor type-1 (PAI-1) [45] and resistin [46]....

    [...]

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