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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: As excess visceral body fat is strongly associated with higher risk of hypertension and prehypertension, measurements of VFI or VFI/PBF ratio, in addition to PBF, will provide a better understanding of adiposity-related risks for hypertension.
Abstract: Objective:This article investigates the relative effects of percentage body fat (PBF) and visceral fat index (VFI) on the prevalence of hypertension and prehypertension, and evaluates if excess visceral deposition of body fat increased the risk of hypertension or prehypertension.Methods:A general po

51 citations


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

  • ...subcutaneous abdominal fat confer different metabolic risk profiles, which are influenced by ethnicity and gender [20]....

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  • ...This difference could be partly because of the gender differences in the association of visceral and subcutaneous adiposity with adiponectin [20] and the stronger visceral fat-associated sympathoactivation seen in young boys versus girls [11], but a better explanation may require further research....

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  • ...However, this study did not adjust the confounding effects from visceral fat, which is generally positively associated with PBF [18,20]....

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Journal ArticleDOI
TL;DR: More work is needed to understand barriers to behavior change for black women, and knowledge gaps remain in identifying mechanisms by which pharmacologic and surgical treatments for obesity modify cardiovascular risk in black women.
Abstract: Black women in the United States are disproportionately affected by obesity, with almost two-thirds considered obese based on body mass index Obesity has been directly linked to cardiovascular morbidity and mortality in black women Therefore, understanding contributors to the genesis of obesity in black women is imperative While biologic differences likely result in varying obesity prevalence across racial/ethnic groups, behaviors such as post-partum weight retention and limited leisure-time physical activity, may especially contribute to obesity in black women Black women also appear to be particularly susceptible to cultural, psychosocial, and environmental factors that can promote weight gain Therapeutic interventions are being tailored to specifically address these social determinants of health and to foster lifestyle modification; however, more work is needed to understand barriers to behavior change for black women Knowledge gaps also remain in identifying mechanisms by which pharmacologic and surgical treatments for obesity modify cardiovascular risk in black women

49 citations

Journal ArticleDOI
TL;DR: The findings reinforce the advantages of being born with an appropriate birth weight, and the hazards of rapid postnatal gains in weight relative to linear growth, particularly after the critical window of the first 1000 days.
Abstract: Associations of birth weight, linear growth and relative weight gain throughout life with abdominal fat depots in adulthood: the 1982 Pelotas (Brazil) birth cohort study

42 citations

Journal ArticleDOI
TL;DR: For each given decrease in HMW adiponectin concentrations a greater increase in HOMA-IR is observed in Aboriginals, Chinese, and South Asians than Europeans.
Abstract: Background Ethnic-specific differences in insulin resistance (IR) are well described but the underlying mechanisms are unknown. Adiponectin is an insulin sensitizing adipocytokine that circulates as multiple isoforms, with high molecular weight (HMW) adiponectin associated with greatest insulin sensitivity. The objective of this study is to determine if plasma total and HMW adiponectin concentrations underlie ethnic-specific differences in IR.

40 citations


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

  • ...Direct measures of adiposity have rarely been utilized and were predominantly explored in African, Caucasian, and Hispanic American populations [15,16]....

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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]....

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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]....

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  • ..., 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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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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