Visceral fat accumulation in men is positively associated with insulin, glucose, and C-peptide levels, but negatively with testosterone levels

Seidell, Jacob C.; Björntorp, Per; Sjöström, Lars; Kvist, Henry; Sannerstedt, Rune

doi:10.1016/0026-0495(90)90297-p

Cited by 523 publications

(320 citation statements)

References 23 publications

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“…5,35 Endogenous testosterone levels are also inversely related to central adiposity in men in this and other cross-sectional studies, 36,37 and testosterone therapy in men reduces visceral fat. 38 Thus, the positive association of testosterone with adiponectin in men could be mediated by testosterone effects on the size of the visceral fat mass, rather than a direct effect of testosterone on adiponectin synthesis or secretion.…”

Section: Discussionsupporting

confidence: 62%

Sex-specific determinants of serum adiponectin in older adults: the role of endogenous sex hormones

2006

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Objective: To assess the sex-specific association of adiponectin with multiple factors thought to influence its levels, with a special emphasis on endogenous sex hormones. Design and methods: A cross-sectional study of determinants of serum adiponectin in 873 men and 673 postmenopausal women, ages 50-92. Factors evaluated include age, body size, fat distribution, lifestyle (exercise, smoking, alcohol intake), insulin resistance, renal function and endogenous sex hormone levels (total and bioavailable testosterone and estradiol). Results: Median serum adiponectin was 50% higher in women than men (Po0.001). In unadjusted analyses, adiponectin was positively related to age, alcohol intake, high-density lipoprotein (HDL) and testosterone, and negatively related to waist girth, body mass index, Homeostasis Model Assessment for Insulin Resistance (HOMA-IR), triglycerides and bioavailable estradiol in both sexes (all Po0.01). Adiponectin was positively related to blood urea nitrogen, a measure of renal function, in men only (Po0.001). Sex-specific multivariate linear regressions adjusting for HDL and triglycerides showed that only age, HOMA-IR and sex hormones independently predicted circulating adiponectin for both men and women. Higher levels of endogenous testosterone and lower bioavailable estradiol concentrations each predicted higher adiponectin; this was true for both sexes, and was not explained by differences in age, adiposity, alcohol intake, insulin resistance or lipoprotein levels. Conclusions: The association of adiponectin with the factors studied here is strikingly similar for men and women. Sex differences in circulating adiponectin levels in older adults cannot be explained by sex hormone regulation.

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Section: Discussionsupporting

confidence: 62%

Sex-specific determinants of serum adiponectin in older adults: the role of endogenous sex hormones

2006

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“…Central or abdominal obesity, long recognised as a factor predisposing to diabetes and coronary disease [29] in both sexes, is linked with glucose intolerance, insulin resistance and disturbances of lipoprotein metabolism [30,31]. Each of these components of the metabolic syndrome showed a close inverse association with employment grade in the Whitehall II data.…”

Section: Discussionmentioning

confidence: 99%

Social inequality in coronary risk: Central obesity and the metabolic syndrome. Evidence from the Whitehall II study

et al. 1997

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SummaryThis report describes the social distribution of central obesity and the metabolic syndrome at the Whitehall II study phase 3 examination, and assesses the contribution of health related behaviours to their distribution. Cross-sectional analyses were conducted utilising data collected in 1991-1993 from 4978 men and 2035 women aged 39-63 years who completed an oral glucose tolerance test. There was an inverse social gradient in prevalence of the metabolic syndrome. The odds ratio (95 % confidence interval) for having the metabolic syndrome comparing lowest with highest employment grade was: men 2.2 (1.6-2.9), women 2.8 (1.6-4.8). Odds ratios for occupying the top quintile of the following variables, comparing lowest with highest grade, were, for waist-hip ratio: men 2.2 (1.8-2.8), women 1.6 (1.1-2.4); postload glucose: men 1.4 (1.1-1.8), women 1.8 (1.2-2.6); triglycerides: men 1.6 (1.2-2.0), women 2.2 (1.5-3.3); fibrinogen: men 1.7 (1.4-2.3), women 1.9 (1.2-2.8). Current smoking status, alcohol consumption and exercise level made a small contribution (men 11%, women 9 %) to the inverse association between socioeconomic status and metabolic syndrome prevalence. In conclusion, central obesity, components of the metabolic syndrome and plasma fibrinogen are strongly and inversely associated with socioeconomic status. Our findings suggest the metabolic syndrome may contribute to the biological explanation of social inequalities in coronary risk. Health related behaviours appear to account for little of the social patterning of metabolic syndrome prevalence. [Diabetologia (1997[Diabetologia ( ) 40: 1341[Diabetologia ( -1349

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“…Concerning body fat distribution, however, one has to consider the sexual status of an individual, as gonadal steroids are known to mediate body fat deposition [43,44]. In this study and in the study of Hoenig et al all cats were neutered; this could influence body fat distribution and possibly GC receptor expression.…”

Section: Discussionmentioning

confidence: 78%

Effect of hyperlipidemia on 11β-hydroxysteroid-dehydrogenase, glucocorticoid receptor, and leptin expression in insulin-sensitive tissues of cats

Sieber-Ruckstuhl

Zini

Osto

et al. 2010

Domestic Animal Endocrinology

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Visceral fat accumulation in men is positively associated with insulin, glucose, and C-peptide levels, but negatively with testosterone levels

Cited by 523 publications

References 23 publications

Sex-specific determinants of serum adiponectin in older adults: the role of endogenous sex hormones

Sex-specific determinants of serum adiponectin in older adults: the role of endogenous sex hormones

Social inequality in coronary risk: Central obesity and the metabolic syndrome. Evidence from the Whitehall II study

Effect of hyperlipidemia on 11β-hydroxysteroid-dehydrogenase, glucocorticoid receptor, and leptin expression in insulin-sensitive tissues of cats

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