Reciprocal association between visceral obesity and adiponectin: in healthy premenopausal women

Kwon, Kihwan; Jung, Sang Hyuk; Choi, Chulhee; Park, Si-Hoon

doi:10.1016/j.ijcard.2004.03.050

Cited by 42 publications

(35 citation statements)

References 43 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: 63%

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: 63%

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

2006

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“…Although the negative association between overall obesity, as estimated by BMI and adiponectin levels, is quite consistent in numerous studies, the association between DXA-measured body fat mass or body fat percentage and adiponectin has been found to be less consistent (27,28). Regarding fat distribution, waist circumference or waist-to-hip ratio were stronger and negatively associated with adiponectin than BMI (6,27,29), and CT-measured visceral fat was a stronger negative determinant than abdominal s.c. fat (30,31). One study revealed that waist-to-hip ratio was even more strongly associated with adiponectin than visceral fat tissue (6), which may be due to the additional effect of femoral-gluteal fat tissue (measured by hip circumference) on adiponectin levels.…”

Section: Discussionmentioning

confidence: 99%

Relationship of adiposity with arterial stiffness as mediated by adiponectin in older men and women: the Hoorn Study

Snijder

Flyvbjerg

Stehouwer

et al. 2009

European Journal of Endocrinology

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Objective: To investigate whether adiponectin is associated with arterial stiffness, and whether adiponectin explains the association between body composition and arterial stiffness. Design: Cross-sectional cohort study. Methods: Subjects were participants (nZ456, mean age 68.9G6.1 years; age range 60-86 years) of the third follow-up examination of the Hoorn Study. Trunk fat, leg fat, trunk lean, and leg lean mass were measured by dual-energy X-ray absorptiometry. Ultrasound was used to measure distensibility and compliance of the carotid, femoral, and brachial arteries, and carotid Young's elastic modulus (as estimates of peripheral arterial stiffness). Results: Trunk fat mass was negatively associated with (ln-transformed) adiponectin (standardized bZK0.49, P!0.001), while leg fat mass was positively associated with adiponectin (bZ0.44, P!0.001), after adjustment for each other, age, and lean mass. After adjustment for age, sex, mean arterial pressure, and estimated glomerular filtration rate, higher adiponectin was associated with decreased peripheral arterial stiffness (b of mean Z-scores of all three arteriesZ0.14, PZ0.001). However, the associations of trunk fat (bZK0.26, P!0.001) and leg fat (bZ0.16, PZ0.006) with peripheral arterial stiffness were only minimally explained by adiponectin levels. Conclusion: Trunk fat and leg fat are oppositely associated with adiponectin. Although low adiponectin was a determinant of increased peripheral arterial stiffness, it only explained a small part of the association between body fat and peripheral arterial stiffness. This indicated that factors other than adiponectin may be more important in the pathophysiological mechanisms by which abdominal obesity leads to arterial stiffness.

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“…Its levels are decreased in obesity (50)(51)(52)(53)(54) and are increased by caloric restriction (55,56), a condition known to inhibit carcinogenesis (44)(45)(46)(47). Although adiponectin was only somewhat suppressed in ob/ob mice, it was undetectable in ZIP mice (Table 1).…”

Section: Discussionmentioning

confidence: 99%

Susceptibility to Induced and Spontaneous Carcinogenesis Is Increased in Fatless A-ZIP/F-1 but not in Obese ob/ob Mice

Ablamunits

Cohen²,

Brazee³

et al. 2006

Cancer Research

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Obesity is typically associated with increased tumor susceptibility, whereas caloric restriction, a regimen resulting in leanness, inhibits carcinogenesis. The link between adiposity and malignancies suggests that adipose tissue may influence carcinogenesis. An adipose tissue hormone, leptin, could be procarcinogenic because it stimulates proliferation in various tissues and tumor cell lines. Leptin may contribute to the correlation between adiposity and malignancies as its levels are usually increased in obese subjects and reduced by caloric restriction. We hypothesized that leptin deficiency, despite obesity, would inhibit carcinogenesis in leptin-null ob/ob mice and tested this hypothesis in two models: (a) two-stage skin carcinogenesis initiated by 7,12-dimethylbenz(a)anthracene and promoted by phorbol 12-myristate 13-acetate (PMA) and (b) p53 deficiency. Contrary to a typical association between obesity and enhanced carcinogenesis, obese ob/ob mice developed induced skin papillomas and spontaneous p53-deficient malignancies, mostly lymphomas, similarly to their lean littermates. Surprisingly, lipodystrophic (ZIP) mice that had very little both adipose tissue and leptin were highly susceptible to carcinogenesis. Hyperphagia, hyperinsulinemia, and hyperglycemia are unlikely to have contributed significantly to the enhancement of carcinogenesis in ZIP mice because similarly hyperphagic, hyperinsulinemic, and hyperglycemic ob/ob mice had normal susceptibility to carcinogenesis. Our data suggest that, in contrast to a well-known correlation between obesity and cancer, the direct effect of adipose tissue may rather be protective. (Cancer Res 2006; 66(17): 8897-902)

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Reciprocal association between visceral obesity and adiponectin: in healthy premenopausal women

Cited by 42 publications

References 43 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

Relationship of adiposity with arterial stiffness as mediated by adiponectin in older men and women: the Hoorn Study

Susceptibility to Induced and Spontaneous Carcinogenesis Is Increased in Fatless A-ZIP/F-1 but not in Obese ob/ob Mice

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