Contribution of androgens to the gender difference in leptin production in obese children and adolescents.

Wabitsch, Martin; Blum, WF; Muche, Rainer; Braun, Mike; Hube, F; Rascher, Wolfgang; Heinze, E.; Teller, W. M.; Hauner, Hans

doi:10.1172/jci119595

Cited by 338 publications

(256 citation statements)

References 34 publications

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“…Sexual dimorphism in circulating leptin concentrations M Rosenbaum et al (r ¼70.35, P < 0.0001), 13,26 and among adult men (r ¼70.32, P < 0.01). 27 Horlick et al 13 reported that there was a marked suppression of circulating leptin concentrations corrected for body composition in males at Tanner stages IV and V and a smaller increase in circulating concentrations of leptin corrected for body composition in females at these later Tanner stages.…”

Section: Discussionmentioning

confidence: 97%

Sexual dimorphism in circulating leptin concentrations is not accounted for by differences in adipose tissue distribution

et al. 2001

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BACKGROUND: Circulating concentrations of leptin normalized to total adipose tissue mass are significantly greater in females than in males. Rates of leptin expression (per gram of adipose tissue) are significantly greater in subcutaneous (SAT) than visceral (VAT) adipose tissue and the relative amount of fat stored as SAT vs VAT is significantly greater in pre-menopausal females than in males. Gender-related differences in the relative amounts of SAT and VAT may account for the greater circulating leptin concentration relative to fat-mass in females than males. METHODS: We examined body composition and anatomic fat distribution by dual energy X-ray-absorptiometry (DEXA) and magnetic resonance imaging (MRI), and post-absorptive circulating concentrations of leptin and insulin in 58 subjects (26 females, 32 males). Stepwise multiple linear regression analyses, treating gender as a dichotomous variable, were performed to determine inter-relationships among leptin concentrations and insulin concentrations, VAT and SAT. RESULTS: Body composition by DEXA and MRI were highly correlated (r 2 ¼ 0.97, P < 0.0001). There were significant gender effects on leptin=total fat mass (males, 0.17 AE 0.01 ng=ml=kg; females, 0.49 AE 0.05 ng=ml=kg; P < 0.0001) and relative amounts of fat in SAT and VAT depots (ratio of SAT=VAT; males, 12.3 AE 1.5; females, 32.9 AE 3.2; P < 0.0001). Circulating leptin concentration was significantly correlated with insulin concentration (P ¼ 0.001), SAT (P < 0.0001) and gender (P ¼ 0.033). Circulating concentrations of insulin were significantly correlated with VAT, but not SAT, in males and with SAT, but not VAT, in females. CONCLUSIONS: The sexual dimorphism in the relationship between leptin and adipose tissue mass cannot be explained by differences in the relative amounts of VAT and SAT. Thus, the sexual dimorphism in plasma leptin concentration appears to reflect, at least in part, effects of circulating concentrations of gonadal steroids (especially androgens) and=or primary genetic differences that are independent of amounts of VAT or SAT.

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Section: Discussionmentioning

confidence: 97%

Sexual dimorphism in circulating leptin concentrations is not accounted for by differences in adipose tissue distribution

et al. 2001

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“…Studies in vitro and in vivo would suggest that sex steroids are directly responsible for the gender difference, with a direct inhibitory effect of testosterone on leptin in humans 18,19 and an increase in response to oestrogen in humans and rats. 20 Other researchers also show a higher leptin concentration in female mice, 21 however one study in rats has documented a reversal in the sexual dimorphism.…”

Section: Discussionmentioning

confidence: 99%

Gender difference in the leptin response to feeding in peroxisome-proliferator-activated receptor-alpha knockout mice

Brismar

2002

Int J Obes

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OBJECTIVE: Peroxisome-proliferator-activated receptor-alpha (PPARa) has a central role in lipid metabolism. Mice lacking PPARa accumulate hepatic fat and are prone to late onset obesity. Leptin, an adipocyte-derived hormone, also plays an important role in regulating energy balance. In order to test the hypothesis that leptin secretion increases in response to PPARa knockout, we determined leptin concentrations including the effect of nutritional status in male and female PPARa knockout mice compared with wild-type controls. DESIGN: We studied the effect of 16 h fasting and 4 h refeeding on plasma leptin concentrations in male and female wild-type and PPARa-knockout mice, aged 14 weeks. In female mice the effect of daily growth hormone (GH) injection on the leptin response to refeeding was determined. RESULTS: Circulating leptin concentrations were higher in female mice compared with males and increased in both sexes after PPARa-knockout. There was no change in leptin levels after a 16 h fast, compared with ad libitum feeding. However leptin increased with refeeding, to the greatest extent in female PPARa-knockout mice. Intermittent GH administration decreased leptin concentrations in female, wild-type and PPARa-knockout animals and abolished the exaggerated leptin response to refeeding. CONCLUSIONS: Leptin concentrations are increased in PPARa-knockout mice. There are gender differences in the leptin response to feeding which may be due to differences in insulin sensitivity.

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“…13,14 To study the time-course of expression of adipocyte-speci®c genes during differentiation of SGBS cells total RNA was extracted by the method of Chomczynski and Sacchi 15 at different time points during differentiation (day 0: undifferentiated cells, day 10: during adipose differentiation; day 20: after differentiation). RNAspeci®c primer pairs (GC-content about 50%, PCR product length 200 ± 500 bp) were selected from human cDNA libraries (Wisconsin Package Version 9.1, Genetic Computer Group, Madison, WI) and were used for semiquantitative duplex PCR with the transcription factor Sp1 as internal standard.…”

Section: Cell Proliferationmentioning

confidence: 99%

Characterization of a human preadipocyte cell strain with high capacity for adipose differentiation

et al. 2001

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OBJECTIVE:To develop and to characterize a human preadipocyte cell strain with high capacity for adipose differentiation serving as a model for studying human adipocyte development and metabolism in vitro. METHODS: Cells were derived from the stromal cells fraction of subcutaneous adipose tissue of an infant with Simpson ± Golabi ± Behmel syndrome (SGBS). Adipose differentiation was induced under serum-free culture conditions by exposure to 10 nM insulin, 200 pM triiodothyronine, 1 mM cortisol and 2 mM BRL 49653, a PPARg agonist. RESULTS: During the differentiation process SGBS cells developed a gene expression pattern similar to that found in differentiating human preadipocytes with a characteristic increase in fat cell-speci®c mRNAs encoding lipoprotein lipase (LPL), glycero-3-phosphate dehydrogenase (GPDH), GLUT4, leptin and others. Differentiated SGBS cells exhibited an increase in glucose uptake upon insulin stimulation and in glycerol release upon catecholamine exposure. SGBS adipocytes were morphologically, biochemically and functionally identical to in vitro differentiated adipocytes from healthy subjects. However, while preadipocytes from healthy control infants rapidly lost their capacity to differentiate after a few cell divisions in culture, SGBS cells maintained their differentiation capacity over many generations: upon appropriate stimulation 95% of SGBS cells of generation 30 developed into adipocytes. A mutation in the glypican 3 gene was not detected in the patient. Thus, it remains unclear whether the molecular alteration in SGBS cells is also responsible for the high differentiation capacity and further investigations are required. CONCLUSION: The human cell strain described here provides an almost unlimited source of human preadipocytes with high capacity for adipose differentiation and may, therefore, represent a unique tool for studying human fat cell development and metabolism. International Journal of Obesity (2001) 25, 8 ± 15

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Contribution of androgens to the gender difference in leptin production in obese children and adolescents.

Cited by 338 publications

References 34 publications

Sexual dimorphism in circulating leptin concentrations is not accounted for by differences in adipose tissue distribution

Sexual dimorphism in circulating leptin concentrations is not accounted for by differences in adipose tissue distribution

Gender difference in the leptin response to feeding in peroxisome-proliferator-activated receptor-alpha knockout mice

Characterization of a human preadipocyte cell strain with high capacity for adipose differentiation

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