The role of androgens in metabolism, obesity, and diabetes in males and females

Navarro, Guadalupe; Allard, C.; Xu, Wei; Mauvais-Jarvis, Franck

doi:10.1002/oby.21033

Cited by 222 publications

(184 citation statements)

References 82 publications

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“…Androgen deficiency in males and androgen excess in females produce metabolic dysfunction via deficient or excessive androgen-receptor (AR) action, respectively, in multiple tissues including the central nervous system, liver, skeletal muscle, adipose and β-cells [48].…”

Section: Androgensmentioning

confidence: 99%

“…Generally, insulin sensitivity is shown to be improved when hyperandrogenism is reversed with anti-androgen therapy, in association with weight loss [63][64][65]. Androgen excess also prevents leptin from activating brown adipose tissue thermogenesis, which is associated with reduced energy expenditure and visceral obesity [48]. Summarily, in women with a prior β-cell defect, excess testosterone may increase predisposition to β-cell failure through the cumulative action of various β-cell stresses, including insulin resistance and circulating oxidative stress [58].…”

Section: Androgensmentioning

confidence: 99%

See 1 more Smart Citation

Obesity and diabetes: An update

Verma

Hussain

2017

Diabetes & Metabolic Syndrome: Clinical Research & Revi

245

149

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Section: Androgensmentioning

confidence: 99%

Section: Androgensmentioning

confidence: 99%

Obesity and diabetes: An update

Verma

Hussain

2017

Diabetes & Metabolic Syndrome: Clinical Research & Revi

245

149

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“…PCOS) females but in hypoandrogenemic males (Navarro et al 2015) ( Table 2). Thus, it appears that androgens are necessary for the maintenance of metabolic homeostasis in men and are detrimental to the maintenance of metabolic homeostasis in women.…”

Section: Insulin Sensitivitymentioning

confidence: 99%

The role of sex steroids in white adipose tissue adipocyte function

Newell-Fugate

2017

Reproduction

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Abstractwith the increasing knowledge that gender influences normal physiology, much biomedical research has begun to focus on the differential effects of sex on tissue function. Sexual dimorphism in mammals is due to the combined effects of both genetic and hormonal factors. Hormonal factors are mutable particularly in females in whom the estrous cycle dominates the hormonal milieu. Given the severity of the obesity epidemic and the fact that there are differences in the obesity rates in men and women, the role of sex in white adipose tissue function is being recognized as increasingly important. Although sex differences in white adipose tissue distribution are well established, the mechanisms affecting differential function of adipocytes within white adipose tissue in males and females remain largely understudied and poorly understood. One of the largest differences in the endocrine environment in males and females is the concentration of circulating androgens and estrogens. This review examines the effects of androgens and estrogens on lipolysis/lipogenesis, adipocyte differentiation, insulin sensitivity and adipokine production in adipocytes from white adipose tissue with a specific emphasis on the sexual dimorphism of adipocyte function in white adipose tissue during both health and disease.Reproduction (2017) 153 R133-R149

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“…It is well established that sexhormones regulate energy metabolism. Estrogen and androgen promote energy homeostasis, reduce fat body mass and ameliorate insulin resistance (ie enhance insulin sensitivity) (Mauvais-Jarvis et al, 2013;Navarro et al, 2015). However, suboptimal or deficient levels of estrogens have been linked to the fat accumulation and obesity in female (Litwak et al, 2014).…”

Section: Figmentioning

confidence: 99%

Obesogen effects after perinatal exposure of 4,4′-sulfonyldiphenol (Bisphenol S) in C57BL/6 mice

et al. 2016

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Bisphenol A were removed from consumer products and replaced by chemical substitutes such as Bisphenol S (BPS). Based on their structural similarity, BPS may be obesogen like Bisphenol A in mice. Our objective was to determine the impact of BPS on lipid homeostasis in C57Bl/6 mice after perinatal and chronic exposure. Pregnant mice were exposed to BPS via the drinking water (0.2; 1.5; 50μg/kg bw/d). Treatment began at gestational day 0 and continued in offspring up to 23-weeks old. Then, offspring mice were fed with a standard or high fat diet. The body weight, food consumption, fat mass and energy expenditure were measured. A lipid load test was performed to check the postprandial triglyceridemia. Plasma parameters and mRNA gene expression in adipose tissues were also analysed. BPS induced overweight in male mice offspring fed with a HFD at the two highest doses. There was no change in food intake and energy expenditure. The overweight was correlated to the fat mass, hyperinsulinemia and hyperleptinemia. The plasma triglyceride clearance was significantly increased with BPS and tyloxapol(®) (triglyceride clearance inhibitor) reversed this phenomenon. BPS induced alteration in mRNA expression of marker genes involved in adipose tissue homeostasis: hormone sensitive lipase, PPARγ, insulin receptor, SOCS3 and adiponectin. This is the first time that BPS is described as obesogenic at low doses and after perinatal and chronic exposure in male mice. BPS potentiated the obesity induced by a HFD by inducing the lipid storage linked to faster lipid plasma clearance.

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The role of androgens in metabolism, obesity, and diabetes in males and females

Cited by 222 publications

References 82 publications

Obesity and diabetes: An update

Obesity and diabetes: An update

The role of sex steroids in white adipose tissue adipocyte function

Obesogen effects after perinatal exposure of 4,4′-sulfonyldiphenol (Bisphenol S) in C57BL/6 mice

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