Sex differences in the regulation of body weight

Department of Psychiatry, College of Medicine, University of Cincinnati, Cincinnati, OH 45237, USA.
Physiology & Behavior (Impact Factor: 2.98). 03/2009; 97(2):199-204. DOI: 10.1016/j.physbeh.2009.02.017
Source: PubMed


Obesity and its associated health disorders and costs are increasing. Males and females differ in terms of how and where body fat is stored, the hormones they secrete in proportion to their fat, and the way their brains respond to signals that regulate body fat. Fat accumulation in the intra-abdominal adipose depot is associated with the risk for developing cardiovascular problems, type-2 diabetes mellitus, certain cancers and other disorders. Men and postmenopausal women accumulate more fat in the intra-abdominal depot than do pre-menopausal women, and therefore have a greater risk of developing metabolic complications associated with obesity. The goal of this review is to explore what we know about sexual dimorphisms in adipose tissue accrual and deposition. Elucidating the mechanisms by which sex hormones may modulate the way in which fat is accumulated and stored is a critical area of research due to the prevalence of obesity and the metabolic syndrome, and the rapid increase in propensity for these diseases following menopause.

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    • "We hypothesize that FF treatment can obviously improve EDV responses to Ach and endothelial dysfunction via alleviating ER stress in endothelial cells induced by high-fat diet (HFD) and high circulated FFAs. HFD usually induces obesity and hypertriglyceridemia more easily in male SD rats than in female SD rats, because females experienced slower adipose gains compared with males when fed obesogenic diets [7]. We adopted an international standard HFD (D12451) to feed female SD rats for consecutive 5 months to make them obese, then they were treated with FF for another 2 months. "
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    ABSTRACT: Fenofibrate (FF) is widely used to lower blood lipids in clinical practice, but whether its protective effect on endothelium-dependent vasodilatation (EDV) in thoracic aorta is related with endoplasmic reticulum (ER) stress remains unknown. In this study, female Sprauge Dawley rats were divided into standard chow diets (SCD), high-fat diets (HFD) and HFD plus FF treatment group (HFD+FF) randomly. The rats of latter two groups were given HFD feeding for 5 months, then HFD+FF rats were treated with FF (30 mg/kg, once daily) via gavage for another 2 months. The pathological and tensional changes, protein expression of eNOS, and ER stress related genes in thoracic aorta were measured. Then impacts of palmitic acid (PA) and FF on EDV of thoracic aorta from normal female SD rats were observed. Ultimately the expression of ER stress related genes were assessed in primary mouse aortic endothelial cells (MAEC) treated by fenofibric acid (FA) and PA. We found that FF treatment improved serum lipid levels and pathological changes in thoracic aorta, accompanied with decreased ER stress and increased phosphorylation of eNOS. FF pretreatment also improved EDV impaired by different concentrations of PA treatment. The dose- and time-dependent inhibition of cell proliferation by PA were inverted by FA pretreatment. Phosphorylation of eNOS and expression of ER stress related genes were all inverted by FA pretreatment in PA-treated MAEC. Our findings shows that fenofibrate recovers damaged EDV by chronic HFD feeding and acute stimulation of PA, this effect is related with decreased ER stress and increased phosphorylation of eNOS. Copyright © 2015. Published by Elsevier Inc.
    Biochemical and Biophysical Research Communications 01/2015; 458(1). DOI:10.1016/j.bbrc.2014.12.123 · 2.30 Impact Factor
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    • "suggesting that a smaller " available space " exists in male than female AT. Available data suggest that there is also a definite difference between sexes in age-related changes of whole-body fat distribution, especially in the abdominal fat tissues, and that the accumulation of visceral fat is markedly accelerated after menopause (Toth et al., 2000; Poehlman, 2002; Shi et al., 2009). "
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    ABSTRACT: The biological differences between males and females are determined by a different set of genes and by a different reactivity to environmental stimuli, including the diet, in general. These differences are further emphasized and driven by the exposure to a different hormone flux throughout the life. These differences have not been taken into appropriate consideration by the scientific community. Nutritional sciences are not immune from this “bias” and when nutritional needs are concerned, females are considered only when pregnant, lactating or when their hormonal profile is returning back to “normal,” i.e., to the male-like profile. The authors highlight some of the most evident differences in aspects of biology that are associated with nutrition. This review presents and describes available data addressing differences and similarities of the “reference man” vs. the “reference woman” in term of metabolic activity and nutritional needs. According to this assumption, available evidences of sex-associated differences of specific biochemical pathways involved in substrate metabolism are reported and discussed. The modulation by sexual hormones affecting glucose, amino acid and protein metabolism and the metabolization of nutritional fats and the distribution of fat depots, is considered targeting a tentative starting up background for a gender concerned nutritional science.
    Critical Reviews in Food Science and Nutrition 01/2015; 55(2):227-41. DOI:10.1080/10408398.2011.651177 · 5.18 Impact Factor
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    • "Importantly , sex plays a role in determining susceptibility to these pathologies . For example, women generally possess a higher total body fat percentage than men, but men tend to accrue a higher percentage of visceral adipose tissue (VAT) [23], which increases the risk of MetS and cardiovascular disease [24] [25]. Premenopausal women are protected from T2DM and heart disease but lose this protection with increasing visceral adiposity after menopause. "
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    ABSTRACT: Hypoxia Inducible Factor 1 (HIF-1) promotes fibrosis and inflammation in adipose tissues, while estrogens and Estrogen Receptor-α (ERα) have the opposite effect. Here we identify an Estrogen Response Element (ERE) in the promoter of Phd3, which is a negative regulatory enzyme of HIF-1, and we demonstrate HIF-1α is ubiquitinated following 17-β estradiol (E2)/ERα mediated Phd3 transcription. Manipulating ERα in vivo increases Phd3 transcription and reduces HIF-1 activity, while addition of PHD3 ameliorates adipose tissue fibrosis and inflammation. Our findings outline a novel regulatory relationship between E2/ERα, PHD3 and HIF-1 in adipose tissues, providing a mechanistic explanation for the protective effect of E2/ERα in adipose tissue.
    Molecular Metabolism 09/2014; 3(6). DOI:10.1016/j.molmet.2014.05.007
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