Direct effects of sex steroid hormones on adipose tissues and obesity

Abstract

Sex steroid hormones are involved in the metabolism, accumulation and distribution of adipose tissues. It is now known that oestrogen receptor, progesterone receptor and androgen receptor exist in adipose tissues, so their actions could be direct. Sex steroid hormones carry out their function in adipose tissues by both genomic and nongenomic mechanisms. In the genomic mechanism, the sex steroid hormone binds to its receptor and the steroid-receptor complex regulates the transcription of given genes. Leptin and lipoprotein lipase are two key proteins in adipose tissues that are regulated by transcriptional control with sex steroid hormones. In the nongenomic mechanism, the sex steroid hormone binds to its receptor in the plasma membrane, and second messengers are formed. This involves both the cAMP cascade and the phosphoinositide cascade. Activation of the cAMP cascade by sex steroid hormones would activate hormone-sensitive lipase leading to lipolysis in adipose tissues. In the phosphoinositide cascade, diacylglycerol and inositol 1,4,5-trisphosphate are formed as second messengers ultimately causing the activation of protein kinase C. Their activation appears to be involved in the control of preadipocyte proliferation and differentiation. In the presence of sex steroid hormones, a normal distribution of body fat exists, but with a decrease in sex steroid hormones, as occurs with ageing or gonadectomy, there is a tendency to increase central obesity, a major risk for cardiovascular disease, type 2 diabetes and certain cancers. Because sex steroid hormones regulate the amount and distribution of adipose tissues, they or adipose tissue-specific selective receptor modulators might be used to ameliorate obesity. In fact, hormone replacement therapy in postmenopausal women and testosterone replacement therapy in older men appear to reduce the degree of central obesity. However, these therapies have numerous side effects limiting their use, and selective receptor modulators of sex steroid hormones are needed that are more specific for adipose tissues with fewer side effects.

Effect of high-fat diet feeding on leptin receptor expression in white adipose tissue in rats: depot- and sex-related differential response

“…In addition to these factors, a sex differential regulation of the leptin receptor in WAT could be expected, as sex steroid hormones are closely involved in the metabolism, accumulation and distribution of adipose tissues [11], and a sex-dependent regulation of the expression of metabolic and fat partitioning-related genes has been previously described by our group [16].…”

Genetic and environmental correlations between obesity phenotypes and age at menarche

“…26 On the other hand, low SHBG and high estrogen levels are associated with increased total and central adiposity in women. 20,[27][28][29] SHBG is a protein that binds primarily to steroids such as estrogen. As only the unbound steroid fraction is biologically active, SHBG may play an important role in both AAM and obesity through determining the amount of free estrogen.…”

“…30,31 Estrogen may also decrease lipolysis in adipose tissues by increasing the number of antilipolytic a2A-adrenergic receptors. 20,32 Besides, it was suggested that estrogen may attenuate growth hormone (GH) signaling 33 and GH was reported to increase lipid oxidation 34 and reduce body fatness. 35 In sum, estrogen can affect obesity phenotypes through different pathways which may interact with each other, and much work is needed to understand its precise role in obesity.…”

“…The potential confounding effects of menopause status and HRT use were adjusted as they generally affect obesity phenotypes in Caucasians. 20 The bivariate quantitative genetic analysis is a powerful method to directly assess the degree of genetic and environmental correlations between pairs of traits. This method decomposes the phenotypic correlations (r P ) between obesity phenotypes and AAM into the portion due to genes shared in common and that due to shared environment.…”

Effect of Artificial and Natural Day Light Intensities on some Behavioral Activities, Plumage Conditions, Productive and Physiological Changes for Japanese Quail

“…In males, LH controls the production of the major sex steroid hormone (testosterone), which secreted by Leydig cells in the testes. In females, the secretion of LH and FSH control the secretion of estrogen, which necessary for yolk precursor lipoprotein secretion by the liver and oviduct and ovarian follicles development (Mayes and Watson, 2004;Chen et al, 2005). Dim light may not be able to penetrate the skull and may be unable or less likely to excite receptors to release GnRH (Morgan et al, 1995).…”