Hypothalamic growth hormone secretagogue receptor regulates growth hormone secretion, feeding, and adiposity

Growth hormone secretagogues (GHSs) stimulate GH secretion and food intake. GHS receptor (GHS-R) mRNA has been identified mainly in the arcuate nucleus (Arc) and ventromedial nucleus of the hypothalamus and in the pituitary. Ghrelin, an endogenous ligand for GHS-R, has recently been purified from rat stomach. Although ghrelin is also expressed in the hypothalamus, the physiological significance of the ghrelin/GHS-R system is still unknown. We have created transgenic (Tg) rats expressing an antisense GHS-R mRNA under the control of the promoter for tyrosine hydroxylase (TH), thus selectively attenuating GHS-R protein expression in the Arc. Tg rats had lower body weight and less adipose tissue than did control rats. Daily food intake was reduced, and the stimulatory effect of GHS treatment on feeding was abolished in Tg rats. GH secretion and plasma insulin-like growth factor-I levels were reduced in female Tg rats. These results suggest that GHS-R in the Arc is involved in the regulation of GH secretion, food intake, and adiposity

Expression and Epigenetic Change of the AR and FSHR Genes in the Granulosa Cells of Endometriosis Patients

Background Endometriosis is one of the most common gynecological diseases associated with infertility. Endometriosis may affect the androgen receptor (AR) mRNA expression in human granulosa cells and the methylation of the promoter region of AR. We investigated 28 patients with endometriosis and 47 subjects without endometriosis undertaking IVF treatment. Methods Granulosa cells were obtained from 28 patients with endometriosis and 47 subjects without endometriosis as a control. Expressions of AR and FSHR mRNA were then evaluated by OneStep real-time PCR analysis, and the level of methylation of the promoter region was qualified by methylation-specified PCR (MSP). Results The expression of AR mRNA in the endometriosis group was statistically lower than that in the control group. As well, FSHR mRNA expression in the control group showed a positive correlation with AR mRNA expression; however, there was no such correlation in endometriosis patients. In the control group, AR mRNA expression was statistically higher in pregnant subjects compared with non-pregnant subjects; however, in the endometriosis group, no significant difference was identified. The promoter of AR was heavily methylated in all endometriosis cases; however, only 5 (45.4%) were methylated in the control group. Conclusion Lower AR mRNA expression and methylation of the AR promoter region might affect the expression of AR and FSHR the presence of endometriosis, thus leading to a disturbance in the regulation of AR and FSHR