- 期刊
瘦體激素在生殖醫學之角色
Leptin in Human Reproduction
摘要
在婦產科領域裹，過度肥胖或過分消瘦，都會導致月經異常、無排卵，甚至是無月經。臨床上最常見的相關疾病，就是多囊性卵巢症候群(polycystic ovary Syndrome)、過度減重、運動選手無月經(athletic amenorrhea)或厭食症(anorexia nervosa)等，這些疾病發生之生理學機轉，有許多理論被提出，但其中大部分仍然未明。直到1994年，肥胖基因所產生之蛋白荷爾蒙瘦體激素(leptin)被發現以後，我們對於這些疾病之病態生理，纔較有深一層的認識。瘦體激素接受器(leptin receptor, Ob-R)可以在生殖內分泌系統的下視丘、腦下腺前葉細胞、卵巢之顆粒(granulosa cell)之間質細胞(interstitial cell)、睪丸之Leydig細胞以及子宮內膜細胞被檢測出來，目前許多的研究顯示肥胖基因所產生之瘦體激素濃度，與生殖生理機能有密切的相關。換言之，急速的營養變動所引起的肥胖或消瘦，都可能改變肥胖基因瘦體激素的增減，而使生殖內分泌系統的下視丘、腦下腺及卵巢功能失調。
並列摘要
It is generally accepted that, in women of reproductive age, an excessive increase or decrease in body weight induces menstrual disorders, anovulation, and amenorrhea. Clinically, polycystic ovary syndrome, excessive dieting, running, and anorexia nervosa are often associated with these kinds of abnormalities. Leptin is a protein encoded by the ob gene and expressed in adipocytes. Since its discovery in 1994 by means of positional cloning of the mouse obese gene, leptin is well known to be a sensitive marker of a subject's nutritional status. Leptin receptors (Ob-Rs) have been identified in the hypothalamus, anterior pituitary gland, ovaries, testes, and endometrial cells of the uterus. This varied distribution of receptors indicates that the nutritional modulation of leptin during marked changes in body weight and its effects on the reproductive function may involve a complex network of interactions. These interactions occur at multiple levels to regulate the hypothalamic-pituitary-ovarian axis through the endocrine and/or paracrine systems.