Insulin Modulation of Luteinizing Hormone Secretion in Normal Female Volunteers and Lean Polycystic Ovary Syndrome Patients

• Published in: Neuroendocrinology Vol. 89; no. 2; pp. 131 - 139
• Main Authors: Moret, Mallory, Stettler, Rodrigue, Rodieux, Frederique, Gaillard, Rolf C., Waeber, Gérard, Wirthner, Daniel, Giusti, Vittorio, Tappy, Luc, Pralong, Francois P.
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland Karger 01.02.2009; S. Karger AG
• Subjects: Adult; Biological and medical sciences; Female; Female genital diseases; Fundamental and applied biological sciences. Psychology; Glucose Clamp Technique; GnRH, Gonadotropins, Gonadal Steroids and Reproduction; Gonadotropin-Releasing Hormone - metabolism; Gynecology. Andrology. Obstetrics; Humans; Hypothalamus - metabolism; Insulin - administration & dosage; Insulin - blood; Insulin - pharmacology; Luteinizing Hormone - blood; Luteinizing Hormone - drug effects; Luteinizing Hormone - secretion; Medical sciences; Non tumoral diseases; Polycystic Ovary Syndrome - metabolism; Thinness; Vertebrates: endocrinology; Pituitary; Clinical neuroendocrinology; Pulsatility; Polycystic ovary; Gonadotropin; Hypothalamus; Insulin; Human; Pancreatic hormone; Endocrine gland; Secretion; Central nervous system; Female sterility; Encephalon; Female genital diseases; Ovarian diseases; Adenohypophyseal hormone; Modulation; Cyst; Luteinizing hormone; Female; Pituitary gland; Benign neoplasm
• ISSN: 0028-3835; 1423-0194
• DOI: 10.1159/000160911

Background/Aims: Endocrine features of polycystic ovary syndrome (PCOS) include altered ovarian steroidogenesis, hyperinsulinemia and abnormal luteinizing hormone (LH) secretion. This study was undertaken to further evaluate the role of insulin to modulate LH secretion in lean PCOS patients with normal insulin sensitivity and normal volunteers. Methods: The study was performed in five nonobese patients diagnosed with PCOS on the basis of amenorrhea and a polycystic morphology at ovarian ultrasound, and 5 normal controls in early to mid-follicular phase and matched for weight and age. All subjects were phenotyped, and then admitted for 12 h of frequent (q 10’) blood sampling on two separate occasions, once for a baseline study and the other time for a hyperinsulinemic and euglycemic clamp study. LH was measured in samples obtained throughout each admission in order to perform LH pulse analysis. Results: Baseline LH secretion in PCOS subjects was significantly different from controls: they had higher LH levels, higher LH/FSH ratios as well as a faster LH pulse frequency than normal women. Insulin administration did not affect the pattern of LH secretion of PCOS patients, whereas it significantly increased the LH pulse frequency while decreasing the LH interpulse intervals in the controls. Conclusions: These data confirm that an abnormal pattern of LH secretion characteristic of PCOS can be observed in lean patients, and appears independent of peripheral insulin levels. Furthermore, our results in lean controls provide the first direct evidence that peripheral insulin can modulate the activity of hypothalamic gonadotropin-releasing hormone (GnRH) neurons in the human.