Browse > Article

The Effects of Body Mass Index on Baseline Hormonal Status and Glucose Metabolism in Women with Chronic Anovulation  

Rhee, Jeong-Ho (Department of Obstetrics and Gynecology, School of Medicine, Keimyung University)
Jeong, Eun-Jeong (Department of Obstetrics and Gynecology, School of Medicine, Keimyung University)
Kim, Jong-In (Department of Obstetrics and Gynecology, School of Medicine, Keimyung University)
Publication Information
Clinical and Experimental Reproductive Medicine / v.29, no.1, 2002 , pp. 67-76 More about this Journal
Abstract
Objective: To assess the difference of baseline hormonal status and pathophysio logy, and confirm the risk factors for long term complication according to Body Mass Index in women with polycystic ovary syndrome. Materials and Methods: Serum level of LH, FSH, Estradiol, Prolactin, Testosterone, DHEA-S, fasting insulin were measured and 100 gm oral glucose tolerance test and endometrial biopsy were performed in total 75 chronic anovulation patients and 20 normal cycling infertility patients. 95 evaluated patients were divided into 3 groups including patients with chronic anovulation having BMI below 25, BMI beyond 25.1, normal cycling infertility patients, Group 1 (n=39), Group 2 (n=36), Group 3 (n=20), respectively. Statistical analysis was performed respect to relationship between BMI and measured hormone level, sum of glucose level during 100 gm OGTT, insulin resistance using t-test, ANOVA test, Post Hoc test, Mann-Whitney test. p<0.05 was considered as statistically significant. Results: Serum LH level and LH/FSH ratio was significantly higher in Group 1, compared than Group 2 or 3 (p<0.05), BMI and LH, LH/FSH ratio was negatively correlated (r=-0.351, r=-0.318). There was no significant difference according to BMI in FSH, testosterone, estradiol, prolactin, DHEA-S level. Fasting insulin and sum of glucose level during 100 gm OGTT were significantly higher in Group 2 compared than Group 1 or Group 3 (p<0.05), there was no significant difference between Group 1 and Group 3. Insulin resistance was more frequently identified in Group 2 compared than Group 1 (p=0.001). Conclusions: BMI and LH, LH/FSH ratio were negatively correlated, so clinical significance of LH, LH/FSH ratio in diagnosis of PCOS may be attenuated by increasing body weight. Overweight patients with chronic anovulation may be the risk group for developing insulin resistance, hyperinsulinemia, glucose intolerance, later type 2 DM. Hyperinsulinemia may operate mainly in overweight chronic anovulation patients in development of hyperandrogenism.
Keywords
Body mass index; Chronic anovulation; LH and LH/FSH ratio; Insulin resistance; Glucose intolerance;
Citations & Related Records
연도 인용수 순위
  • Reference
1 Franks S. Polycystic ovary syndrome. New Engl J Med 1995; 333: 853-61   DOI   ScienceOn
2 Carmina E, Rosato F, Janni A. Increased DHEAs levels in PCO syndrome: evidence for the existence of two subgroups of patients. J Endocrinol Invest 1986; 9: 5-9   DOI   PUBMED
3 Guzick DS, Berga SL, Wing R, Winters SJ, Smith D. Endocrine consequences of weight loss in obese, hyperandrogenic, anovulatory women. Fertil Steril 1994; 61: 598-604   DOI   PUBMED
4 Ciaraldi TP, El-Roeiy A, Madar Z, Reichart D, Olefsky JM, Yen SSC. Cellular mechanisms of insulin resistance in polycystic ovarian syndrome. J Clin Endocrinol Metab 1992; 75: 577-83   DOI
5 Chang RJ, Nakamura RM, Judd HL, Kaplan SA. Insulin resistance in nonobese patients with polycystic ovarian disease. J Clin Endocrinol Metab 1983; 57: 356-9   DOI
6 Legro RS, Kunselman AR, Dodson WC, Dunaif A. Prevalence and predictors of risk for type 2 diabetes mellitus and impaired glucose tolerance in policystic ovary syndrome: A prospective, controlled study in 254 affected woman. J Clin Endocrinol Metab 1999; 84: 165-9   DOI
7 Dunaif A, Segal KR, Futterweit W, Dobrjansky A. Profound peripheral insulin resistance, independent of obesity, in polycystic ovary syndrome. Diabetes 1989; 38: 1165-74   DOI   ScienceOn
8 Ostlund RE Jr, Staten M, Kohrt WM, Schultz J, Malley M. The ratio of waist-to-hip circumference, plasma insulin level, and glucose intolerance as independent predictors of the HDL$_2$ cholesterol level in older adults. New Engl J Med 1990; 322: 229-34   DOI   ScienceOn
9 Nestler JE. Role of hyperinsulinemia in the pathogenesis of the polycystic ovary syndrome, and its clinical implication. Seminars Reprod Endocrinol 1997; 15: 111-22   DOI
10 Ovesen P, Moller J, Ingerslev HJ, Jorgensen JOL, Mengel A, Schmitz O, et al. Normal basal and insulin-stimulated fuel metabolism in lean women with the polycystic ovary syndrome. J Clin Endocrinol Metab 1993; 77: 1636-40   DOI
11 Hollmann M, Runnebaum B, Gerhard I. Effects of weight loss on the hormonal profile in obese, infertile women. Hum Reprod 1996; 11: 1884-91   DOI   PUBMED
12 Kiddy DS, Hamilton-Fairley D, Bush A, Short F, Anyaoku V, Reed MJ, et al. Improvement in endocrine and ovarian function during dietary treatment of obese women with polycystic ovary syndrome. Clin Endocrinol 1992; 36: 105-11   DOI
13 Morales AJ, Laughlin GA, Butzow T, Maheshwari H, Baumann G, Yen SSC. Insulin, somatotropic, and luteinizing hormone axes in lean and obese women with polycystic ovary syndrome: Common and distinct features. J Clin Endocrinol Metab 1996; 81: 2854-64   DOI
14 Anttila L, Erkkola R, Ding YQ, Irjala K, Ruutiainen K, Huhtaniemi I. Clinical features and circulating gonadotropin, insulin, and androgen interactions in women with polycystic ovarian disease. Fertil Steril 1991; 55: 1057-61   DOI   PUBMED
15 Dale PO, Tanbo T, Vaaler S, Abyholm T. Body weight, hyperinsulinemia, and gonadotropin levels in the polycystic ovarian syndrome: evidence of two distinct populations. Fertil Steril 1992; 58: 487-91   DOI   PUBMED
16 Insler V, Shoham Z, Barash A, Koistinen R, Seppala M, Hen M, et al. Polycystic ovaries in non-obese and obese patients: possible pathophysiological mechanism based on new interpretation of facts and findings. Hum Reprod 1993; 8: 379-84   DOI   PUBMED
17 Legro RS, Finegood D, Dunaif A. A fasting glucose to insulin ratio is a useful measure of insulin sensitivity in women with polycystic ovary syndrome. J Clin Endocrinol Metab 1998; 83: 2694-8   DOI
18 Kirschner MA, Samojlik E, Drejka M, Szmal E, Schneider G, Ertel N. Androgen-estrogen metabolism in women with upper body versus lower body obesity. J Clin Endocrinol Metab 1990; 70: 473-9   DOI
19 Conover CA, Lee PDK, Kanaley JA, Clarkson JT, Jensen MD. Insulin regulation of insulin-like growth factor binding protein-l in obese and nonobese humans. J Clin Endocrinol Metab 1992; 74: 1355-60   DOI
20 Campbell PJ, Gerich JE. Impact of obesity on insulin action in volunteers with normal glucose tolerance: Demonstration of a threshold for the adverse effect of obesity. J Clin Endocrinol Metab 1990; 70: 1114-8   DOI
21 Wabitsch M, Hauner H, Heinze E, Bockmann A, Benz R, Mayer H, et al. Body fat distribution and steroid hormone concentrations in obese adolescent girls before and after weight reduction. J Clin Endocrinol Metab 1995; 80: 3469-75   DOI
22 Arroyo A, Laughlin GA, Morales AJ, Yen SSC. Inappropriate gonadotropin secretion in polycystic ovary syndrome: Influence of adiposity. J Clin Endocrinol Metab 1997; 82: 3728-33   DOI
23 Jiala1 I, Naiker P, Reddi K, Moodley J, Joubert SM. Evidence for insulin resistance in nonobese patients with polycystic ovarian disease. J Clin Endocrinol Metab 1987; 64: 1066-9   DOI
24 Peiris AN, Sothmann MS, Aiman EJ, Kissebah AH. The relationship of insulin to sex hormone-binding globulin: role of adiposity. Fertil Steril 1989; 52: 69-72   DOI   PUBMED
25 Clayton RN, Ogden V, Hodgkinson J, Worswick L, Rodin DA, Dyer S, et al. How common are polycystic ovaries in normal women and what is their significance for the fertility of the population? Clin Endocrinol 1992; 37: 127-34