Restoration of Reproductive Potential by Lifestyle Modification in Obese Polycystic Ovary Syndrome: Role of Insulin Sensitivity and Luteinizing Hormone

1999 ◽  
Vol 84 (4) ◽  
pp. 1470-1474 ◽  
Author(s):  
M.-M. Huber-Buchholz
1999 ◽  
Vol 71 (3) ◽  
pp. 425-430 ◽  
Author(s):  
Koray Elter ◽  
C.Tamer Erel ◽  
Naci Cine ◽  
Ugur Ozbek ◽  
Burak Hacihanefioglu ◽  
...  

Gene ◽  
2012 ◽  
Vol 494 (1) ◽  
pp. 51-56 ◽  
Author(s):  
Shilpi Dasgupta ◽  
P.V.S. Sirisha ◽  
K. Neelaveni ◽  
K. Anuradha ◽  
G. Sudhakar ◽  
...  

2002 ◽  
Vol 13 (6) ◽  
pp. 251-257 ◽  
Author(s):  
Robert J. Norman ◽  
Michael J. Davies ◽  
Jonathan Lord ◽  
Lisa J. Moran

1996 ◽  
Vol 135 (3) ◽  
pp. 335-339 ◽  
Author(s):  
Tarek M Fiad ◽  
Sean K Cunningham ◽  
T Joseph McKenna

Fiad TM, Cunningham SK, McKenna TJ. Role of progesterone deficiency in the development of luteinizing hormone and androgen abnormalities in polycystic ovary syndrome. Eur J Endocrinol 1996;135:335–9. ISSN 0804–4643 The aetiology of polycystic ovary syndrome (PCOS) is unknown. It is uniquely characterized by oligomenorrhoea or amenorrhoea associated with normal or high oestrogen levels. This prospective clinical study was designed to examine the possible role of the lack of cyclical exposure to progesterone in the development of gonadotrophin and androgen abnormalities in PCOS. Gonadotrophin, androgen and oestrogen levels were measured in 15 PCOS patients and 10 normal subjects untreated and following treatment with the progestogen medroxyprogesterone acetate (MPA). When compared to control subjects, PCOS patients had significantly higher luteinizing hormone (LH) pulse height, pulse amplitude, integrated LH levels, LH response to gonadotrophin-releasing hormone (GnRH) and LH/FSH ratio; LH pulse frequency was similar in the two groups. In addition, the testosterone/sex hormone binding globulin ratio (T/SHBG), androstenedione and oestrone concentrations in the plasma were significantly higher in PCOS than in control subjects. When PCOS patients were treated with MPA for 5 days, there were significant decreases (p < 0.02–0.001) to values no longer different from normal: from 8.7 ± 1.2 to 5.6 ± 0.8 IU/l for integrated LH levels (untreated and MPA-treated PCOS); from 31.2 ±3.5 to 12.9 ±1.5 IU/l for LH response to GnRH; from 2.4 ± 0.26 to 1.3 ± 0.2 for LH/FSH ratio; and from 10.4 ± 0.63 to 8.5 ± for androstenedione. Significant decreases (p < 0.05–0.005) to values that still remained significantly higher than in normal subjects occurred for: LH pulse height, 11.05 ± 1.3 to 6.88 ± 0.79 IU/l (untreated and MPA-treated PCOS); LH pulse amplitude, 2.8 ± 0.5 to 1.8 ± 0.2 IU/l; total testosterone, 2.5 ± 0.2 to 2.0± 0.2 nmol/l; T/SHBG ratio, 14.1 ± 1.7 to 11 ± 1.5; and oestrone, 265 ± 24 to 208 ± 29 pmol/l. These results are consistent with the concept that ovulation failure and progesterone deficiency play a facilitatory role in the development of the hypothalamic-pituitary abnormality giving rise to disordered LH secretion in PCOS. TJ McKenna. Department of Investigative Endocrinology. St Vincent's Hospital, Elm Park. Dublin 4, Ireland


1999 ◽  
Vol 84 (4) ◽  
pp. 1470-1474 ◽  
Author(s):  
M.-M. Huber-Buchholz ◽  
D. G. P. Carey ◽  
R. J. Norman

Weight reduction and exercise have been shown to help with menstrual disturbance and infertility in obese women with polycystic ovary syndrome. We studied the relationship between insulin sensitivity and ovulation patterns in 18 infertile anovulatory obese polycystic ovary syndrome (PCOS) women (NO) with normal glucose tolerance, aged between 22–39 yr with a body mass index of 27–45 kg/m2, before and after a 6-month diet and exercise program. This program promotes healthy lifestyle factors, but does not lead to rapid weight loss. The anthropometric, metabolic, and endocrine factors of these subjects were compared to those of 10 age- and weight-matched PCOS women with regular monthly ovulation (RO). Before lifestyle modification, the anovulatory subjects had greater central obesity than regular ovulators, as assessed by percent central fat (NO, 45.7 ± 0.8%; RO, 42.2 ± 1.6%; P &lt; 0.05), higher glucose increment after glucose challenge (NO, 10.1 ± 1.0 mmol/L; RO, 6.4 ± 1.1 mmol/L; P &lt; 0.02), lower insulin sensitivity index (NO, 1.2 ± 0.2; RO, 2.8 ± 0.6 μmol/kg·min/pmol/L; P &lt; 0.005), higher plasma LH (NO, 8.9 ± 0.9; RO, 4.6 ± 0.9 IU/L; P &lt; 0.005), and lower plasma sex hormone-binding globulin (NO, 18.0 ± 2.5; RO, 27.8 ± 5.7 nmol/L; P &lt; 0.05]. Anovulatory subjects were classified as responders (R) to the intervention if they regained ovulation during the study. As a result of intervention, R showed an 11% reduction in central fat, a 71% improvement in insulin sensitivity index, a 33% fall in fasting insulin levels, and a 39% reduction in LH levels. None of these parameters changed significantly in nonresponders (NR). At the end of the study, R had lower fasting insulin (R, 13.6 ± 1.7; NR, 23.0 ± 3.5 mU/L) and LH levels (R,5.0 ± 1.7; NR, 7.4± 1.4 IU/L), but similar androgen levels compared to NR. We conclude that lifestyle modification without rapid weight loss leads to a reduction of central fat and improved insulin sensitivity, which restores ovulation in overweight infertile women with PCOS. Lifestyle modification is the best initial management for obese women seeking to improve their reproductive function.


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