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Am J Physiol Endocrinol Metab (December 11, 2001). doi:10.1152/ajpendo.00458.2001
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Articles in PresS, published online ahead of print December 11, 2001
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00458.2001
Submitted on October 11, 2001
Accepted on November 28, 2001

Increase in daily LH secretion in response to caloric restriction in obese women with polycystic ovary disease

Eveline W van Dam1, Ferdinand Roelfsema2, Johannes D Veldhuis3, Frans M Helmerhorst4, Marijke Frolich5, Arend E Meinders5, Michiel J Krans2, and Hanno Pijl5*

1 Internal Medicine, University Hospital Vrije Universiteit, Amsterdam, Netherlands
2 Endocrinology, Leiden University Medical Center, Leiden, Netherlands
3 Internal Medicine, University of Virginia Medical School, Charlottesville, VA, USA
4 Gynecology, Leiden University Medical Center, Leiden, Netherlands
5 Internal Medicine, Leiden University Medical Center, Leiden, Netherlands

* To whom correspondence should be addressed. E-mail: h.pijl{at}lumc.nl.

We hypothesized that short-term caloric restriction would blunt LH hypersecretion in obese women with PCOS, and thereby ameliorate the anovulatory endocrine milieu. To test this postulate, 15 obese patients with PCOS and 9 age- and body mass index-matched healthy women underwent 24 h sampling to quantitate plasma LH, leptin and insulin levels. PCOS subjects were prescribed a very low caloric liquid diet (4.2 MJ per day) for 7 days and then resampled. Basal and pusatile LH secretion were threefold higher in PCOS subjects, but plasma insulin and leptin levels were not different in the calorie-replete state. Contrary to expectation, caloric restriction enhanced basal and pulsatile LH secretion even further. As expected, plasma glucose, insulin and leptin concentration decreased by 18%, 75%, and 50% respectively. Serum total testosterone concentrations fell by 23%, whereas serum estrone, estradiol, SHBG and androstenedione concentrations remained unchanged. Enhanced LH secretion in the presence of normal metabolic and hormonal adaptations to caloric restriction points to anomalous feedback control of pituitary LH release in PCOS.




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