Serum soluble leptin receptor levels and free leptin index in women with polycystic ovary syndrome: relationship to insulin resistance and androgens.
OBJECTIVE
To evaluate levels of soluble receptor (sOB-R) and free leptin in women with polycystic ovarian syndrome (PCOS) and note any relationships with insulin resistance, adiposity, and androgens. Leptin is an adipokine that circulates in a free form and bound to an sOB-R. Only free leptin is biologically active.


METHODS
Prospective, case-control study.


METHODS
University-based reproductive endocrinology practice.


METHODS
Forty women with PCOS and severe insulin resistance and 15 body mass index (BMI)-matched ovulatory controls.


METHODS
Measurements of serum insulin, leptin, sOB-R at fasting and during a standard oral glucose tolerance test (OGTT), and measurements before and after treatment with rosiglitazone.


METHODS
Fasting glucose, insulin, leptin, sOB-R, T, and DHEAS levels in women with PCOS and controls were measured to investigate the relationship of sOB-R and the free leptin index (FLI) to insulin, adipocity, and androgens and to investigate the effect of acute hyperinsulinemia during OGTT and the effect of improvement of insulin resistance with rosiglitazone on the leptin system. FLI was calculated by dividing leptin levels by sOB-R.


RESULTS
Total leptin and FLI correlated significantly with BMI in both patients with PCOS and in controls. There was a significant negative correlation between DHEAS and sOB-R in PCOS. Leptin, sOB-R, and FLI were not significantly different in the two groups, and neither sOB-R nor FLI correlated with insulin or glucose levels. The sOB-R levels increased significantly 3 hours after oral glucose ingestion, resulting in a significant decline in FLI.


CONCLUSIONS
[1] Adiposity rather than insulin resistance appears to be the main determinant of leptin levels and FLI. [2] Acute increase in insulin levels during OGTT is associated with an increase in levels of sOB-R. [3] DHEAS may play a role in leptin bioavailability by modulating sOB-R levels.
Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, Texas 77555-0587, USA.
Vicken P
VP
Sepilian
John R
JR
Crochet
Manubai
M
Nagamani
D000052:Acanthosis Nigricans / Q000097:blood / Q000453:epidemiology; D050154:Adiposity; D000328:Adult; D000728:Androgens / Q000097:blood*; D015992:Body Mass Index; D016022:Case-Control Studies; D015897:Comorbidity; D005260:Female; D006801:Humans; D015994:Incidence; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood*; D009765:Obesity / Q000097:blood / Q000453:epidemiology; D011085:Polycystic Ovary Syndrome / Q000097:blood* / Q000453:epidemiology*; D011956:Receptors, Cell Surface / Q000097:blood* / Q000737:chemistry; D054411:Receptors, Leptin; D018570:Risk Assessment / Q000379:methods; D012307:Risk Factors; D013781:Texas / Q000453:epidemiology
D000728:Androgens; C515448:LEPR protein, human; D020738:Leptin; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin