Hum. Reprod. Advance Access originally published online on March 29, 2007
Human Reproduction 2007 22(6):1555-1561; doi:10.1093/humrep/dem041
Influence of hypo- and hyperglycaemia on plasma leptin concentrations in healthy women and in women with polycystic ovary syndrome
1 Department of Gynaecology and Obstetrics, University of Schleswig-Holstein, Campus Lübeck, Germany 2 Department of Psychiatry and Psychotherapy, University of Schleswig-Holstein, Campus Lübeck, Germany 3 Department of Internal Medicine I, University of Schleswig-Holstein, Campus Lübeck, Germany 4 Department of Neuroendocrinology, University of Schleswig-Holstein, Campus Lübeck, Germany
5 Correspondence address: Department of Gynaecology and Obstetrics, University of Schleswig-Holstein, Campus Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany. Tel: +49 451 5002148; Fax: +49 451 5002139; E-mail: a.k.ludwig{at}web.de
BACKGROUND: Insulin resistance and obesity play an important role in the pathogenesis of polycystic ovary syndrome (PCOS). It is known that experimentally induced insulin resistance diminishes the stimulatory effect of insulin on leptin secretion. It is not yet known whether the long-term insulin resistance as found in PCOS patients alters the leptin response to hypo- and hyperglycaemia.
METHODS: We induced hyper- and hypoglycaemia by glucose clamp technique in 7 patients with PCOS and 20 healthy controls. After a plasma glucose level of 8.8 mmol/l was reached, the plasma glucose level was reduced stepwise to 6.8, 4.8 and 2.8 mmol/l.
RESULTS: The PCOS patients required lower glucose infusion rates to reach the glycaemic targets (P < 0.05). Serum insulin and C-peptide concentrations increased significantly during the clamp compared with the baseline in both groups (P < 0.001 for insulin, and P < 0.001, P < 0.005 for C-peptide control and PCOS, respectively) and increased significantly more in PCOS patients compared with the control group (both P < 0.05). Basal leptin levels were significantly higher in the PCOS group than in the control group (P = 0.005). In the controls, the leptin concentration increased significantly during the clamp (P < 0.001 for each glycaemic target), whereas in the PCOS group, leptin secretion increased only during hypoglycaemia (P = 0.04).
CONCLUSIONS: Compared with the healthy controls, the response of leptin secretion to hyper- and hypoglycaemia was diminished in PCOS patients. Changes in leptin secretion seem not to be caused by hyper- and hypoglycaemia, but rather by hyperinsulinaemia. Reduced insulin sensitivity seems to be responsible for the diminished leptin response, which might contribute to the obesity found in PCOS patients.
Key words: glucose clamp/hyperinsulinaemia/leptin/obesity/polycystic ovary syndrome
Submitted on October 3, 2006; resubmitted on August 17, 2006; resubmitted on October 3, 2006; resubmitted on November 17, 2006; accepted on November 29, 2006.
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