Insulin resistance is a sufficient basis for hyperandrogenism in lipodystrophic women with polycystic ovarian syndrome
AO Lungu, E Safar Zadeh, A Goodling… - The journal of …, 2012 - academic.oup.com
AO Lungu, E Safar Zadeh, A Goodling, E Cochran, P Gorden
The journal of clinical endocrinology & Metabolism, 2012•academic.oup.comContext: The lipodystrophies (LD) are characterized by metabolic abnormalities (insulin
resistance, hypertriglyceridemia, and diabetes) and a polycystic ovarian syndrome (PCOS)
phenotype. Therapeutic administration of leptin improves insulin sensitivity and the
metabolic features. Objective: The objective of the study was to investigate whether the
PCOS features are corrected by increasing insulin sensitivity as a function of leptin
treatment. Design: This was a prospective, open-label trial using leptin replacement in …
resistance, hypertriglyceridemia, and diabetes) and a polycystic ovarian syndrome (PCOS)
phenotype. Therapeutic administration of leptin improves insulin sensitivity and the
metabolic features. Objective: The objective of the study was to investigate whether the
PCOS features are corrected by increasing insulin sensitivity as a function of leptin
treatment. Design: This was a prospective, open-label trial using leptin replacement in …
Context
The lipodystrophies (LD) are characterized by metabolic abnormalities (insulin resistance, hypertriglyceridemia, and diabetes) and a polycystic ovarian syndrome (PCOS) phenotype. Therapeutic administration of leptin improves insulin sensitivity and the metabolic features.
Objective
The objective of the study was to investigate whether the PCOS features are corrected by increasing insulin sensitivity as a function of leptin treatment.
Design
This was a prospective, open-label trial using leptin replacement in various forms of lipodystrophy.
Setting
The study was performed at the Clinical Center at the National Institutes of Health.
Patients or Other Participants
Twenty-three female patients with LD were enrolled in a leptin replacement trial from 2000 to the present. Different parameters were assessed at baseline and after 1 yr of therapy.
Intervention(s)
Patients were treated with leptin for at least 1 yr.
Main Outcome Measure(s)
We evaluated free testosterone, SHBG, and IGF-I at baseline and after 1 yr of leptin.
Results
Testosterone levels decreased from 3.05 ±0.6 ng/ml at baseline to 1.7 ±0.3 ng/ml (P = 0.02). SHBG increased from 14.5 ±2 to 25 ±3.5 nmol/liter after 1 yr of leptin therapy. There were no significant changes in the levels of gonadotropins and ovarian size as a result of leptin replacement therapy. IGF-I increased significantly after leptin therapy from 150 ±14 to 195 ±17. There was a significant decrease in triglycerides and glycosylated hemoglobin in the context of reduced insulin requirements.
Conclusions
In the present study, we show that LD may be a model for the common forms of PCOS and that the endocrine features are corrected by leptin therapy, which reduces insulin resistance.
Oxford University Press