Elevated Insulin in Obese Women Relates to Low Endogenous Luteinizing Hormone

Abstract

INTRODUCTION: Obesity is a state of insulin resistance as it is also a state of relative hypogonadotropic hypogonadism. The physiology behind this is still unclear and may be the result of hypothalamic or pituitary factors or pharmacokinetics of gonadotropins. We sought to investigate if insulin, directly or indirectly, suppresses pituitary luteinizing hormone (LH) secretion. METHODS: A luteal phase frequent blood sampling study was undertaken in regularly menstruating obese (n=10) and normal-weight women (n=10). The study included 12 hours of unstimulated monitoring (to evaluate endogenous hypothalamic–pituitary function) with subsequent administration of intravenous bolus of gonadotropin-releasing hormone (to evaluate pituitary sensitivity). Luteinizing hormone was measured with an immunofluorometric assay. Luteinizing hormone pulsatility was evaluated using an objective, widely accepted method. RESULTS: All women were ovulatory. The obese group was significantly older than the normal weight group (32.5±4.7 compared with 27.3±2.6 years, P=.006). Insulin was significantly higher in the obese group than the normal-weight group (21.5 [14.3–28.7] compared with 11.7 [8.9–14.5] mU/L, P=.01). In the 2-hour postprandial period, there was a rise in insulin that was significantly higher (35.6 [17.1–54.1] compared with 16.5 [8.4–24.7] mU/L, P=.04) and LH that trended lower in the obese women (8.1 [3.5–12.7] compared with 4.2 [2.8–5.6] IU/L) (Figure 1).CONCLUSIONS: Higher insulin in obese women may be associated with lower endogenous LH output. A direct role of insulin in suppressing pituitary LH secretion should be further investigated.