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Leptin does not directly regulate the pancreatic hormones, amylin and pancreatic polypeptide: interventional studies in humans

¹Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA
²Department of Nutrition and Dietetics, Harokopio University, Athens, Greece
³Division of Developmental Medicine, Glasgow University, Glasgow, Scotland, UK

cmantzor{at}bidmc.harvard.edu

ABSTRACT

Objective: Leptin and the pancreatic hormones, amylin and pancreatic polypeptide (PP), are being evaluated alone or in combination for the treatment of obesity, but their physiological regulation has not yet been fully elucidated. Thus, we examined whether amylin and PP are regulated by caloric intake and/or short- and long-term energy deprivation and whether any potential regulation is mediated by changes in leptin levels.

Research Design and Methods: We measured circulating levels of amylin and PP after: 1) a 75-gram glucose load in 28 healthy, normal-weight women; 2) 72-hour complete energy deficiency (severe hypoleptinemia) with administration of either placebo or replacement-dose recombinant human leptin (r-metHuLeptin) in normal-weight men (n=6) and women (n=7); and 3) chronic mild energy deficiency (mild hypoleptinemia) in 7 women with hypothalamic amenorrhea (HA) before and after r-metHuLeptin administration for 3 months.

Results: Amylin and PP levels increased 15 minutes after a 75-gram glucose load and remained elevated at 60 and 120 minutes (P<0.0001). Fasting for 72 hours decreased leptin (to 21%) and amylin (to 67%) of baseline, but not PP levels. Normalizing leptin levels with r-metHuLeptin did not alter the fasting-induced decrease in amylin and had no effect on PP levels. Neither amylin nor PP levels were different in leptin-deficient HA women compared to weight-matched controls, and normalization of leptin levels with r-metHuLeptin treatment did not alter amylin or PP levels.

Conclusions: Circulating amylin levels increase after a glucose load and decrease in response to short-term complete fasting; but, these changes are not mediated by leptin.

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