This Article Full Text Full Text (PDF) Submit a related Letter to the Editor Purchase Article View Shopping Cart Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Prasad, C. Articles by Hermon-Taylor, J. Search for Related Content PubMed PubMed Citation Articles by Prasad, C. Articles by Hermon-Taylor, J.

Hyperenterostatinemia in Premenopausal Obese Women¹

Louisiana State University-Tulane General Clinical Research Center and the Obesity Research Program, Section of Endocrinology, Department of Medicine (C.P., M.I., C.D., F.S.), Louisiana State University Medical Center, New Orleans, Louisiana 70112; and the Department of Surgery (N.S., J.H.-T.), St. George’s Hospital Medical School, London SW17 ORE, United Kingdom

Address all correspondence and requests for reprints to: Dr. Chandan Prasad, Section of Endocrinology, Department of Medicine, Louisiana State University Medical Center, 1542 Tulane Avenue, New Orleans, Louisiana 70112. E-mail: cprasa{at}lsumc.edu

Enterostatins [Val-Pro-Asp-Pro-Arg (VPDPR), Val-Pro-Gly-Pro-Arg (VPGPR), and Ala-Pro-Gly-Pro-Arg (APGPR)] are pentapeptides derived from the NH₂-terminus of procolipase after tryptic cleavage and belong to the family of gut-brain peptides. Although enterostatin-like immunoreactivities exist in blood, brain, and gut, and exogenous enterostatins decrease fat appetite and insulin secretion in rats, the roles of these peptides in human obesity remain to be examined. To determine whether VPDPR and APGPR secretion is altered in obesity, serum VPDPR and APGPR levels were measured in 38 overnight-fasted subjects (body mass index, 17.9–54.7 kg/m²) before and after a meal. The mean fasting VPDPR in the serum of lean subjects was significantly lower than that in obese subjects [lean = 603 ± 86 nmol/L (n = 17); obese, 1516 ± 227 nmol/L (n = 21); P = 0.0023]. In addition, the rise in serum APGPR after a meal (postmeal/fasting ratio) was significantly higher in lean than in obese subjects [lean, 1.71 ± 0.24 (n = 17); obese, 1.05 ± 0.14 (n = 21); P = 0.0332]. The results of these studies show hyperenterostatinemia in obesity and a diminution in enterostatin secretion after satiety.