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Neural Plasticity
Volume 2014, Article ID 917981, 10 pages
Research Article

Glucagon-Like Peptide-1 as Predictor of Body Mass Index and Dentate Gyrus Neurogenesis: Neuroplasticity and the Metabolic Milieu

1Department of Psychiatry & Behavioral Sciences, Division of Neuropsychopharmacology, State University of New York, Downstate Medical Center (SUNY DMC), Brooklyn, NY 11203, USA
2Downstate College of Medicine, SUNY DMC, Brooklyn, NY 11203, USA
3New York State Psychiatric Institute, New York, NY 10032, USA
4Division of Endocrinology, Department of Internal Medicine, SUNY DMC, Brooklyn, NY 11203, USA
5Department of Molecular Imaging and Neuropathology, New York State Psychiatric Institute, New York, NY 10032, USA
6Departments of Psychiatry and Pathology and Cell Biology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
7Departments of Surgery and Internal Medicine, SUNY DMC, Brooklyn, NY 11203, USA

Received 5 July 2014; Revised 14 October 2014; Accepted 15 October 2014; Published 23 November 2014

Academic Editor: Lucas Pozzo-Miller

Copyright © 2014 Jeremy D. Coplan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Glucagon-like peptide-1 (GLP-1) regulates carbohydrate metabolism and promotes neurogenesis. We reported an inverse correlation between adult body mass and neurogenesis in nonhuman primates. Here we examine relationships between physiological levels of the neurotrophic incretin, plasma GLP-1 (pGLP-1), and body mass index (BMI) in adolescence to adult neurogenesis and associations with a diabesity diathesis and infant stress. Morphometry, fasting pGLP-1, insulin resistance, and lipid profiles were measured in early adolescence in 10 stressed and 4 unstressed male bonnet macaques. As adults, dentate gyrus neurogenesis was assessed by doublecortin staining. High pGLP-1, low body weight, and low central adiposity, yet peripheral insulin resistance and high plasma lipids, during adolescence were associated with relatively high adult neurogenesis rates. High pGLP-1 also predicted low body weight with, paradoxically, insulin resistance and high plasma lipids. No rearing effects for neurogenesis rates were observed. We replicated an inverse relationship between BMI and neurogenesis. Adolescent pGLP-1 directly predicted adult neurogenesis. Two divergent processes relevant to human diabesity emerge—high BMI, low pGLP-1, and low neurogenesis and low BMI, high pGLP-1, high neurogenesis, insulin resistance, and lipid elevations. Diabesity markers putatively reflect high nutrient levels necessary for neurogenesis at the expense of peripheral tissues.