Journal Articles

Central GIP signaling stimulates peripheral GIP release and promotes insulin and pancreatic polypeptide secretion in nonhuman primates.

August 25, 2016

Paul B. Higgins, Robert E. Shade, Iram P. Rodríguez-Sánchez, Magdalena Garcia-Forey, M. Elizabeth Tejero-Barrera, V. Saroja Voruganti, Shelley A. Cole, Anthony G Comuzzie, Franco Folli. 2016. Central GIP signaling stimulates peripheral GIP release and promotes insulin and pancreatic polypeptide secretion in nonhuman primates. American Journal of Physiology – Endocrinology and Metabolism.

Author Affiliations

1. Texas Biomedical Research Institute
2. Texas Institute for Biomedical Research
3. Autonomous University of Nuevo León (Universidad Autonoma de Nuevo León)
4. National Institute of Genomic Medicine (Instituto Nacional de Medicina Genómica-INMEGEN),
5. University of North Carolina at Chapel Hill
6. University of Texas Health Science Center at San Antonio

Abstract

Glucose-dependent insulinotropic polypeptide (GIP) has important actions on whole body metabolic function. GIP and its receptor are also present in the central nervous system and have been linked to neurotrophic actions. Metabolic effects of central nervous system GIP signaling have not been reported. We investigated whether centrally administered GIP could increase peripheral plasma GIP concentrations and influence the metabolic response to a mixed macronutrient meal in nonhuman primates. An infusion and sampling system was developed to enable continuous intracerebroventricular (ICV) infusions with serial venous sampling in conscious nonhuman primates. Male baboons (Papio Sp.) that were healthy and had normal body weights (28.9 ±2.1Kg) were studied (n=3). Animals were randomized to receive continuous intracerebroventricular (ICV) infusions of GIP (20pmol.kg-1.hr-1) or vehicle prior to and over the course of a 300min. mixed meal test (15kcal/kg, 1.5g glucose/kg) on two occasions. A significant increase in plasma GIP concentration was observed under ICV GIP infusion (66.5 ±8.0 vs. 680.6 ±412.8pg/mL, p=0.04), before administration of the mixed meal. Increases in postprandial, but not fasted, insulin (p=0.01) and pancreatic polypeptide (p=0.04) were also observed under ICV GIP. Effects of ICV GIP on fasted or postprandial glucagon, glucose, triglyceride, and free fatty acids were not observed. Our data demonstrate that central GIP signaling can promote increased plasma GIP concentrations independent of nutrient stimulation and increase insulin and pancreatic polypeptide responses to a mixed meal.

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