Glucagon-Like Peptide-1 Induced Signaling and Insulin Secretion Do Not Drive Fuel and Energy Metabolism in Primary Rodent Pancreatic β-Cells (Extract)

In the present study we examined whether the acute stimulation of GSIS by GLP-1 or Ex-4 involves the modulation of glucose, fatty acid and energy metabolism in the β-cells, as studied using isolated islets of both rats and mice. The study was designed to respond to four questions of general interest for β-cell neuropeptide and fuel signaling. 1) Does GLP-1 amplify GSIS in part by metabolic signaling? 2) Does the activation of major cellular signaling processes (Ca2+, cAMP, PKB etc) in response to a physiological peptide agonist changes β-cell metabolism? 3) Does enhanced insulin secretion contribute significantly to total energy consuming processes in the β-cell? 4) Is the β-cell similar or different from most tissues in term of metabolic activation, specifically whether it is primarily governed by a “push” (fuel substrate driven) process, rather than a “pull” mechanism secondary to enhanced activation of its major cellular function?