Endogenously released GLP-1 is not sufficient to alter postprandial glucose regulation in the dog.

Johnson KM, Farmer T, Schurr K, Patrick Donahue E, Farmer B, Neal D, Cherrington AD
Endocrine. 2011 39 (3): 229-34

PMID: 21547512 · PMCID: PMC5371028 · DOI:10.1007/s12020-011-9441-x

Glucagon-like peptide-1 (GLP-1) is secreted from the L cell of the gut in response to oral nutrient delivery. To determine if endogenously released GLP-1 contributes to the incretin effect and postprandial glucose regulation, conscious dogs (n = 8) underwent an acclimation period (t = -60 to -20 min), followed by a basal sampling period (t = -20 to 0 min) and an experimental period (t = 0-320 min). At the beginning of the experimental period, t = 0 min, a peripheral infusion of either saline or GLP-1 receptor (GLP-1R) antagonist, exendin (9-39) (Ex-9, 500 pmol/kg/min), was started. At t = 30 min, animals consumed a liquid mixed meal, spiked with acetaminophen. All animals were studied twice (± Ex-9) in random fashion, and the experiments were separated by a 1-2-week washout period. Antagonism of the GLP-1R did not have an effect, as indicated by repeated-measures MANOVA analysis of the Δ AUC from t = 45-320 min of arterial plasma glucose, GLP-1, insulin, glucagon, and acetaminophen levels. Therefore, endogenous GLP-1 is not sufficient to alter postprandial glucose regulation in the dog.

MeSH Terms (17)

Acetaminophen Animals Blood Glucose Dogs Enteroendocrine Cells Female Food Gastric Emptying Glucagon Glucagon-Like Peptide-1 Receptor Glucagon-Like Peptide 1 Homeostasis Insulin Kinetics Male Peptide Fragments Receptors, Glucagon

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