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Publication
Chronic high-fat feeding increases GIP and GLP-1 secretion without altering body
weight.
Authors Wang F, Yoder SM, Yang Q, Kohan AB, Kindel TL, Wang J, Tso P
Submitted By Submitted Externally on 4/21/2017
Status Published
Journal American journal of physiology. Gastrointestinal and liver physiology
Year 2015
Date Published 11/1/2015
Volume : Pages 309 : G807 - 15
PubMed Reference 26336929
Abstract The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and
glucagon-like peptide-1 (GLP-1), enhance postprandial insulin secretion, promote
adipogenesis, and regulate gastrointestinal motility and food intake. To date, a
consensus on how the incretin response is altered in obesity is lacking. We
investigated the effects of chronic high-fat (HF) feeding on incretin secretion
in the lymph fistula rat model. Male Sprague-Dawley rats (8 wk) were provided a
semipurified AIN93M HF or low-fat (LF) diet ad libitum for 3 or 13 wk; a HF
pair-fed (HF-PF) group was included as a control during the 3-wk feeding trial.
Energy intake, body weight, and body composition were regularly monitored. At
the culmination of the feeding period, an intestinal lymphatic duct cannula and
duodenal infusion tube were installed. All animals were challenged with a 3-ml
Ensure bolus (3.125 kcal/animal) to measure lymphatic incretin secretion.
Despite a significantly higher energy intake, both the 3-wk and 13-wk HF-fed
animals did not have an increase in body weight and only a slight increase in
body fat compared with LF-fed rats. Following the duodenal Ensure challenge, the
3-wk and 13-wk HF-fed rats had significantly greater lymphatic GIP and GLP-1
secretion than the LF-fed animals. Additionally, the HF-PF group displayed a
secretion profile similar to the HF-fed animals for GIP but a similar pattern to
the LF-fed animals for GLP-1. The HF-PF data suggest that the increased GIP
secretion is driven by the greater percentage of fat intake, whereas the
increased GLP-1 secretion is driven by the excess caloric intake.




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