Faculty Collaboration Database

Nutrient-driven incretin secretion into intestinal lymph is different between diabetic Goto-Kakizaki rats and Wistar rats. Am J Physiol Gastrointest Liver Physiol 2009 Feb;296(2):G168-74

Date

12/06/2008

Pubmed ID

19056762

Pubmed Central ID

PMC2643916

DOI

10.1152/ajpgi.90506.2008

Scopus ID

2-s2.0-59449102829 (requires institutional sign-in at Scopus site)   12 Citations

Abstract

The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) augment postprandial glucose-mediated insulin release from pancreatic beta-cells. The Goto-Kakizaki (GK) rat is a widely used, lean rodent model of Type 2 diabetes; however, little is known regarding the incretin secretion profile to different nutrients in these rats. We have recently shown that lymph is a sensitive medium to measure incretin secretion in rodents and probably the preferred compartment for GLP-1 monitoring. To characterize the meal-induced incretin profile, we compared lymphatic incretin concentrations in the GK and Wistar rat after enteral macronutrient administration. After cannulation of the major mesenteric lymphatic duct and duodenum, each animal received an intraduodenal bolus of either a fat emulsion, dextrin, a mixed meal, or saline. Lymph was collected for 3 h and analyzed for triglyceride, glucose, GLP-1, and GIP content. There was no statistical difference in GIP or GLP-1 secretion after a lipid bolus between GK and Wistar rats. Dextrin and a mixed meal both increased incretin concentration area under the curve, however, significantly less in GK rats compared with Wistar rats (dextrin GIP: 707 +/- 106 vs. 1,373 +/- 114 pg ml(-1) h, respectively, P < 0.001; dextrin GLP-1: 82.7 +/- 24.3 vs. 208.3 +/- 26.3 pM/h, respectively, P = 0.001). After administration of a carbohydrate-containing meal, GK rats were unable to mount as robust a response of both GIP and GLP-1 compared with Wistar rats, a phenomenon not seen after a lipid meal. We propose a similar, glucose-mediated incretin secretion pathway defect of both K and L cells in GK rats.

Author List

Kindel TL, Yang Q, Yoder SM, Tso P

Author

Tammy Lyn Kindel MD, PhD Associate Professor in the Surgery department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Animals
Dextrins
Diabetes Mellitus, Type 2
Diet
Dietary Carbohydrates
Dietary Fats
Disease Models, Animal
Duodenum
Enteroendocrine Cells
Gastric Inhibitory Polypeptide
Glucagon-Like Peptide 1
Glucose
Intestinal Secretions
Lymph
Male
Postprandial Period
Rats
Rats, Wistar
Sodium Chloride, Dietary
Time Factors
Triglycerides