Glucagon-like peptide-2 (GLP-2) is a potent trophic gut hormone, yet its function in ruminants is relatively unknown. Experiment 1 was conducted as a pilot study to establish the presence of GLP-2 in ruminants and to ascertain whether it was responsive to increased nutrition, as in non-ruminants. Concentrations of intact GLP-2 in the blood and gut epithelial mRNA expression of proglucagon (GCG) and the GLP-2 receptor (GLP2R) were measured in 4 ruminally, duodenally, and ileally cannulated steers. Steers were fed to meet 0.75 ± NEM for 21 d, and then increased to 1.75 ± NEM requirement for another 29 d. Blood samples and ruminal, duodenal, and ileal epithelium biopsies were collected at low intake (Days -6 and -3), acute high intake (Days 1 and 3), and chronic high intake (Days 7 and 29) periods. Experiment 2 investigated the mRNA expression pattern of GCG and GLP2R in epithelial tissue obtained from the forestomachs (rumen, omasum, and abomasum) and intestines (duodenum, jejunum, ileum, and colon) of 18 forage-fed Angus steers (260 kg BW). In Experiments 1 and 2, real-time polymerase chain reaction showed that expression of GCG and GLP2R mRNA was detectable in forestomach tissues, but expression was greater (P < 0.001) in small intestinal and colon tissue. High energy intake tended (P = 0.07) to increase plasma GLP-2 during the acute period and was paralleled by a 78% increase (P = 0.07) in ileal GCG mRNA expression. After this initial adaptation, duodenal GCG mRNA expression increased (P = 0.08) during the chronic high intake period. Duodenal GLP2R mRNA expression was not affected by energy intake, but ileal GLP2R expression was increased after 29 d of high energy intake compared to both the low and acute high intake periods (P = 0.001 and P = 0.01, respectively). These data demonstrate that cattle express GCG and GLP2R mRNA primarily in small intestinal and colon tissues. Increased nutrient intake increases ileal GCG mRNA and plasma GLP-2, suggesting that GLP-2 may play a role in the trophic response of the ruminant gastrointestinal tract to increased feed intake.
|Number of pages||13|
|Journal||Domestic Animal Endocrinology|
|State||Published - Oct 2010|
Bibliographical noteFunding Information:
Support for this research was provided by the Kentucky Agricultural Experiment Station Publication No. 10-07-072. Products used in this research were donated or purchased. Suppliers had no input into the design or conduct of these studies. The authors express gratitude to Julie Cannon, Alma True, Kelly Brown, Anne Koontz, Kyle Earing, and Susanna Kitts for assistance with tissue collection; to Alma True for validation of the DPPIV plasma assay; and to Louis Dionissopoulus and Shengfa Liao for assistance with RT-PCR assays.
C.C. Taylor-Edwards is presently affiliated with the Center for Veterinary Medicine, US Food and Drug Administration, Rockville, MD. This manuscript was written by C.C. Taylor-Edwards in her private capacity. No official support or endorsement by the FDA is intended or should be inferred. All authors have approved the final article. The authors declare no conflicts of interest. Source of funding: Specific Cooperative Agreement between USDA-ARS-Forage Animal Production Research Unit and the University of Kentucky and the Faculty Research Support Program , University of Kentucky.
ASJC Scopus subject areas
- Food Animals
- Animal Science and Zoology