Location: Children's Nutrition Research Center
Title: Expression of mRNA for proglucagon and glucagon-like peptide-2(GLP-2) receptor in the ruminant gastrointestinal tract and the influence of energy intake Authors
|Taylor-Edwards, C -|
|Matthews, J -|
|Mcleod, K -|
|Holst, J -|
|Harmon, D -|
Submitted to: Domestic Animal Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 1, 2010
Publication Date: September 30, 2010
Citation: Taylor-Edwards, C.C., Burrin, D.G., Matthews, J.C., McLeod, K.R., Holst, J.J., Harmon, D.L. 2010. Expression of mRNA for proglucagon and glucagon-like peptide-2(GLP-2) receptor in the ruminant gastrointestinal tract and the influence of energy intake. Domestic Animal Endocrinology. 39:181-193. Interpretive Summary: The mechanisms that explain how food stimulates intestinal growth are not completely understood, especially in agriculturally important, domestic animals. Glucagon-like peptide 2 (GLP-2) is a hormone produced by the intestine after ingesting food. GLP-2 is produced from the proglucagon gene in the intestine. Our previous studies in neonatal piglets showed that feeding stimulates GLP-2 secretion and that the blood concentration of GLP-2 is correlated with intestinal growth. We previously also showed the expression of the GLP-2 receptor in the piglet small intestine. The aim of the current collaborative study was to characterize the expression of the proglucagon and GLP-2R genes in the gastrointestinal tissues of the ruminant calf. The results show that both the proglucagon and GLP-2R genes are expressed in the stomach, small intestine, and colon, but greatest in the small intestine and colon. In addition, the blood concentration of GLP-2 and expression of proglucagon gene were increased with an energy rich diet. The results of this study show that the ruminant GLP-2 secretion process is responsive to food intake and functions in ruminants similar to that of non-ruminants.
Technical Abstract: 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 x net energy for maintenance for 21 d, and then increased to 1.75 x net energy for maintenance 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.