Intestinal Proglucagon-Derived Peptides

Brubaker, Patricia L.; Drucker, Daniel J.

doi:10.1007/978-1-59259-695-9_20

Cited by 1 publication

(2 citation statements)

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“…The only report describing the distribution of the GLP-2 receptor showed that, although the mRNA is predominantly confined to the gastrointestinal tissues, the highest level of expression occurred in the proximal small intestine and decreased along the longitudinal axis toward the colon (18). This finding may seem paradoxical, since proglucagon mRNA expression and hence the secretion of the GLP-2 peptide have been shown to be localized in the distal intestine (1,14,4). It should be noted that we did not observe a stimulation of growth in the stomach, pancreas, or large intestine with GLP-2 treatment, although another recent study has shown that GLP-2 stimulates colonic growth (17).…”

Section: Discussionmentioning

confidence: 99%

“…GLUCAGON-LIKE PEPTIDE (GLP)-2, along with GLP-1, represent the major secretory peptides derived from the posttranslational processing of the proglucagon gene expressed in the enteroendocrine L cells localized in the distal intestine (4,14). Studies indicate that a primary stimulus for GLP-2 secretion, like that of GLP-1, is enteral nutrient intake, especially lipid and carbohydrate (13,30).…”

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GLP-2 stimulates intestinal growth in premature TPN-fed pigs by suppressing proteolysis and apoptosis

Burrin

Stoll

Jiang

et al. 2000

American Journal of Physiology-Gastrointestinal and Liver Physi

153

119

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We wished to determine whether exogenous glucagon-like peptide (GLP)-2 infusion stimulates intestinal growth in parenterally fed immature pigs. Piglets (106-108 days gestation) were given parenteral nutrient infusion (TPN), TPN + human GLP-2 (25 nmol. kg(-1). day(-1)), or sow's milk enterally (ENT) for 6 days. Intestinal protein synthesis was then measured in vivo after a bolus dose of [1-(13)C]phenylalanine, and degradation was calculated from the difference between protein accretion and synthesis. Crypt cell proliferation and apoptosis were measured in situ by 5-bromodeoxyuridine (BrdU) and terminal dUTP nick-end labeling (TUNEL), respectively. Intestinal protein and DNA accretion rates and villus heights were similar in GLP-2 and ENT pigs, and both were higher (P < 0.05) than in TPN pigs. GLP-2 decreased fractional protein degradation rate, whereas ENT increased fractional protein synthesis rate compared with TPN pigs. Percentage of TUNEL-positive cells in GLP-2 and ENT groups was 48 and 64% lower, respectively, than in TPN group (P < 0.05). However, ENT, but not GLP-2, increased percentage of BrdU-positive crypt cells above that in TPN piglets. We conclude that GLP-2 increases intestinal growth in premature, TPN-fed pigs by decreasing proteolysis and apoptosis, whereas enteral nutrition acts via increased protein synthesis and cell proliferation and decreased apoptosis.

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