A Physiological Level of Rhubarb Fiber Increases Proglucagon Gene Expression and Modulates Intestinal Glucose Uptake in Rats ,

Abstract

Previous work demonstrated that a high fiber diet upregulates proglucagon mRNA and secretion of glucagon-like peptide-1 [GLP-1(7-37)] and insulin compared with an elemental fiber-free diet. This study examined whether similar intakes of fibers differing in physiochemical and fermentative properties alter the expression of intestinal hormones and intestinal absorptive properties. Sprague-Dawley rats were fed either a 50 g/kg cellulose or rhubarb fiber diet for 14 d. Ileal proglucagon mRNA levels were significantly higher in rats fed rhubarb fiber than in those fed cellulose fiber (9.3 +/- 0.9 vs. 6.2 +/- 1.0 densitometer units). Proglucagon mRNA in the colon did not differ between diet treatments. Plasma c-peptide concentrations were significantly higher 30 min after an oral glucose tolerance test in the rhubarb vs. cellulose group (1627 +/- 67 vs. 1290 +/- 71 pmol/L). Passive permeability, measured by the uptake of L-glucose, was significantly higher in the jejunum of rats fed cellulose compared with those fed rhubarb fiber. Adjusting total glucose uptake for passive permeability and unstirred water layer resistance resulted in a higher Km being calculated for the jejunum and ileum of the cellulose fiber group. Jejunal and ileal carrier-mediated uptakes (Vmax) were not altered by diet and reflected the lack of difference between groups in sodium-dependent glucose cotransporter (SGLT-1) and sodium-independent glucose transporter (GLUT2) mRNA levels. Replacing cellulose fiber with rhubarb fiber in a diet upregulated ileal proglucagon mRNA and resulted in a reduced passive permeability but did not affect glucose transport of the small intestine. This work establishes the importance of dietary fiber fermentability in modulating intestinal proglucagon expression and possibly glucose homeostasis.

Dairy protein and leucine alter GLP-1 release and mRNA of genes involved in intestinal lipid metabolism in vitro

“…It is not inherently obvious why we would have observed the null results of GLP-1 in response to whey. From our previous studies demonstrating that soluble dietary fiber, which slows gastrointestinal transit, promotes GLP-1 release [19,21], it may be argued that a slower emptying rate and prolonged intestinal absorption of casein may stimulate GLP-1 release from the L cells of the distal small intestine and colon. It is interesting to note the recent observation by Diepvens et al [34] that GLP-1 concentrations after milk protein and whey protein ingestion in humans were 145.3 ± 194.9 and 96.7 ± 150.2 pmol/L, respectively.…”

“…We previously demonstrated in vivo and in vitro that dietary fiber and meat hydrolysate increase the secretion of glucagon-like peptide-1 (GLP-1), a key satiety hormone, and modulate proglucagon gene expression [17][18][19][20][21][22]. Distinct from alterations in satiety, additional mechanisms may also play a role in body weight regulation by dairy and BCAAs.…”

Increased plasma PYY levels following supplementation with the functional fiber PolyGlycopleX in healthy adults

“…Fermentable dietary fibers are more effective at promoting secretion of glucagon-like peptide-1 (GLP-1), one of many known anorexigenic peptides, than non-fermentable fibers (Reimer et al, 1997;Zhou et al, 2008). In addition to fermentability, dietary fibers are also classified according to solubility.…”

Co-requirement of Cyclic AMP- and Calcium-dependent Protein Kinases for Transcriptional Activation of Cholecystokinin Gene by Protein Hydrolysates

“…Intestinal genes, expressed by epithelial cells of which the apical pole is in direct contact with the luminal contents, are potential targets for a nutritional control of transcription. Thus, expression of hormone genes such as those of glucose-dependent insulinotropic peptide, proglucagon, and cholecystokinin (CCK) 1 has been shown to be up-regulated in the intestine of rodents by glucose, dietary fibers, or protein hydrolysates (1)(2)(3). CCK, produced by intestinal endocrine I-cells regulates several key digestive functions such as gallbladder contraction or pancreatic enzyme secretion (4).…”