Intestinal Growth in Parenterally‐Fed Rats Induced by the Combined Effects of Glucagon‐like Peptide 2 and Epidermal Growth Factor

Abstract

Both GLP-2 and EGF upregulate growth of the small intestine, and this is augmented when GLP-2 and EGF are combined. These findings may lead to improved treatment of patients receiving PN.

Synergistic Effect of Glucagon-Like Peptide 2 (GLP-2) and of Key Growth Factors on the Proliferation of Cultured Rat Astrocytes. Evidence for Reciprocal Upregulation of the mRNAs for GLP-2 and IGF-I Receptors

“…No synergistic changes were observed when the effects of EGF, IGF-I, IGF-II and GH, either alone or in combination with GLP-2, on the control of intestinal growth were studied in mice [32]. Nevertheless, a synergistic effect between GLP-2 and EGF on cellular proliferation in the small intestine was observed in parenterally fed rats [33].…”

The Correlation Between the Expression of Differentiation Markers in Rat Small Intestinal Mucosa and the Transcript Levels of Schlafen 3

“…Notch signaling has been shown to regulate the fate of the cells of the mucosal crypt in differentiation after postmitotic events, 1 whereas exogenous growth factors affect cell proliferation and differentiation along the rat gastrointestinal tract. 34,35 Although the potential interaction between the Notch signal pathway and Slfn3 awaits further study, at least 1 growth factor, TGF-β, appears to stimulate Slfn3 expression. 6 A previous in vitro study 6 suggested that Slfn3 is necessary for the induction of enterocytic differentiation by repetitive deformation, TGF-β, and butyrate and that this effect might involve phosphatidylinositol 3-kinase (PI3K), focal adhesion kinase (FAK), or p38 signaling.…”

The Intestinotrophic Peptide, GLP-2, Counteracts the Gastrointestinal Atrophy in Mice Induced by the Epidermal Growth Factor Receptor Inhibitor, Erlotinib, and Cisplatin

“…It has been shown in vivo that EGF infusion increases the mitotic activity in the intestinal crypts in rats [11,12]. No former study has investigated the effect of antagonizing the EGFR system on the apoptotic or mitotic activity in the gastrointestinal tract.…”

“…The receptor is located at the basolateral membrane of the surface epithelium in the small intestine and is activated primarily by epidermal growth factor (EGF) or transforming growth factor alpha (TGF-a) [9]. The EGFR pathway has been demonstrated to stimulate proliferation of enterocytes in the gastrointestinal tract [11][12][13][14]; to up-regulate electrolyte and nutrient transport in the enterocyte [15], increase the expression of brush border enzymes [16], and to induce epithelial restitution [17][18][19][20]. An inhibition of these functions by erlotinib could explain the gastrointestinal symptoms experienced by the patients.…”