Effects of porcine gastric fundic factor, somatostatin, substance P, glucagon, neurotensin, bombesin, VIP, motilin, and pentagastrin on jejunal glucose absorption in the rat.

Abstract

SUMMARY The effects of a porcine gastric fundic mucosal extract (molecular weight <10 000) has been compared with the effects of eight candidate gastrointestinal peptides on glucose absorption from the jejunum in a rat model. Bolus injection of the extract produced immediate and marked depression of glucose absorption. None of the candidate peptides tested produced this response, although somatostatin and substance P depressed absorption as a late phenomenon after 30 minutes. We conclude that the effects of the fundic extract are not reproduced by any of these candidate peptides. This strengthens the evidence for a novel gastrointestinal peptide, resident in fundic mucosa, which affects absorption from upper small bowel.There is evidence for a peptide factor, secreted from gastric fundic mucosa, which affects jejunal mucosal absorption. 1-4 Stimulation of gastric fundic mucosa by distension or raised pH significantly reduced luminal loss of glucose, 14C-labelled 3-0-methyl glucose and tracer ions 22Na and 99mTc, from the jejunum. An extract of porcine gastric mucosa also reduced jejunal absorption when infused intravenously in a rat model.4Samples of the porcine gastric fundic mucosal extract contained only small and variable amounts of some of the known gastrointestinal peptides (Bloom, personal communication; Table 1). The present series of experiments was designed to see if the effects of the fundic extract on jejunal absorption could be because of the action of a specific candidate gastrointestinal peptide.

Metformin Alters Upper Small Intestinal Microbiota that Impact a Glucose-SGLT1-Sensing Glucoregulatory Pathway

“…The following treatments were infused into the lumen of the upper small intestine during the basal insulin euglycemic clamp at a rate of 2 mL/min for 50 min: 1) saline, 2-6) glucose, fructose, galactose, 3-O-methyl glucose, sucralose (2 mM, Sigma-Aldrich, St. Louis, MO, USA), 7) phlorizin (50 mM; 40 pmol min-1; Sigma Aldrich), 8) MK-329 (979 mM; 2 nmol min-1; Tocris Bioscience), 9) Exendin-9 (75 mg mL À1 ; 0.15 mg min À1 ; Tocris Bioscience). Intestinal glucose is absorbed from the lumen into the small intestinal mucosa at a rate of 600 nmol min-1 in rats at comparable weight (250 g) (Andrews et al, 1983). A lower glucose dose of 20 nmol min-1 was originally used in a previous study from our lab investigating the effects of a glucose infusion into the lower jejunum (Breen et al, 2012).…”

Substance P-induced intestinal secretion of water and electrolytes.

“…14 15 In addition, jejunal glucose absorption has also been shown to be decreased by substance P in vivo. 28 Other, as yet untested mechanisms of action include the central and/or peripheral neurologic effects of substance P as well as its interactions with other gastrointestinal peptides. Humoural mediation is suggested by the reports of a suppressive effect of substance P on gastric somatostatin release29 30 Along with other neurohumoural substances that alter intestinal transport, such as serotonin and neurotensin, substance P appears to effect intestinal transport by increasing Ca" + entry across the basolateral membrane of intestinal epithelial cells.32 3 Its secretory effects are unaffected in vitro by atropine, indomethacin, diphenhydramine, and somatostatin, but can be reversed by removal of extracellular Ca++ ions or the addition of Verapamil, a calcium-channel blocker, to the serosal bathing solution.…”

The Influence of Estradiol and Diet on Small Intestinal Glucose Transport in Ovariectomized Rats

“…The basolateral membrane of enterocytes has receptors for cholecystokinin, gastrin, and other regulatory peptides associated with the GIT, which are known to modulate enterocyte absorption of ions (6)(7)(8)(9) and carrier-mediated uptake of glucose by the sodium-dependent transporter SGLT-l (10)(11)(12)(13)(14). Less is known about the responses to signaling molecules that originate from sources other than the GIT and associated organs.…”