A rat intestinal perfusion technique has been used to assess the ability of a number of monosaccharides, monosaccharide analogues and disaccharides to stimulate intestinal release of immunoreactive gastric inhibitory polypeptide (GIP).
Perfusates containing glucose, sucrose, galactose, maltose, 3-O-methylglucose or α- or β-methylglucoside at concentrations of 100 mmol/l in Krebs–Ringer phosphate buffer (KRP) produced significant stimulation of GIP release compared with the control perfusions with KRP alone (P < 0·02). Mannose, 6-deoxygalactose, 2-deoxyglucose, myoinositol, fructose or lactose (100 mmol/1 of each) did not stimulate GIP release compared with controls. There was no significant difference in the ability of sucrose, maltose or β-methylglucoside (100 mmol/1 of each) to release GIP compared with 100 mmol glucose/1, but galactose, 3-O-methylglucose and α-methylglucoside (100 mmol/1 of each) produced significantly lower GIP responses than did glucose (P <0·02). Addition of 5 mmol phloridzin/1 to a perfusate containing 50 mmol glucose/1 prevented intestinal absorption of glucose and abolished the GIP response.
The molecular configuration of monosaccharides which have the ability to stimulate GIP release agreed well with the structural requirements for active transport by the sodium-dependent hexose pathway.
Stimulation of insulin-like growth factor II receptor binding and insulin receptor kinase activity in rat adipocytes. Effects of vanadate and H2O2.