title: In vitro study of the effect of miglitol on carbohydrate digestion and intestinal metabolism in normal and non-insulin-dependent diabetic rats.
abstract: The effect of miglitol was studied (20 mg/kg body weight), administered intraduodenally alone or together with maltose, on the absorption and intestinal metabolism of glucose during its translocation from the lumen of the intestine to the blood, using in vitro perfused preparations of complete small intestine-pancreas, proximal small intestine alone, or distal small intestine alone, isolated from normal and non-insulin-dependent diabetic rats. In the absence of a luminal administration of maltose in normal rats, the glucose uptake from the vascular perfusate was greater in the presence (0.52 +/- 0.04 mmol/h) than in the absence (0.39 +/- 0.02 mmol/h) of miglitol (p < 0.05). In diabetic rats, no significant variations were observed in glucose uptake from the vascular perfusate as an effect of miglitol, but the glucose uptake in the presence of this drug was significantly less (p < 0.05) than that observed in normal rats. Portal lactate was significantly greater (p < 0.05) in diabetic than in normal rats and, after administration of miglitol, rose in both normal and diabetic rats, the rise being significantly greater in normal than in diabetic rats (p < 0.01). When maltose was administered luminally (2 g/kg body weight), the values of portal glucose in both normal and diabetic rats were significantly less in the presence of miglitol in the complete as well as in the distal and proximal small intestine preparations (p < 0.05); the glucose uptake from luminal administered maltose was greater in the presence of miglitol in diabetic (p < 0.05) and in normal (p < 0.05) rats except in the complete small intestine of normal rats; and no significant differences were observed in portal lactate levels between normal and diabetic rats in the presence of miglitol. In conclusion, our results show that miglitol administered luminally at the doses employed here, as well as reducing the transport of glucose from the lumen of the intestine into the blood supply, significantly stimulate intestinal glucose metabolism.
authors.affiliation: Departamento de Fisiología, Facultad de Medicina, Universidad de Extremadura, Badajoz, Spain.
authors.forename: M A
authors.initials: MA
authors.lastname: Tormo
authors.forename: M F
authors.initials: MF
authors.lastname: Ropero
authors.forename: M
authors.initials: M
authors.lastname: Nieto
authors.forename: I M
authors.initials: IM
authors.lastname: Martinez
authors.forename: J E
authors.initials: JE
authors.lastname: Campillo
mesh_terms: D017485:1-Deoxynojirimycin / Q000031:analogs & derivatives; D000818:Animals; D050260:Carbohydrate Metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000139:chemically induced / Q000378:metabolism*; D005944:Glucosamine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology; D065089:Glycoside Hydrolase Inhibitors; D050112:Imino Pyranoses; D066298:In Vitro Techniques; D007408:Intestinal Absorption / Q000187:drug effects*; D007421:Intestine, Small / Q000187:drug effects* / Q000378:metabolism*; D008297:Male; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar
chemical_list: D065089:Glycoside Hydrolase Inhibitors; D050112:Imino Pyranoses; C045621:miglitol; D017485:1-Deoxynojirimycin; D005944:Glucosamine