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Stimulation of Gastric Inhibitory Polypeptide Release in ob/ob Mice by Oral Administration of Sugars and Their Analogues

Peter R. Flatt, Piotr Kwasowski and Clifford J. Bailey^*

Department of Biochemistry, University of Surrey, Guildford, Surrey GU2 5XH Department of Biological and Biomedical Sciences, University of Ulster at Coleraine, Co. Londonderry, BT52 1SA ^* Biology Division, Department of Pharmaceutical Sciences, Aston University, Birmingham, B4 7ET, United Kingdom

The effect of oral administration of sugars and their analogues (glucose, galactose, fructose, mannose, sucrose, N-acetylglucosamine, 2-deoxyglucose, 3-O-methylglucose and -methyl-glucoside) on plasma gastric inhibitory polypeptide (GIP) concentration was examined in 18-h fasted ob/ob mice. Administration of sucrose (5.52 mol/kg body wt), or the monosaccharides (11.04 mol/kg body wt) glucose, galactose or fructose, elicited prompt GIP responses that peaked at 30 min. Similar effects were induced by 3-O-methylglucose or -methyl-glucoside, but the stimulatory action of 2-deoxyglucose was delayed. In contrast to the other sugars, N-acetylglucos-amine decreased plasma GIP concentration, while mannose exerted no effect. The results suggest that sugars using the Na⁺-glucose cotransporter at the luminal brush border stimulate GIP release without the necessity of being metabolized or removed from the cell by the glucose transporter at the basolateral membrane. The ability of fructose to stimulate GIP release in ob/ob mice suggests that the Na⁺-glucose cotransporter does not represent an exclusive trigger for sugar-induced GIP secretion.

KEY WORDS: • enteroinsular axis • gastric inhibitory polypeptide (GIP) • ob/ob mice • mannose • fructose • sucrose • glucose • galactose • sugar analogues

Manuscript received 21 November 1988. Revision accepted 10 April 1989.

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