Adaptation of intestinal glucose transport in rats with diabetes mellitus occurs independent of hyperphagia

Abstract

Chronic diabetes enhances intestinal absorption of glucose and induces hyperphagia. We examined the enhanced intestinal absorption of glucose in ad libitum-fed rats with streptozocin-induced diabetes mellitus and compared these results with those obtained from pair-fed diabetic animals. Maximal transport capacity (Vmax) and carrier affinity (K0.5) were determined by measuring jejunal and ileal short circuit current (Isc) responses to varying concentrations of 3-O-methyl-D-glucopyranose and D-glucose. Pair-fed diabetic animals maintained the same body weight as animals fed ad libitum, although ad libitum-fed diabetic rats had an increased oral chow intake. Age-matched control rats maintained a constant jejunal and ileal Vmax and K0.5 throughout the study. Diabetic rats fed ad libitum demonstrated an enhanced Vmax and K0.5 in both jejunum and ileum. Pair feeding diabetic animals further enhanced jejunal Vmax while lowering jejunal K0.5 levels. In contrast, pair feeding diabetic animals delayed and blunted changes in ileal Vmax and prevented changes in ileal K0.5. In conclusion, signals other than those of hyperphagia regulate kinetic changes in glucose absorption during diabetes mellitus. Furthermore, these changes have differing effects on jejunum and ileum.

Active transport of 3-O-methyl-glucose by the small intestine in chronically catheterized rats.

“…30MG is actively transported by the same sodium-dependent cotransporter as D-glucose with a similar Vm. and Km ( 15,31 ). In this paper, we show that L-glucose absorption is similar to passive 30MG absorption.…”

“…(6) In this study, we are measuring the fraction of 30MG that is active. Therefore, the portal venous-aortic concentration gradient of 30MG (AC30MG) is substituted for ACtow (15,30). L-glucose is absorbed only passively and has the same permeability coefficient as D-glucose (6,29,31,33 We found that the ACLglUCOSe was 20±20 nmoles/gm blood (n = 6) and that the AC30MG in the presence of phloridzin was 30±60 nmoles/gm blood (n = 6).…”

“…30MG is actively transported at the brush border membrane by the major sodiumdependent transporter that transports D-glucose. Fedorak et al showed that the Km for D-glucose and 30MG are similar but that the Vm,, was -30% less (15). Thomson et al showed that the rate of 30MG uptake in rats was 40% less than for Dglucose (33).…”

“…In some studies, the intestinal vasculature is also perfused (9)(10)(11). In vitro methods for studying intestinal glucose transport include everted sleeves of intestinal tissue (4,(12)(13)(14), isolation of membrane vesicles (15)(16)(17)(18), and cell cultures (19).…”

Mechanism and rate of glucose absorption differ between an Australian honeyeater (Meliphagidae) and a lorikeet (Loriidae)

“…Secondly, because of this structural difference, 3-OMG has a lower affinity for glucose transporters compared with D-glucose (Ikeda et al, 1989;Kimmich, 1981). In four mammal species (laboratory rat, rabbit, guinea pig and hamster) and chickens (the only avian species studied), averaging across species where data are available for both D-glucose and 3-OMG in the same study and thus avoiding a myriad of confounding methodological differences, the affinity (defined here as 1/K m , or reciprocal of the Michaelis constant) of the 3-OMG for carrier-mediated glucose transport systems is ~25% that of the D-glucose (Bihler, 1969;Fedorak et al, 1991;Shehata et al, 1981;Thomson et al, 1982). Lower affinity for glucose transporters may result in lower uptake rates of 3-OMG relative to D-glucose.…”