Plasma D-Glucose, D-Fructose and Insulin Responses after Oral Administration of D-Glucose, D-Fructose and Sucrose to Normal Rats

Abstract

Objective: To assess whether oral D-fructose modifies the plasma D-glucose and insulin responses to oral D-glucose administration in normal rats.

Design: Oral D-glucose (1.7, 3.5, 6.9 or 13.9 μmol/g body weight), D-fructose (6.9 μmol/g), both D-glucose and D-fructose (1.7 or 3.5 μmol/g of each hexose) or sucrose (3.7 μmol/g) were administered intragastrically to overnight fasted rats and the plasma concentration of D-glucose, D-fructose and insulin measured over the ensuing 120 minutes. Control experiments were conducted after oral administration of H₂O or saline.

Results: The administration of D-fructose, given as the free hexose or as sucrose, instead of augmenting the plasma D-glucose concentration evoked by the concomitant administration of D-glucose, tended both to improve the insulin response of the pancreatic B-cell and to minimize hyperglycemia, when compared to the results of experiments including the administration of equimolar amounts of D-glucose alone. For instance, the area under the plasma D-glucose curve was comparable in the rats receiving both D-glucose and D-fructose (3.5 μmol/g of each hexose) and the rats receiving only D-glucose (3.5 μmol/g), averaging respectively 836 ± 32 and 850 ± 34 mM · min each. Likewise, the paired ratio between the areas under the plasma insulin and D-glucose curves, when corrected for the threshold concentration for the insulinotropic action of the hexose (2.05 ± 0.10 mM), averaged 44.3 ± 3.0 nmol/mol in the 16 rats receiving D-fructose alone, sucrose alone or both D-glucose and D-fructose, as compared to 37.7 ± 2.9 nmol/mol in the 22 rats receiving increasing amounts of D-glucose alone.

Conclusions: The intake of D-fructose, as the free hexose or as sucrose, favours D-glucose homeostasis. This is likely to be attributable to the reciprocal effects of the aldose and ketose upon their respective phosphorylation by glucokinase in both hepatocytes and insulin-producing pancreatic islet cells.

• D-glucose
• D-fructose
• sucrose
• plasma insulin
• normal rats

This work was supported by grants from the Spanish Institute of Health Carlos III (RGDM-G03/212 and FIS-PI020967), and the Belgian Foundation for Scientific Medical Research (3.4567.97 and 3.4517.02). P.G.P. is a Research Fellow of the Fundación Conchita Rábago de Jiménez Díaz. We are grateful to E. Martin-Crispo for technical assistance and to C. Demesmaeker for secretarial help.