Plasma D-glucose, D-fructose and insulin responses after oral administration of D-glucose, D-fructose and sucrose to normal rats.

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 micromol/g body weight), D-fructose (6.9 micromol/g), both D-glucose and D-fructose (1.7 or 3.5 micromol/g of each hexose) or sucrose (3.7 micromol/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 H(2)O 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 micromol/g of each hexose) and the rats receiving only D-glucose (3.5 micromol/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.