Experimental type 2 diabetes induces enzymatic changes in isolated rat enterocytes.

Abstract

Diabetes in humans and in experimental animals produces changes in the function and structure of the small intestine. The authors determined the activity of intestinal disaccharidases (maltase and sucrase) and of 6-phosphofructo-1-kinase (PFK-1) in enterocytes isolated from the small intestine of male Wistar rats (2.5 to 3 months old) with experimental nonobese type 2 diabetes, induced by streptozotocin (STZ) injection on the day of birth (n0-STZ) or on the 5th day of life (n5-STZ), with different degrees of hyperglycemia and insulinemia (n0-STZ and n5-STZ models). The glycemia (mmol/L) of the diabetic rats (n0-STZ: 8.77 +/- 0.47; n5-STZ: 20.83 +/- 0.63) was higher (P <.01) than that of the nondiabetic (ND) rats (5.99 +/- 0.63); on the contrary, the insulinemia (ng/mL) was significantly lower in both n0-STZ (1.74 +/- 0.53; P <.05) and n5-STZ (1.12 +/- 0.44; P <.01) diabetic rats than in normal rats (3.77 +/- 0.22). The sucrase and maltase activities (U/g protein) in diabetic rats (n0-STZ: 89 +/- 9 and 266 +/- 12; n5-STZ: 142 +/- 23 and 451 +/- 57) were significantly higher than those in the ND group (66 +/- 5 and 228 +/- 22). The PFK-1 activities (mU/mg protein) in the diabetic models (n0-STZ: 14.89 +/- 1.51; n5-STZ: 13.35 +/- 3.12) were significantly lower (P <.05) than in ND rats (20.54 +/- 2.83). The data demonstrated enzymatic alterations in enterocytes isolated from the small intestine of n0-STZ rats that are greater (P <.05) than in the more hyperglycemic and hypoinsulinemic n5-STZ animals. The results also show that nonobese type 2-like diabetes in the rat produces modifications that favor an increase in glucose absorption rates.