Partial recovery of erythrocyte glycogen in diabetic rats treated with phenobarbital

ABSTRACT

Erythorocytes may play a role in glucose homeostasis during the postprandial period. Erythrocytes from diabetic patients are defective in glucose transport and metabolism, functions that may affect glycogen storage. Phenobarbital, a hepatic enzyme inducer, has been used in the treatment of patients with non-insulin-dependent diabetes mellitus (NIDDM), increasing the insulin-mediated glucose disposal. We studied the effects of phenobarbital treatment in vivo on glycemia and erythrocyte glycogen content in control and alloxan-diabetic rats during the postprandial period. In control rats (blood glucose, 73 to 111 mg/dl in femoral and suprahepatic veins) the erythrocyte glycogens content was 45.4 + 1.1 and 39.1 + 0.8 mug/g Hb (mean + SEM, N = 4-6) in the femoral artery and vein, respectively, and 37.9 +1.1 in the portal vein and 47.5 + 0.9 in the suprahepatic vein. Diabetic rats (blood glucose 300-350 mg/dl) presented low (p<0.05) erythrocyte glycogen content, i.e., 9.6 + 0.1 and 7.1 + 0.7 mug/g Hb in the femoral artery and vein, respectively, and 10.0 + 0.7 and 10.7 + 0.5 in the portal and suprahepatic veins, respectively. After 10 days of tratment, phenobarbital (0.5 mg/ml in the drinking water) did not change blood glucose or erythrocyte glycogen content in control rats. In diabetic rats, however, it lowered (P<0.05) blood glucose in the femoral artery (from 305 + 18 to 204 + 45 mg/dl) and femoral vein (from 300 + 11 to 174 + 48 mg/dl) and suprahepatic vein (from 350 + 10 to 174 + 42 mg/dl), but the reduction was not sufficient for complete recovery. Phenobarbital also stimulated the glycogens synthesis, leading to a partial recovery of glycogen stores in erythrocytes. In treated rats, erythrocyte glycogen content increased to 20.7 + 3.8 mug/g Hb in the femoral artery and 30.9 + 0.9 mug/g Hb in the suprahepatic veins (p<0.05). These data indicate that phenobarbital activated some of the insulin-stimulated glucose matabolism steps which were depressed in diabetic srythrocytes, supporting the view that erythrocytes participate in glucose homeostasis.