Abstract

Coconut kernel protein (CKP) has been reported to contain significant amounts of L-arginine. Its potential effect on glucose homeostasis, possibly through the nitric oxide synthase (NO) pathway, was therefore investigated in alloxan-induced diabetic rats. Diabetes was induced by a single intraperitoneal dose of alloxan (150 mg kg⁻¹ body weight). Experimental rats were grouped as follows: Group I, normal control; Group II, diabetic control; Group III, diabetic + CKP; Group IV, diabetic + L-arginine; Group V, diabetic + L-arginine + L-N(G)-Nitroarginine methyl ester (L-NAME). Purified CKP isolated from dried coconut kernel and L-arginine was administered to rats along with a semi-synthetic diet for 45 days. L-NAME (0.5 mg kg⁻¹ body weight) was given to Group V animals. After the experimental period, serum glucose, insulin, activities of liver nitric oxide synthase and arginase, liver glycogen levels and histopathology of the pancreas were evaluated. Serum glucose, insulin and antioxidant enzyme activities and liver glycogen levels were found to be restored to basal levels in CKP-fed rats. Decreased arginase and increased nitric oxide synthase (NOS) activities were found in CKP- and arginine-fed rats. L-NAME treatment showed a partial effect on these parameters. Histopathology revealed that CKP and L-arginine feeding reduced the diabetes-related pancreatic damage in treated rats compared to the diabetic control. The results observed in this study indicate that the potential antidiabetic activity of CKP may be through an arginine-NO pathway leading to pancreatic beta cell regeneration.

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