Abstract

The effects of fibre-enriched biscuit on biomarkers associated with hepatotoxicity in diabetic rats were investigated. Diabetes was induced by single intraperitoneal injection of alloxan monohydrate. Treatment lasted for 14 days after which the rats were sacrificed by cervical dislocation. Blood serum was analyzed to determine hepatic function enzymes. The liver was also analyzed to determine hepatic lipid profile and antioxidant enzymes. Induction of diabetes led to elevated levels of ALP, AST, and ALT. These were, however, significantly (p < 0.05) reduced in the fibre-enriched biscuit fed (treated) group. There was no significant difference in the serum bilirubin and total protein levels of the studied groups. Reduced albumin level was observed in the diabetic group; this was further lowered on feeding with fibre-enriched biscuits. Induction of diabetes led to increased hepatic level of cholesterol, triglyceride (TG), low density lipoprotein (LDL), and lipid peroxidation and decreased activities of glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) and HDL level. These were significantly (p < 0.05) reversed on feeding with fibre-enriched biscuit. This study portrays the protective effect of fibre-enriched biscuit on increased oxidative stress and hyperlipidemia in hepatic tissues of alloxan-induced diabetic rats.

Highlights

  • Diabetes is a chronic disease associated with high morbidity and mortality due to its complications and consequences [1]

  • Series of experimental investigations have shown that hyperglycemia-induced-oxidative stress via free radical generation and oxidative damage to cells plays a major role in these diabetic complications [1, 3]

  • Wannamethee et al [7] suggested that elevated levels of hepatic enzymes could cause insulin resistance and other features of diabetic syndrome

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Summary

Introduction

Diabetes is a chronic disease associated with high morbidity and mortality due to its complications and consequences [1]. It is characterized by chronic hyperglycemia and alterations of cellular homeostasis, which leads to diffuse vascular damage. The progression of this disease causes β-pancreatic cell dysfunction implicated in the development of cardiovascular diseases, neuropathy, nephropathy, and retinopathy [2]. Series of experimental investigations have shown that hyperglycemia-induced-oxidative stress via free radical generation and oxidative damage to cells plays a major role in these diabetic complications [1, 3]. Bakhshaeshi et al [8] and Dey and Lakshmanan [9] have linked hyperglycemiainduced generation of reactive oxygen species (ROS) with development of diabetic liver injury and increased attention on antioxidants in the treatment and management of diabetes

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