The present study investigated the molecular effects of rice bran oil (RBO) on lipid-regulatory genes (sterol regulatory element binding protein-1 [Srebf1] and peroxisome proliferator-activated receptors-α [Ppara]) and the expression of catalase (CAT) and superoxide dismutase (SOD1) genes in insulin-resistant rats. Rats were divided into five groups: animals that received standard diet (control); rats fed standard diet containing RBO as the sole source of fat (RBO); a high-fructose diet (HFD) group, which was further divided into two subgroups: rats fed HFD either for only 1 month (HFD1) or for 2 months (HFD2) and rats fed HFD containing RBO for 1 month; while rats in the last group fed HFD for 30 days then treated with RBO for another 30 days. The HFD induced a state of insulin resistance (IR) as indicated by the hyperinsulinemia and elevated homeostasis model assessment insulin resistance index. Hepatic lipid levels and radical scavenging enzymes were altered by the HFD. Lipid-regulatory genes, Srebf1 and Ppara, were upregulated while Sod1 and Cat were downregulated in insulin-resistant rats. Addition of RBO to the two diet regimens alleviated the disorders of IR to some extent. RBO reduced the hepatic levels of triacylglycerol, malondialdehyde, SREBP, and PPAR-α mRNA. Hepatic SOD and CAT were elevated at gene and protein levels. The HFD induces de novo lipogenesis by upregulating the lipid-regulatory genes resulting in increased serum and hepatic triacylglycerol. Moreover, IR induced by the HFD caused a state of oxidative stress. Supplementation of RBO to fructose-fed rats not only improves insulin resistance but also downregulates lipogenic genes and improves the unbalanced oxidative status.
Background Insulin resistance is an inadequate metabolic response of the peripheral tissue to circulating insulin. It plays an important pathophysiological role in type 2 diabetes mellitus. The purpose of the study was to investigate the molecular effects of rice bran oil (RBO) on the gene expression of insulin receptor (IR), insulin receptor substrate-1 (IRS-1), glucose transporters-4 and 5 (GLUT-4 and 5) in insulin-resistant rats induced by high fructose diet (HFD). Methods Rats were divided into six groups (10 rats each) as follows: Groups 1 and 2: rats received a standard diet with corn oil or RBO (as the sole source of fat), respectively. Group 3: animals fed on HFD, which was furtherly divided into 2 subgroups: rats fed HFD either for one (HFD1) or for 2 months (HFD2). Group 4, rats fed HFD containing RBO for 1 month (HFD1 + RBO), while rats in group 5 fed HFD for 30 days then RBO was added to the diet for another 30 days (HFD2 + RBO). Serum levels of glucose and insulin, as well as hepatic gene expression of insulin receptors and glucose transporters were determined. Livers were isolated for histopathological study. Results HFD induced insulin resistance with a reduction in the hepatic level of insulin receptor and glucose transporters at both protein and molecular levels. Addition of RBO improved the insulin sensitivity and up-regulated the expression of the tested genes. Conclusion HFD impaired the insulin sensitivity of the hepatocytes by down-regulating the insulin receptor genes. Addition of RBO alleviated all the hazardous effects.
Background: insulin resistance (IR) is a pathological condition characterized by inadequate peripheral tissue metabolic response to circulating insulin. It plays pathophysiological role in type 2 diabetes mellitus (T2DM). High dosage of fructose in the diet (60 g/100 g diet) may induce insulin resistance accompanied by deleterious metabolic consequences including hyperglycemia and hyperinsulinemia. Rice bran oil (RBO), is a rich source of antioxidants especially γ-oryzanol, αtocopherols and tocotrienols which contribute to high oxidative stability, longer shelf life than other edible oils and high antioxidant property against free radicals. The present work was undertaken to study if the addition of rice bran oil in rat's diets ameliorate the insulin resistance. Materials and methods: to achieve this target, plasma fasting glucose, serum insulin and calculated HOMA-IR, which assesse the presence of insulin resistance, was evaluated. Serum lipid profile (cholesterol, triglycerides, high-density lipoprotein-cholesterol (HDL) and low-density lipoproteincholesterol (LDL) was also evaluated. In addition, the oxidative stress was assessed through hepatic malondialdehyd (MDA) as an oxidative biomarker and the antioxidant enzyme superoxide dismutase (SOD) was also estimated. Results: RBO ameliorated HOMA-IR, oxidative biomarker (MDA) and increased SOD activity. Conclusion: high fructose diet induced oxidative stress which lead to insulin resistance, this was ameliorated by addition of RBO.
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