Abstract

Purpose: To investigate the protective potential of rice bran water extract (RBE) from Khao Dawk Mali 105 on pancreatic abnormalities in high-fat diet (HFD)-induced obese rats.Methods: Male Sprague-Dawley rats were divided into 4 groups: control group, HFD group, and HFD group treated with RBE at 2,205 or 4,410 mg/kg/day. After 4 weeks, body weight, glucose homeostatic parameters, and pancreatic fat accumulation were assessed. mRNA expression levels of sterol regulatory element-binding protein-1c (SREBP-1c), insulin receptor substrate-2 (IRS-2), glucose transporter-2 (GLUT-2) and glucokinase (GK) genes in pancreas were also analyzed.Results: Compared with HFD group, two doses of RBE-treated rats significantly (p < 0.05) reversed HFD-induced obesity, hyperglycemia, impaired glucose tolerance and pancreatic triglyceride accumulation in rats. Histological examination of HFD-induced obese rats revealed fat droplets in acinar cells, but these alterations were ameliorated in RBE-treated rats. RBE treatment showed significantly (p < 0.05) decreased SREBP-1c expression, and also significantly (p < 0.05) increased IRS-2, GLUT-2 and GK expressions in pancreas.Conclusion: RBE consumption may attenuate pancreatic abnormalities by inhibiting fat accumulation, as well as enhancing insulin sensitivity and glucose sensing in the pancreas of HFD-induced obese rats.Keywords: Rice bran, Obesity, Pancreatic steatosis, Insulin signaling, Glucose sensor

Highlights

  • Obesity, especially abdominal obesity, appears to play an important role in the impairment of glucose and lipid metabolism, such as hyperglycemia, insulin resistance, ectopic fat deposition and dyslipidemia [1,2]

  • Samples were subjected to quantitative amplification using TaqMan probe and primer sets for rat SREBP-1c (Rn01495769_m1), insulin receptor substrate-2 (IRS-2) (Rn01482270_s1), glucose transporter-2 (GLUT-2) (Rn00563565_m1) and GK (Rn00561265_m1)

  • In agreement with previous reports, we found that after high-fat diet (HFD) feeding, pancreatic IRS-2, GLUT-2 and GK mRNA levels were decreased, suggesting that HFD might interfere with insulin signaling and glucose-sensing pathways in the pancreas

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Summary

Introduction

Especially abdominal obesity, appears to play an important role in the impairment of glucose and lipid metabolism, such as hyperglycemia, insulin resistance, ectopic fat deposition and dyslipidemia [1,2]. Consumption of high-energy diets with increased saturated and/or trans-fats, an important environmental cause of obesity, are associated with the initiation of these metabolic disturbances [2]. The pancreas is an important organ for the regulation of cellular and whole-body energy homeostasis. Pancreatic abnormalities linked to the development of obesity, insulin resistance and type 2 diabetes (T2D) [3,4]. A previous report has indicated that activation of SREBP-1c is essential for impaired insulin secretion and islet mass associated with the accumulation of triglycerides (TG) [7]

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