Protective effect of rice bran water extract on pancreas of rats fed a high-fat diet

Name: Wason Parklak

keyword: Rice bran

; Obesity

; Pancreatic steatosis

; Insulin signaling

; Glucose sensing

; Pancreatic senescence

; Oxidative stress

Abstract: Obesity is generally associated with the infiltration of fat in multiple organs including the liver, heart, kidneys, as well as pancreas. This ectopic fat deposition in the pancreas may trigger lipotoxicity in the pancreas and leads to the pancreatic abnormalities. Many studies have reported the beneficial effects of rice bran water extract (RBE) against obesity, insulin resistance, hyperglycemia, dyslipidemia and oxidative stress. However, the mechanisms of how RBE can modulate fat accumulation, insulin signaling, glucose sensing, and cellular senescence, particularly in the pancreas, are still unknown. Thus, this study aimed to investigate the effects of RBE on the pancreatic abnormalities in high-fat diet (HFD)-fed rats. The study was performed on male Sprague-Dawley rats. The rats were divided into five groups including the control group (C), HFD alone group (HF), HFD treated with RBE at 2,205 or 4,410 mg/kg/day groups (HFR1 and HFR2, respectively) and HFD treated with metformin at 19.1 mg/kg/day group (HFM). After 4 weeks, body weight, glucose homeostasis parameters, blood lipid profile, lipid peroxidation marker (both in serum and pancreas) and pancreatic fat accumulation were assessed. The mRNA expression levels of sterol regulatory element-binding protein-1c (SREBP-1c), insulin receptor substrate-2 (IRS-2), glucose transporter-2 (GLUT-2), glucokinase (GK), and nuclear factor-kappa B p50 and p65 (NF-κB p50 and p65) genes in pancreas were also analyzed. Moreover, senescence in rat pancreatic islet cells were analyzed by immunohistochemistry. The results showed the rats in HF group developed metabolic disturbances compared with the control rats ; these disturbances were characterized by obesity, hyperglycemia, hyperinsulinemia, impaired glucose tolerance and dyslipidemia. However, two doses of RBE-treated rats significantly reversed the HFD-induced obesity, hyperglycemia, impaired glucose tolerance and hyperlipidemia in rats when compared with HF group. Metformin treatment had no effect on levels of fasting blood glucose (FBG) and serum insulin, but body weight gain, the area under the curve of blood glucose levels (AUC-G), and serum total-cholesterol (total-C) and low-density lipoprotein-cholesterol (LDL-C) levels were significantly decreased in the HFM group. Histological examination of HFD-induced obese rats revealed fat droplets in acinar cells, and irregular and larger shapes of islets, but these alterations were ameliorated in RBE- and metformin-treated rats. Moreover, the pancreatic triglyceride (TG) and SREBP-1c mRNA levels were also significantly decreased in RBE- and metformin-treated rats compared with the rats fed an HFD alone. The HF group also exhibited impaired insulin signaling and glucose-sensing pathways, which RBE could prevent these alterations via the improvement of IRS-2, GLUT-2, and GK expression. Unfortunately, metformin-treated rats had no effect on transcript levels of IRS-2 and GK, however GLUT-2 mRNA levels were significantly increased in the HFM group when compared with HF group. In addition, islet cell senescence was also observed in the HF group accompanied by enhanced malondialdehyde (MDA) level, and NF-κB expression. Interestingly, all RBE treatments resulted in a decrease in these alterations. The oxidative markers in pancreas were not significantly improved in the HFM group. However, metformin treatment effectively reduced serum MDA level and pancreatic islet senescence in rats fed an HFD. In conclusion, RBE consumption may attenuate pancreatic abnormalities by inhibiting fat accumulation, senescence, and oxidative damage, as well as enhancing insulin sensitivity and glucose sensing in the pancreas of HFD-induced obese rats. These data are likely to be associated with the improvement of impaired glucose homeostasis

Thammasat University. Thammasat University Library

Address: BANGKOK

Email: preserv@tu.ac.th

Name: Nusiri Lerdvuthisopon

Role: advisor

Created: 2016

Modified: 2021-07-15

Issued: 2021-07-15

วิทยานิพนธ์/Thesis

application/pdf

DOI: 10.14457/TU.the.2016.1471

eng

DegreeName: Doctor of Philosophy

Level: Doctoral Degree

Descipline: Medical Sciences

Grantor: Thammasat University

©copyrights Thammasat University

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