Abstract
BackgroundType 2 diabetes mellitus (DM), characterized by peripheral insulin resistance, is the most common form of diabetes. Probiotics are live micro-organisms that, when administered in adequate amounts, confer delaying effect on DM development. In this study, the effects Lactobacillus reuteri GMNL-263 (Lr263), a new probiotic strain developed by our laboratory, on insulin resistance and the development of hepatic steatosis in high-fructose fed rats were explored. Furthermore, the relevant regulatory pathways involved were also investigated.MethodMale Sprague–Dawley rats were fed a high-fructose diet with or without Lr263 administration for 14 weeks. The composition of fecal microbiota, oral glucose tolerance, glycated haemoglobin, insulin, leptin, C-peptide, and incretins were measured. The markers of liver injury, serum and hepatic lipids profile, activity of hepatic antioxidant enzyme, and proinflammatory cytokines in adipose tissue were investigated. Additionally, the expression of hepatic lipogenic genes and insulin signaling related genes in adipose tissue were also studied. Liver sections were examined for hepatic steatosis using hematoxylin-eosin staining.ResultsThe levels of serum glucose, insulin, leptin, C-peptide, glycated hemoglobin, GLP-1, liver injury markers, lipid profile in serum and liver were significantly increased in high-fructose-fed rats. However, after Lr263 administration, the elevation of these parameters was significantly suppressed. Feeding of Lr263 reversed the decreased number of bifidobacterium species and lactobacillus species and increased number of clostridium species induced by high fructose treatment. The decreased activities of hepatic antioxidant enzymes in HFD rats were dramatically reversed by Lr263 treatment. Concentrations of IL-6 and TNF-α in adipose tissue which were elevated in high fructose treatment were markedly decreased after Lr263 feeding. Decreased levels of PPAR-γ and GLUT4 mRNA after high fructose treatment were significantly enhanced by Lr263 administration. Lr263 consumption normalized the increased lipogenic gene (Srebp-1c, FAS, and Elvol6) expressions stimulated by high fructose. Administration of Lr263 significantly ameliorated hepatic steatosis observed in high fructose treated rats.ConclusionOur study provided evidences clarifying the effectiveness of Lr263 on reducing insulin resistance as well as hepatic steatosis formation in high-fructose-fed rats and suggested that Lr263 may be a promising therapeutic agent in treating type 2 diabetes.
Highlights
Type 2 diabetes mellitus (DM), characterized by peripheral insulin resistance, is the most common form of diabetes
Our study provided evidences clarifying the effectiveness of Lactobacillus reuteri GMNL-263 (Lr263) on reducing insulin resistance as well as hepatic steatosis formation in high-fructose-fed rats and suggested that Lr263 may be a promising therapeutic agent in treating type 2 diabetes
Our results from histological analysis demonstrated that a prominent hepatic steatosis was observed in high fructose-diet group (HFD) rats, whereas administration of Lr263 significantly ameliorated fat accumulation in liver as compared to HFD group. These findings indicated that hyperlipidemia and insulin resistance caused by high fructose treatment were improved by administration of Lr263, which may ameliorate the development of hepatic steatosis in HFD rats
Summary
Type 2 diabetes mellitus (DM), characterized by peripheral insulin resistance, is the most common form of diabetes. Type 2 diabetes is the most common form of diabetes comprising about 80% of all diabetic population characterizing by insulin resistance, dyslipidemia, and hyperglycemia [4,5,6]. A major abnormality underlying type 2 diabetes mellitus, is defined as the pathophysiological condition reducing insulin responsiveness in liver, muscle, and adipose tissue [8,9]. Aberrations of metabolism caused by insulin resistance may increase levels of circulating free fatty acids and liver fat accumulation, which leads to liver inflammation and fibrosis [10]. High levels of free fatty acids induce the overexpression of cytochrome P450 (CYP) 2E1 and increase oxidative stress via lipid peroxidation, which may lead to liver injury [11]
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