Oral administration of Lactobacillus reuteri GMNL-263 improves insulin resistance and ameliorates hepatic steatosis in high fructose-fed rats

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.

Sardine protein diet increases plasma glucagon-like peptide-1 levels and prevents tissue oxidative stress in rats fed a high-fructose diet

“…The results from the current study indicate that the weight gain and liver, kidney, heart and muscle weights in the HF group were significantly greater than those of control groups, despite reduced energy intake, suggesting a low energy expenditure. These results are in line with a previous study (37). Intake of sardine protein suppressed HF-diet-mediated body, liver and muscle weight gain compared with casein, which is attributable in part to the satietogenic effects of sardine protein.…”

Gamma-linolenic acid ameliorated glycation-induced memory impairment in rats

“…Our data showed that the fructose treatment caused significant elevation of the HbA1c levels as compared to normal salinetreated rats (Figure 8). This is in line with the previous findings that manifested positive co-relation between blood HbA1c levels and high fructose diet (Hsieh et al 2013). To the best of our knowledge, it is the first report attributing higher level of HbA1c in rats with the memory impairment.…”

Antioxidant Properties of Proanthocyanidins Attenuate Carbon Tetrachloride (CCl4)–Induced Steatosis and Liver Injury in Rats via CYP2E1 Regulation

“…16 Furthermore, proanthocyanidin treatment decreased the oxidative stress within the liver tissue by lowering the levels of oxidative products and oxidative-stress-induced DNA damage due to CCl 4 (Table 1 and Fig. 5), and restoring the antioxidant enzyme levels ( Table 1) that were depleted after battling against CCl 4 -mediated oxidative stress.…”