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Bifidobacteria and its rice fermented products on diet induced obese mice: analysis of physical status, serum profile and gene expressions

In: Beneficial Microbes
Authors:
M. Ray Department of Microbiology, Vidyasagar University, Midnapore, West Bengal 721102, India

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P.K. Hor Department of Microbiology, Vidyasagar University, Midnapore, West Bengal 721102, India

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D. Ojha ICMR Virus Unit, I.D. & B.G. Hospital, Dr. S.C. Banerjee Road, Beliaghata, West Bengal 700010, India

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J.P. Soren Department of Microbiology, Vidyasagar University, Midnapore, West Bengal 721102, India

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S.N. Singh Division of Nutrition, Defence Institute of Physiology and Allied Sciences, Lucknow Road, Timarpur, Delhi 110054, India

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K.C. Mondal Department of Microbiology, Vidyasagar University, Midnapore, West Bengal 721102, India

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Obesity is highly correlated with the dysbiosis of intestinal microbiota, and bifidobacteria are one of the soft targets of this metabolic syndrome. The aim of this study is to evaluate the efficacy of Bifidobacterium sp. MKK4 and rice-based fermented foods on physical, haematological, gut microbiota and lypogenic-lypolytic marker genes in diet-induced obese mice. Adult male mice (21±0.7 g) were randomly divided into four groups (n=10) according to the type of diet: normal diet (ND), high fat diet (HFD), HFD supplemented with Bifidobacterium sp. MKK4 and HFD supplemented with MKK4 associated rice-fermented food. 8 weeks of bacterial therapy in the obese mice resulted in significant reduction of body and organ weights, improved serum levels of glucose, triglyceride and cholesterol, the histological structure of the liver (steatosis), and re-establishment of gut Lactobacillus, Bifidobacterium and Bacteroides species. The bacterial therapy led to up-regulation of lipolytic transcription factors, such as peroxisome proliferator-activated receptor (PPAR)-α, PPAR-δ, and their regulated gene products in fatty acid metabolism and glucose uptake, such as acyl-CoA oxidase, carnitine palmitoyl-transferase-1, uncoupling protein-3 and glucose transporter-4. Concomitantly, both adipocytogenesis and fatty acid synthesis were arrested as reflected by the down-regulation of sterol regulatory element binding protein-1c, acetyl-CoA carboxylase, fatty acid synthase and tumour necrosis factor alpha genes. The effectiveness of the fermented product was more profound than the single bacterium. These data provide experimental support with regard to the use of Bifidobacterium sp. MKK4 as a natural therapeutic agent to control obesity.

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