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Bifidobacterium lactis IDCC 4301 exerts anti-obesity effects in high-fat diet-fed mice model by regulating lipid metabolism

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Chronic hypernutrition and lack of physical activity promote lipid accumulation in the white adipose tissue, and excessive lipid accumulation leads to obesity. An increase in the number and size of adipocytes, a characteristic of obesity, is closely associated with adipose dysfunction. Recent in vitro and in vivo studies have proven that probiotics may prevent this dysfunction by regulating lipid metabolism. However, the mechanisms of action of probiotics in obesity are not fully understood, and hence, their usage for treating obesity remains limited. In this study, Bifidobacterium lactis IDCC 4301 was selected for its anti-obesity potential after evaluating inhibitory activity of pancreatic lipase and cholesterol reducing activity. Next, we investigated the roles of B. lactis IDCC 4301 on lipid metabolism in 3T3-L1 cells and high-fat diet (HFD)-fed mice. Our results show that B. lactis IDCC 4301 inhibits cell differentiation and lipid accumulation by suppressing the expression of adipogenic enzymes in 3T3-L1 cells. Moreover, the administration of B. lactis IDCC 4301 resulted in decreased body and epididymal adipose tissue weight, improvement in serum lipid levels, and downregulated adipogenic mRNA expression in HFD-fed mice. Additionally, metabolomic analysis suggested that 2-ketobutyrate might be a possible target compound against obesity. Collectively, these results support that B. lactis IDCC 4301 could be used as an alternative treatment for obesity.

저자정보

  • Minjee Lee IBS R&D Center, Ildong Bioscience, Gyeonggi-do 17957, Republic of Korea
  • Won Yeong Bang IBS R&D Center, Ildong Bioscience, Gyeonggi-do 17957, Republic of Korea
  • O-Hyun Ban IBS R&D Center, Ildong Bioscience, Gyeonggi-do 17957, Republic of Korea
  • Jungwoo Yang IBS R&D Center, Ildong Bioscience, Gyeonggi-do 17957, Republic of Korea

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