Soy Isoflavone Genistein Is a Potential Agent for Metabolic Syndrome Treatment: A Narrative Review

نویسندگان

  • Darya Ghadimi Dept. of Biochemistry, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran
  • Mina Hemmati Dept. of Biochemistry, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran
  • Negar Karimi Dept. of Biochemistry, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran
  • Tooka Khadive Dept. of Biochemistry, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran
چکیده مقاله:

Metabolic syndrome has a high prevalence (about 22.4% in adult individuals) in developed countries. Inflammation due to obesity and fat accumulation is the most important factor in the progression of metabolic syndrome. In cells which have a receptor for insulin hormone, inflammatory mediators target the insulin signaling pathway and cause insulin resistance. Peroxisome proliferator-activated receptors are a group of ligand inducible transcription factors, whose activation can improve insulin resistance and their agonists such as Genistein, which seems to be useful in prevention of insulin resistance development. Genistein is one of the soy derived isoflavonoids that affects carbohydrate and lipid metabolism resulting in prevention of insulin resistance. The current narrative review has concentrated mainly on highlighting the usefulness of Genistein in the improvement of insulin resistance and therapeutic potential of it in both in-vitro and in-vivo models. Genistein can increase fatty acid β-oxidation, decrease lipogenesis and improve insulin resistance in hepatocytes. In adipocytes, Genistein prevents downregulation of adiponectin expression and facilitates the upregulation of adiponectin expression. In β-islet cells, Genistein initiates the special cascade which leads to proliferation of β cells, resulting in increased secretion of insulin. Based on findings of the studies, it can be concluded that Genistein can be a useful agent in prevention of de novo lipid synthesis as well as proliferation of β cells. In this way the development of metabolic syndrome can be prevented.

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عنوان ژورنال

دوره 28  شماره None

صفحات  64- 75

تاریخ انتشار 2020-03

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