Polyphenols have multiple functions for prevention of various diseases, including those related to lifestyle. It is known that polyphenols possess strong antioxidant activity, which contributes to prevention of certain diseases. However, polyphenols also have the ability to modulate metabolism through mechanisms that are separate from their antioxidant activity. In this review, we discuss the mechanism by which flavonoids modulate drug-metabolizing enzymes and help to prevent obesity and hyperglycemia. In the former process, the aryl hydrocarbon receptor (AhR) is a key molecule. The mechanism by which suppression of AhR transformation is dependent on the sub-class structure of flavonoids: flavones and flavonols act as AhR antagonists, indicating that they have the potential to prevent AhR agonist-induced carcinogenesis. In the latter process, AMP-activated protein kinase (AMPK) and glucose transporter 4 (GLUT4) are key molecules related to obesity and hyperglycemia, respectively. AMPK is known to act as an energy sensor for the whole body. In muscle cells, activation of AMPK promotes translocation of GLUT4, indicating that both AMPK and GLUT4 play a pivotal role in prevention of hyperglycemia. We show that polyphenols activate AMPK in various tissues and promote GLUT4 translocation in skeletal muscle.
Pancreatic β-cells play a pivotal role in glucose metabolism through secretion of insulin in response to glucose concentration. In order to prevent type 2 diabetes mellitus, it is important to maintain the secretion of insulin from β-cells. An attractive option to prevent the onset of type 2 diabetes is the use of food or supplements that improve β-cell function. In this study, a bioactive food supplement was examined to determine its effect on cultured β-cells, isolated mouse pancreatic islets, and mice. S-Equol (7-hydroxy-3- (4′-hydroxyphenyl) chroman) is produced by gut microbiota from the isoflavone daidzein, which is found in Pueraria montana (Kudzu) root or Glycine max (soybean) . S-Equol enhanced the proliferation and insulin secretion of β-cells and decreased their susceptibility to oxidative stress by activating protein A signaling in an enantioselective manner. These effects were stronger with S-equol than with daidzein. These results indicate that S-equol boosts β-cell function, suggesting that it may help to prevent type 2 diabetes mellitus.
We conducted a crossover trial to investigate the effect of vitamin-enriched egg consumption on serum 25-hydroxy-vitamin D (HVD) levels in healthy young women (aged 21±0 years) . Forty-one female subjects were divided into two groups. One group was given two vitamin-enriched eggs in addition to their usual diet every day for 4 weeks followed by a washout period, and then normal eggs were provided for 4 weeks. The other group received with same diets, but in reverse order. Before the investigation, the mean serum HVD levels in 53.7％ of the subjects were less than 50 nmol/L, indicating vitamin D deficiency. At the end of the period of vitamin-enriched egg consumption, the HVD level increased and reached more than 50 nmol/L in 92.7％ of the subjects, indicating adequate intake of vitamin D. During both the normal egg consumption and washout periods, the serum HVD level was less than 50 nmol/L in 34.1％ of the subjects, and no significant difference was detected between the periods before and after normal egg consumption. Throughout the investigation periods, food intake did not change. These findings suggest that vitamin-enriched egg consumption could improve serum HVD levels in healthy young women.
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