ABSTRACT
There is significant cultivation of persimmon (Diospyros kaki) in East Asia, a plant whose fruit has abundant nutrients, including vitamins, polyphenols, and dietary fiber. Persimmon dietary supplements can benefit health by amelioration of diabetes, cardiovascular disease, and obesity. There are also persimmon-based beverages produced via fermentation, such as wines and vinegars, and increasing consumption of these products in East Asia. Although there is great interest in functional foods, the health effects of fermented persimmon extract (FPE) are completely unknown. We examined the effects of FPE on the metabolic parameters of mice fed a high-fat diet (HFD). Our results indicated that FPE supplementation led to an approx. 15% reduction of body weight, reduced abdominal and liver fat, and reduced serum levels of triglycerides, total cholesterol, and glucose. FPE also blocked the differentiation of murine 3T3-L1 pre-adipocyte cells into mature adipocytes. We suggest that gallic acid is a major bioactive component of FPE, and that AMP-activated protein kinase mediates the beneficial effects of FPE and gallic acid.
Subject(s)
AMP-Activated Protein Kinases/metabolism , Diospyros/chemistry , Obesity/diet therapy , Obesity/metabolism , Plant Extracts/pharmacology , 3T3-L1 Cells/metabolism , Abdominal Fat/drug effects , Adipocytes/drug effects , Adipocytes/metabolism , Animals , Blood Glucose , Body Weight/drug effects , Fermentation , Fruit , Gallic Acid/pharmacology , Intra-Abdominal Fat/drug effects , Lipids/blood , Male , Mice , Mice, Inbred C57BL , Plant Extracts/chemistryABSTRACT
AMP-activated protein kinase (AMPK) functions as a cellular energy sensor by monitoring the cellular AMP:ATP ratio and plays a central role in cellular and whole-body energy homeostasis. Recent studies have suggested that AMPK also contribute to cell cycle regulation, but its role in this field remains almost elusive. In the present study, we report that AMPKα1 was transiently activated during G1/S transition phase in NIH3T3 cells in the absence of any metabolic stress. Inhibition of AMPK activity at G1/S transition phase completely blocked cells from entering S phase; in contrast, persistent activation of AMPK at G1/S transition phase allowed cells to normally enter S phase, but these cells failed to proceed to G2/M phase, stacking at S phase. We further demonstrated that activation of AMPK at G1/S transition phase depends on Ca2+ transients and CaMKKß activity, but not on energy status. Collectively, these data indicate that temporal regulation of AMPK is required for proper control of S phase in NIH3T3 cells.
