Phloridzin reduces blood glucose levels and alters hepatic gene expression in normal BALB/c mice

► Phloridzin (0.5% and 1%) diets significantly reduce the blood glucose levels in BALB/c mice. ► Phloridzin (0.1%) diet altered of the hepatic gene expressions related to carbohydrate and fatty acid metabolism in mice. ► Phloridzin (0.5%) diets suppressed the gene expressions related to citrate cycl...

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Veröffentlicht in:Food and chemical toxicology 2012-07, Vol.50 (7), p.2547-2553
Hauptverfasser: Kobori, Masuko, Masumoto, Saeko, Akimoto, Yukari, Oike, Hideaki
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Sprache:eng
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Zusammenfassung:► Phloridzin (0.5% and 1%) diets significantly reduce the blood glucose levels in BALB/c mice. ► Phloridzin (0.1%) diet altered of the hepatic gene expressions related to carbohydrate and fatty acid metabolism in mice. ► Phloridzin (0.5%) diets suppressed the gene expressions related to citrate cycle, gluconeogenesis and fatty acid metabolism. ► Phloridzin reduces the blood glucose levels and the hepatic gene expressions associated with some metabolic functions in mice. We previously showed that a diet containing phloridzin suppressed the blood glucose levels in streptozotocin-induced diabetic mice most likely by inhibiting glucose absorption from the small intestine. In this study, we showed that 0.5% and 1% phloridzin diets significantly reduce the blood glucose levels in healthy normal BALB/c mice after 7days of feeding. The 0.1% phloridzin diet did not suppress blood glucose levels but induced the alteration of the hepatic gene expressions related to carbohydrate and fatty acid metabolism in mice after 14days. Ingenuity Pathway Analysis showed that 0.5% and 1% phloridzin diets suppressed the hepatic gene expressions related to the citrate cycle, gluconeogenesis, fatty acid metabolism, and valine, leucine, and isoleucine degradation in mice when compared with mice fed a control diet after 14days. Thus the diet containing phloridzin reduces the blood glucose levels and the hepatic gene expressions associated with some metabolic functions in mice.
ISSN:0278-6915
1873-6351
DOI:10.1016/j.fct.2012.04.017