Abstract
ScopePreviously, we showed that the intake of a persimmon peel (PP) extract altered hepatic gene expression associated with the insulin signaling pathway and enhanced tyrosine phosphorylation of insulin receptors in nonobese type 2 diabetic Goto‐Kakizaki rats. Our objective was to evaluate the effect of fat‐soluble PP extract on obese type 2 diabetic KK‐Ay mice with insulin resistance.Methods and results KK‐Ay mice were fed a diet mixed with 0.1% of the extract for 8 weeks. The total ketone body levels in the plasma of PP extract‐fed mice were significantly lower than those in the normal diet‐fed mice. Hepatic nonesterified palmitic acid content was higher in the PP extract‐fed mice than in normal diet‐fed mice. The hepatic gene expression profiles of the treated mice indicated upregulation of fatty acid synthesis and downregulation of inflammation‐associated genes, predicting SREBP‐1c and PPARγ activation.ConclusionThese results suggest that the PP extract enhances hepatic fatty acid synthesis via SREBP‐1c and PPARγ, as well as anti‐inflammatory activity in KK‐Ay mice.
Highlights
| MATERIALS AND METHODSThe persimmon peel (PP) extract was prepared as described previously (Izuchi et al, 2009). In brief, dried PP powder was extracted with ethanol; a methyl tert-butyl ether-soluble fraction of the extract was collected and evaporated
The incidence of type 2 diabetes mellitus induced by obesity is increasing; certain approaches are required to prevent or reduce its deterioration
These results suggest that persimmon peel (PP) extract has the potential to reduce insulin resistance in Goto- Kakizaki (GK) rats
Summary
The PP extract was prepared as described previously (Izuchi et al, 2009). In brief, dried PP powder was extracted with ethanol; a methyl tert-butyl ether-soluble fraction of the extract was collected and evaporated. TA B L E 1 Plasma biochemical parameters and hepatic nonesterified fatty acid levels in KK-Ay mice administered with PP extract for 8 weeks. We evaluated the effects of PP extract administration on plasma biochemical parameters and nonesterified fatty acids of KK-Ay mice (Table 1). The predicted transcription factors that activated DEGs upstream after PP extract administration were SREBP (sterol regulatory element-binding protein) -1 and -2 and PPARγ (peroxisome proliferator-activated receptor gamma). The predicted transcription factors that inhibited DEGs upstream after PP extract administration were NR3C1 (nuclear receptor subfamily 3, group C, member 1), STAT3 (signal transducer and activator of transcription 3), CREB1 (cAMP responsive element binding protein 1), NF-κB (nuclear factor- kappa B) (Table 2)
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