Hepatic fatty acid biosynthesis in KK‐Ay mice is modulated by administration of persimmon peel extract: A DNA microarray study. Issue 6 (20th July 2018)

• Record Type: Journal Article
• Authors: Izuchi, Ryoichi; Ishijima, Tomoko; Okada, Shinji; Abe, Keiko; Nakai, Yuji
• Is Part Of: Food science & nutrition. Volume 6:Issue 6(2018)
• Page Start: 1657
• Page End: 1663
• Publication Date: 2018-07-20
• Subjects: DNA microarray -- fatty acid biosynthesis -- ketone body -- obese diabetic KK‐Ay mouse -- persimmon peel; Food industry and trade -- Periodicals; Food -- Periodicals; Nutrition -- Periodicals; 664
• DOI: 10.1002/fsn3.728
• Languages: English
• ISSNs: 2048-7177

Abstract

Abstract: Scope: Previously, 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‐A y mice with insulin resistance. Methods and results: KK‐A y 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. Conclusion: These results suggest that the PP extract enhances hepatic fatty acid synthesis via SREBP‐1c and PPARγ, as well as anti‐inflammatory activity in KK‐A y mice. Abstract : Intake of persimmon peel extract altered gene expression of lipid metabolism, including fatty acid biosynthesis, in the liver of diabetic KK‐Ay mice. Moreover, upstream factor analysis predicted that these gene expressions were caused by SREBPs and PPARγ activation.