Amelioration of obesity in high-fat diet-fed mice by chestnut starch modified by amylosucrase from Deinococcus geothermalis

The ameliorative effect of enzymatically modified chestnut starch on high-fat diet (HFD)-induced obesity in a mouse model and the underlying mechanism were investigated. Chestnut starch was enzymatically modified by amylosucrase from Deinococcus geothermalis (DGAS). In vitro analyses including Englyst's assay and determination of the starch digestive pattern to investigate starch digestibility revealed that chestnut starch naturally contained higher slowly digestible starch and resistant starch than corn starch. Modification of chestnut native starch by DGAS increased the proportion of resistant starch, rendering it unavailable for catalysis by small-intestinal mucosal α-glucosidase. The amylose ratio and branch-chain of amylopectin in chestnut starch were increased by DGAS. In an in vivo study, HFD (45% kcal from fat)-induced obese C57BL/6 model mice were orally administered DGAS-modified chestnut starch at the dose of 1500 mg/kg b·w for 10 weeks. Supplementation of DGAS-modified chestnut starch to obese mice significantly reduced features of obesity as compared with HFD- or native chestnut starch-fed mice. Food intake and the gut hormones PYY and GLP-1 were not significantly changed. However, we found that feeding DGAS-modified chestnut starch led to a significant increase in empty cecum weight, indicating short-chain fatty acid production in the cecum. Additionally, DGAS-modified chestnut starch induced the short-chain fatty acid receptor GPR43-mediated suppression of insulin signaling. Changes in all these factors were resistant starch content-dependent. In conclusion, DGAS modification of chestnut starch increases non-digestible resistant starch and this ameliorates diet-induced obesity via GPR43-mediated suppression of insulin signaling, thereby presumably reducing fat accumulation in white adipose tissue.