Poster Topical Area: Energy and Macronutrient Metabolism
Location: Hall D
Poster Board Number: 466
In this study, we investigated whether modification of chestnut starch by amylosucrase from Deinococcus geothermalis (DGAS) increases the resistant starch (RS) content and regulates the obesity. Furthermore, we aimed to elucidate the mechanism to prevent the fat accumulation by prebiotic activity of RS from chestnut starch.
Chestnut starch was enzymatically modified by DGAS. In vitro analyses including Englyst's assay and determination of the starch digestive pattern by mammalian mucosal α-glucosidases were used to determine the ratio of slowly digestible starch and RS in enzymatically modified chestnut starch. In an in vivo study, high-fat diet (45% kcal from fat, HFD)-induced obese C57BL/6 model mice were applied to investigate the physiological effect of DGAS-modified chestnut starch.
Enzymatic modification of chestnut native starch by DGAS increased the proportion of RS, rendering it unavailable for hydrolysis by small-intestinal mucosal α-glucosidases. Structurally, the amylose ratio and branch-chain of amylopectin in chestnut starch were increased by DGAS treatment. Furthermore, supplementation of DGAS-modified chestnut starch to obese mice significantly reduced features of obesity compared to HFD- or NCS-fed mice.
DGAS-modification of chestnut starch increases non-digestible RS and this ameliorates diet-induced obesity via GPR43-mediated suppression of insulin signaling, thereby presumably reducing fat accumulation in white adipose tissue.
Seongnam, Kyonggi-do, Republic of Korea