1791-P: A New Antidiabetic Monomers Composition against Insulin Resistance via Modulation of Bacteria-Cometabolism-Inflammation-Diabetes Axis

Intestinal flora disturbance can cause chronic inflammation, which leads to metabolic disorders such as obesity and insulin resistance. Insulin resistance is the main pathogenesis of T2DM. Recent studies indicated that changes of host-microbiome metabolic axis also play an important role in the path...

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Veröffentlicht in:Diabetes (New York, N.Y.) N.Y.), 2019-06, Vol.68 (Supplement_1)
Hauptverfasser: HAN, LIN, ZHAO, LINHUA, ZHANG, MINGLIANG, DI, SHA, GAO, ZEZHENG, WANG, XINMIAO, WU, HAORAN, JIA, WEIPING, TONG, XIAOLIN
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Sprache:eng
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Zusammenfassung:Intestinal flora disturbance can cause chronic inflammation, which leads to metabolic disorders such as obesity and insulin resistance. Insulin resistance is the main pathogenesis of T2DM. Recent studies indicated that changes of host-microbiome metabolic axis also play an important role in the pathogenic process. Based on previous experiments and literatures, Baicalin, Berberine, Puerarin, Paeoniflorin, Mangiferin, Ginsenoside Rb1 and other effective hypoglycemic compounds were combined to be a new antidiabetic monomers composition (AMC). C57BL/6J mice were used to establish T2DM models with high-fat diet (HFD). The mice in AMC group were observed with an effective weight loss, reduced blood glucose, lower insulin level and content of cholesterol and LDL, and increased metabolic rate and energy consumption compared with HFD group, and impaired glucose tolerance was also alleviated treated with AMC. Further studies showed that AMC improved the disordered of intestinal flora, especially the increase of beneficial bacteria such as Akkermansia, and the decrease of harmful bacteria such as Bacteroides and Collinsella. Afterwards, host-microbial metabolome, inducing inflammatory response, such as Ethylmethylacetic acid and Hydroxyphenyllactic acid reduced. As a result, the level of inflammation in the body decreased as well, and the suppressed signaling pathways related to insulin resistance alleviated. In conclusion, we explored the potential mechanism of AMC against insulin resistance via modulation of bacteria-cometabolism-inflammation-diabetes axis.
ISSN:0012-1797
1939-327X
DOI:10.2337/db19-1791-P