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Published on: April 26, 2019
Resistant starch based on starch-lysine complex alleviated high-fat-diet-induced hyperglycemia via regulating gut
Leyu Yang1, Yukun Yang1, Fan Wang2
1Institute of Nutrition and Health, School of Public Health, Qingdao University, Qingdao, China.
Abstract:
The formation of starch-lysine complex was shown to increase the resistant starch (RS) content and thermal stability of corn starch. In this work, the effects of RS, based on starch-lysine complex, on high-fat diet (HFD)-induced hyperglycemia in mice and its potential mechanisms were studied. Starch-lysine complex was prepared by the heat-moisture treatment of corn starch and lysine and characterized about its RS content, pasting viscosity, complex index, X-ray diffraction and differential scanning calorimetry pattern. Forty male C57BL/6 J mice were distributed in random to four groups: the control, model (using HFD), RS (HFD containing 8.4% RS based on starch-lysine complex), and metformin group. After 9-week intervention, the blood glucose and lipid indices were evaluated; the cecal metabolites and gut microbiota were determined by ultra-performance liquid chromatography connected with tandem mass spectrometry and 16S rRNA sequencing. The RS group possessed significantly lower fasting blood glucose and HOMA-IR (7.1 ± 0.7 mmol/l vs. 9.1 ± 0.9 mmol/l, P < 0.001; 22.7 ± 2.4 vs. 27.6 ± 2.4, P = 0.002) and higher HOMA-β than the HFD group. RS intervention significantly increased the bacterial genera including Blautia, Rikenellaceae_RC9_gut_group, and Lachnospiraceae_UCG_006, which were inversely associated with fasting blood glucose or HOMA-IR (Lachnospiraceae_UCG_006 was positively associated with HOMA-β). These differential gut bacteria were associated with several differential cecal metabolites such as arginylleucine and DG(PGF1α/0:0/2:0), which were associated with blood glucose parameters. In conclusion, RS based on starch-lysine complex alleviated HFD-induced hyperglycemia in mice by modulating gut bacteria including Blautia, Rikenellaceae_RC9_gut_group, and Lachnospiraceae_UCG_006 and cecal metabolites.
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