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    <identifier>10.57760/sciencedb.16045</identifier>
    <datestamp>2024-11-01T09:22:57Z</datestamp>
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  <dc:date>2024-11-01</dc:date>
  <dc:title>Alginate Oligosaccharides Improve Glycolipid Metabolism Disorder</dc:title>
  <dc:identifier>doi:10.57760/sciencedb.16045</dc:identifier>
  <dc:language>en</dc:language>
  <dc:description>	Diabetes, fatty liver, and other disorder of glycolipid diseases threaten human health. Alginate oligosaccharides (AOS) are derived from brown alga by alginate degradation. AOS has many biological activities and is easier to be absorbed. In the present study, the potential beneficial effects of AOS on improving the disorder of glycolipid metabolism by regulating gut microflora was investigated. The results show that AOS improves type 2 diabetes (T2DM) by reducing blood glucose, total cholesterol, and total triglycerides and regulating the expression of PEPCK, G6Pase, HMGCR, CYP7A1, LDLR, SMYD3, SREBP-2 in high-fat-diet-induced mice, and regulates the expression of SREBP-2, HMGCR, and SMYD3 in oleic acid-induced HepG2. Besides, AOS adjusts the abundance of gut microflora in T2DM mice and improves the production of short-chain fatty acids (SCFAs) at the same time. Furthermore, AOS can be efficiently degraded and utilized by the gut microflora of nonalcoholic fatty liver (NAFLD) patients faces while regulating the production of SCFAs and effectively promoting the proliferation of intestinal lactobacillus. To our best knowledge, this study is the first to illustrate that AOS improves glycolipid metabolism disorder by regulating intestinal microflora in both animal model and clinical patient feces.</dc:description>
  <dc:subject>Alginate oligosaccharides; glycolipid metabolism; intestinal flora; short-chain fatty acids; type 2 diabetes; nonalcoholic fatty liver</dc:subject>
  <dc:creator>xiaomin Feng</dc:creator>
  <dc:rights>PUBLIC</dc:rights>
  <dc:rights>https://creativecommons.org/licenses/by-nc-nd/4.0/</dc:rights>
  <dc:type>dataset</dc:type>
  <dc:publisher>Science Data Bank</dc:publisher>
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