Laminaria japonica polysaccharide prevents high-fat-diet-induced insulin resistance in mice via regulating gut microbiota

Insulin resistance has become a worldwide nutrition and metabolic health problem due to the lack of effective protective agents. Laminaria japonica is a well-known marine vegetable. Purified Laminaria japonica polysaccharide (LJP61A) can inhibit atherosclerosis in high-fat-diet (HFD)-fed mice via am...

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Bibliographic Details
Published in:Food & function 2021-06, Vol.12 (12), p.5260-5273
Main Authors: Li, Qiang-Ming, Zha, Xue-Qiang, Zhang, Wei-Nan, Liu, Jian, Pan, Li-Hua, Luo, Jian-Ping
Format: Article
Language:English
Subjects:
Animals
Arteriosclerosis
Atherosclerosis
Atherosclerosis - prevention & control
Diet
Diet, High-Fat - adverse effects
Dietary Carbohydrates - pharmacology
Dysbacteriosis
Dysbiosis
Endotoxemia
Feces - microbiology
Gastrointestinal Microbiome - drug effects
Goblet cells
High fat diet
Homeostasis
Inflammation
Insulin
Insulin Resistance
Intestinal microflora
Laminaria - metabolism
Laminaria japonica
Male
Metabolic Diseases - pathology
Metabolic Diseases - prevention & control
Metabolic disorders
Metabolism
Mice
Mice, Inbred C57BL
Microbiota
Mucin
Nutrition
Obesity
Obesity - prevention & control
Permeability
Polysaccharides
Polysaccharides - pharmacology
Reduction
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Summary:Insulin resistance has become a worldwide nutrition and metabolic health problem due to the lack of effective protective agents. Laminaria japonica is a well-known marine vegetable. Purified Laminaria japonica polysaccharide (LJP61A) can inhibit atherosclerosis in high-fat-diet (HFD)-fed mice via ameliorating insulin resistance. In this study, we aimed to clarify the mechanism by which LJP61A ameliorates HFD-induced insulin resistance. The results indicated that HFD-induced insulin resistance, obesity, systematic inflammation, metabolic endotoxemia, and gut permeability in mice could be reduced by LJP61A. Gut microbiota analysis showed that the gut microbiota dysbiosis of HFD-fed mice, especially the reduction in mucin-degrading Akkermansia, could be reversed by LJP61A. Additionally, the reduction in mucin-producing goblet cells in HFD-fed mice could also be reversed by LJP61A. Moreover, insulin resistance, obesity, systematic inflammation, metabolic endotoxemia, and gut microbiota dysbiosis in HFD-fed mice could also be alleviated by faecal transplant from LJP61A-treated mice. Overall, LJP61A might be used as a prebiotic to ameliorate HFD-induced insulin resistance and associated metabolic disorders via regulating gut microbiota, especially Akkermansia.
ISSN:2042-6496
2042-650X
DOI:10.1039/d0fo02100h