Gut Microbiota Dysbiosis Ameliorates in LNK-Deficient Mouse Models with Obesity-Induced Insulin Resistance Improvement

Abstract

Purpose: To investigate the potential role of gut microbiota in obesity-induced insulin resistance (IR). Methods: Four-week-old male C57BL/6 wild-type mice (n = 6) and whole-body SH2 domain-containing adaptor protein (LNK)-deficient in C57BL/6 genetic backgrounds mice (n = 7) were fed with a high-fat diet (HFD, 60% calories from fat) for 16 weeks. The gut microbiota of 13 mice feces samples was analyzed by using a 16 s rRNA sequencing analysis. Results: The structure and composition of the gut microbiota community of WT mice were significantly different from those in the LNK-/- group. The abundance of the lipopolysaccharide (LPS)-producing genus Proteobacteria was increased in WT mice, while some short-chain fatty acid (SCFA)-producing genera in WT groups were significantly lower than in LNK-/- groups (p 0.05). Conclusions: The structure and composition of the intestinal microbiota community of obese WT mice were significantly different from those in the LNK-/- group. The abnormality of the gut microbial structure and composition might interfere with glucolipid metabolism and exacerbate obesity-induced IR by increasing LPS-producing genera while reducing SCFA-producing probiotics.

Keywords

• gut microbiota
• LNK deficiency
• obesity
• insulin resistance