1. Academic Validation
  2. Leptin improves intestinal flora dysfunction in mice with high-fat diet-induced obesity

Leptin improves intestinal flora dysfunction in mice with high-fat diet-induced obesity

  • J Int Med Res. 2020 Jun;48(6):300060520920062. doi: 10.1177/0300060520920062.
Xiaolin Li 1 Weihong Shi 1 Qinghua Xiong 1 Yungang Hu 1 Xu Qin 1 Guanqun Wan 1 Qi Zeng 1
Affiliations

Affiliation

  • 1 Department of Plastic Maxillofacial Surgery, People's Hospital of Nanchang University, Nanchang, China.
Abstract

Objective: This study investigated the effects of Leptin on intestinal flora and inflammation in mice with high-fat diet (HFD)-induced obesity.

Methods: Mice were fed an HFD for 8 weeks; some were concurrently administered oral Leptin for 4 weeks. Pathological changes in adipose tissue were detected using hematoxylin-eosin staining; endotoxin content in adipose tissue was measured by enzyme-linked immunosorbent assay. Intestinal flora were characterized by 16S Bacterial rDNA sequencing. Levels of Toll-like Receptor 4 (TLR4), nuclear factor-κB inhibitor α (IκB-α), and phosphorylated c-Jun N-terminal kinase (p-JNK) were detected by western blotting.

Results: Mice in the HFD group exhibited weight gain, elevated endotoxin content, and adipocyte hypertrophy, compared with the non-obese control group. Moreover, abundance of bacteria in the Bacteroides genus and community diversity were both reduced in the HFD group; reductions also were observed at corresponding phylum, class, and order levels. Levels of TLR4, IκB-α, and p-JNK were also elevated in the HFD group. Compared with the model group, Leptin administration reduced the weight gain and endotoxin content, while increasing Bacteroides abundance and community diversity; it also reduced the levels of TLR4, IκB-α, and p-JNK.

Conclusion: Leptin administration improved intestinal flora dysfunction and inflammation in mice with HFD-induced obesity.

Keywords

Bacteroides; Leptin; Toll-like receptor 4; adipose tissue; c-Jun N-terminal kinase; high-fat diet; inflammation; intestinal flora; nuclear factor-κB inhibitor α; obesity.

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