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Interleukin‐32β ameliorates metabolic disorder and liver damage in mice fed high‐fat diet
Author(s) -
Lee Dong Hun,
Hong Ji Eun,
Yun HyungMun,
Hwang Chul Ju,
Park Ju Ho,
Han Sang Bae,
Yoon Do Young,
Song Min Jong,
Hong Jin Tae
Publication year - 2015
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.21001
Subject(s) - ampk , endocrinology , medicine , inflammation , steatosis , amp activated protein kinase , immune system , peroxisome proliferator activated receptor , downregulation and upregulation , cytokine , interleukin , lipid metabolism , protein kinase a , chemistry , receptor , kinase , immunology , biochemistry , gene
Objective Chronic excessive food intake leads to energy imbalance, resulting in hepatic steatosis and inflammation. Interleukin‐32 (IL‐32) is known to be a pro‐inflammatory cytokine associated with chronic inflammation and cancer. Therefore, the relationship between IL‐32 and chronic excessive food intake‐induced liver disease was investigated. Methods Male IL‐32β transgenic and wild‐type mice were fed a high‐fat diet (HFD) for 15 weeks. They were compared with wild‐type mice on a standard chow diet. Daily food intake, body and liver weight, serum biochemistry, histopathological analysis of the liver, and hepatic immune response were determined. Results IL‐32β mice on HFD showed lower lipid accumulation, reduced infiltration of immune cells, and lower production of pro‐inflammatory cytokines in the liver. The expression of the peroxisome proliferator‐activated receptor γ (PPARγ) was downregulated and the adenosine 50‐monophosphate (AMP)‐activated protein kinase (AMPK) was activated in the liver of IL‐32β mice compared to wild‐type mice. Furthermore, IL‐32β over‐expression activated the AMPK pathway and IL‐32β downregulation inactivated the AMPK pathway in HepG2 cells under high‐glucose conditions. Conclusions These data suggest that IL‐32β modulates lipid accumulation through inhibition of PPARγ expression and AMPK activation.