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- Title
Interleukin-32β ameliorates metabolic disorder and liver damage in mice fed high-fat diet.
- Authors
Lee, Dong Hun; Hong, Ji Eun; Yun, Hyung‐Mun; Hwang, Chul Ju; Park, Ju Ho; Han, Sang Bae; Yoon, Do Young; Song, Min Jong; Hong, Jin Tae
- Abstract
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.
- Subjects
INTERLEUKIN-32; METABOLIC disorders; LIVER diseases; HIGH-fat diet; LABORATORY mice
- Publication
Obesity (19307381), 2015, Vol 23, Issue 3, p615
- ISSN
1930-7381
- Publication type
Article
- DOI
10.1002/oby.21001