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Published on: April 26, 2019
Interleukin-32β ameliorates metabolic disorder and liver damage in mice fed high-fat diet
Dong Hun Lee1, Ji Eun Hong, Hyung-Mun Yun
1College of Pharmacy, Chungbuk National University, Heungduk-gu, Cheongju, Chungbuk, Republic of Korea.
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.
