title: Interleukin-32β ameliorates metabolic disorder and liver damage in mice fed high-fat diet.
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.
authors: College of Pharmacy, Chungbuk National University, Heungduk-gu, Cheongju, Chungbuk, Republic of Korea.
authors: Dong Hun
authors: DH
authors: Lee
authors: Ji Eun
authors: JE
authors: Hong
authors: Hyung-Mun
authors: HM
authors: Yun
authors: Chul Ju
authors: CJ
authors: Hwang
authors: Ju Ho
authors: JH
authors: Park
authors: Sang Bae
authors: SB
authors: Han
authors: Do Young
authors: DY
authors: Yoon
authors: Min Jong
authors: MJ
authors: Song
authors: Jin Tae
authors: JT
authors: Hong
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D000818:Animals; D001835:Body Weight / Q000187:drug effects / Q000235:genetics; D016207:Cytokines / Q000378:metabolism; D059305:Diet, High-Fat; D005234:Fatty Liver / Q000235:genetics* / Q000378:metabolism; D056945:Hep G2 Cells; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000378:metabolism; D007378:Interleukins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000502:physiology*; D050356:Lipid Metabolism / Q000235:genetics; D008297:Male; D008659:Metabolic Diseases / Q000235:genetics* / Q000378:metabolism; D051379:Mice; D008822:Mice, Transgenic; D047495:PPAR gamma / Q000378:metabolism; D034741:RNA, Small Interfering / Q000494:pharmacology
chemical_list: D016207:Cytokines; D007378:Interleukins; D047495:PPAR gamma; D034741:RNA, Small Interfering; C569037:interleukin-32, mouse; D055372:AMP-Activated Protein Kinases