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Small heterodimer partner (SHP) deficiency protects myocardia from lipid accumulation in high fat diet-fed mice

 Jung Hun Ohn  ;  Ji Yeon Hwang  ;  Min Kyong Moon  ;  Hwa Young Ahn  ;  Hwan Hee Kim  ;  Young Do Koo  ;  Kwang-Il Kim  ;  Hyuk Jae Chang  ;  Hye Seung Lee  ;  Hak Chul Jang  ;  Young Joo Park 
 PLOS ONE, Vol.12(10) : e0186021, 2017-10 
Journal Title
Issue Date
Acyl-CoA Dehydrogenase / genetics ; Acyl-CoA Dehydrogenase / metabolism ; Acyl-CoA Dehydrogenase, Long-Chain / deficiency ; Acyl-CoA Dehydrogenase, Long-Chain / genetics ; Acyl-CoA Dehydrogenase, Long-Chain / metabolism ; Animals ; CD36 Antigens / genetics ; CD36 Antigens / metabolism ; Congenital Bone Marrow Failure Syndromes ; Cytokines / genetics ; Cytokines / metabolism ; Diet, High-Fat ; Fatty Acids / metabolism ; Gene Expression Profiling ; Lipid Metabolism, Inborn Errors / genetics ; Lipid Metabolism, Inborn Errors / metabolism ; Lipogenesis / genetics* ; Liver / metabolism ; Liver / pathology ; Male ; Mice ; Mice, Knockout ; Mitochondrial Diseases / genetics ; Mitochondrial Diseases / metabolism ; Muscular Diseases / genetics ; Muscular Diseases / metabolism ; Myocardium / metabolism* ; Myocardium / pathology ; Obesity / etiology ; Obesity / genetics* ; Obesity / metabolism ; Obesity / pathology ; Oligonucleotide Array Sequence Analysis ; PPAR alpha / genetics ; PPAR alpha / metabolism ; PPAR gamma / genetics ; PPAR gamma / metabolism ; Protective Factors ; Receptors, Cytoplasmic and Nuclear / deficiency ; Receptors, Cytoplasmic and Nuclear / genetics* ; Signal Transduction ; Transcriptome*
The small heterodimer partner (SHP) regulates fatty acid oxidation and lipogenesis in the liver by regulating peroxisome proliferator-activated receptor (PPAR) γ expression. SHP is also abundantly expressed in the myocardium. We investigated the effect of SHP expression on myocardia assessing not only heart structure and function but also lipid metabolism and related gene expression in a SHP deletion animal model. Transcriptional profiling with a microarray revealed that genes participating in cell growth, cytokine signalling, phospholipid metabolism, and extracellular matrix are up-regulated in the myocardia of SHP knockout (KO) mice compared to those of wild-type (WT) mice (nominal p value < 0.05). Consistent with these gene expression changes, the left ventricular masses of SHP KO mice were significantly higher than WT mice (76.8 ± 20.5 mg vs. 52.8 ± 6.8 mg, P = 0.0093). After 12 weeks of high fat diet (HFD), SHP KO mice gained less weight and exhibited less elevation in serum-free fatty acid and less ectopic lipid accumulation in the myocardium than WT mice. According to microarray analysis, genes regulated by PPARγ1 and PPARα were down-regulated in myocardia of SHP KO mice compared to their expression in WT mice after HFD, suggesting that the reduction in lipid accumulation in the myocardium resulted from a decrease in lipogenesis regulated by PPARγ. We confirmed the reduced expression of PPARγ1 and PPARα target genes such as CD36, medium-chain acyl-CoA dehydrogenase, long-chain acyl-CoA dehydrogenase, and very long-chain acyl-CoA dehydrogenase by SHP KO after HFD.
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1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Chang, Hyuk-Jae(장혁재) ORCID logo https://orcid.org/0000-0002-6139-7545
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