Small heterodimer partner (SHP) contributes to insulin resistance in cardiomyocytes

Ricardo Rodriguez-Calvo*, Dipanjan Chanda, Yvonne Oligschlaeger, Marie Miglianico, Will A. Coumans, Emma Barroso, Marta Tajes, Joost J. F. P. Luiken, Jan F. C. Glatz, Manuel Vazquez-Carrera, Dietbert Neumann

*Corresponding author for this work

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Abstract

Small heterodimer partner (SHP) is an atypical nuclear receptor expressed in heart that has been shown to inhibit the hypertrophic response. Here, we assessed the role of SHP in cardiac metabolism and inflammation. Mice fed a high-fat diet (HFD) displayed glucose intolerance accompanied by increased cardiac mRNA levels of Shp. In HL-1 cardiomyocytes, SHP overexpression inhibited both basal and insulin-stimulated glucose uptake and impaired the insulin signalling pathway (evidenced by reduced ART and AS160 phosphorylation), similar to insulin resistant cells generated by high palmitate/high insulin treatment (HP/HI; 500 mu M/100 nM). In addition, SHP overexpression increased Socs3 mRNA and reduced IRS-1 protein levels. SHP overexpression also induced Cd36 expression (similar to 6.2 fold; p

Original languageEnglish
Pages (from-to)541-551
Number of pages11
JournalBiochimica et Biophysica Acta-Molecular and Cell Biology of Lipids
Volume1862
Issue number5
DOIs
Publication statusPublished - May 2017

Keywords

  • Insulin resistance
  • Diabetic cardiomyopathy
  • Nuclear receptors
  • Small heterodimer partner
  • ORPHAN NUCLEAR RECEPTOR
  • FATTY-ACID TRANSPORT
  • FACTOR-KAPPA-B
  • ACTIVATED RECEPTOR
  • CARDIAC-HYPERTROPHY
  • HEPATIC GLUCONEOGENESIS
  • DOWN-REGULATION
  • HEART-DISEASE
  • MOUSE MODELS
  • MUSCLE-CELLS

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