Interleukin-6 stimulates lipolysis in porcine adipocytes

Endocrine. 2008 Jun;33(3):261-9. doi: 10.1007/s12020-008-9085-7.

Abstract

Interleukin (IL)-6 stimulates lipolysis in human and rodents adipocytes. However, the mechanism regulating this process is little known. In this study, we demonstrated that IL-6 increased lipolysis in differentiated porcine adipocytes by activation of extracellular signal-related kinase (ERK), which was inhibited by specific ERK inhibitor PD98059. IL-6 treatment did not elevate intracellular cAMP and specific PKA inhibitor H89 did not affect IL-6-induced lipolysis, which suggested that protein kinase A (PKA) pathway was not involved in IL-6-induced lipolysis. Also, the expressions of perilipin A and PPARgamma2 were significantly reduced in response to IL-6 treatment, but the expressions of peroxisome proliferators-activated receptor gamma coactivator-1 alpha (PGC-1alpha), carnitinepalmitoyl-transferase-1 (CPT-1), and uncoupling protein 2 (UCP2) were significantly elevated. In conclusion, these results suggested that chronic high dose of IL-6 directly stimulated lipolysis in porcine adipocytes through activation of ERK, subsequently repressing perilipin A and promoting PGC-1alpha expression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / cytology
  • Adipocytes / drug effects
  • Adipocytes / metabolism*
  • Animals
  • Carrier Proteins
  • Cell Differentiation
  • Cells, Cultured
  • Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Cytokine Receptor gp130 / genetics
  • Cytokine Receptor gp130 / metabolism
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Fatty Acids, Nonesterified / metabolism
  • Female
  • Flavonoids / pharmacology
  • Gene Expression / physiology
  • Interleukin-6 / metabolism*
  • Interleukin-6 / pharmacology
  • Isoquinolines / pharmacology
  • Lipolysis / drug effects
  • Lipolysis / physiology*
  • MAP Kinase Signaling System / drug effects
  • MAP Kinase Signaling System / physiology*
  • Male
  • Oxidation-Reduction
  • PPAR gamma / genetics
  • PPAR gamma / metabolism
  • Perilipin-1
  • Phosphoproteins / genetics
  • Phosphoproteins / metabolism
  • Protein Kinase Inhibitors / pharmacology
  • Sulfonamides / pharmacology
  • Sus scrofa
  • Transcription Factors / genetics
  • Transcription Factors / metabolism

Substances

  • Carrier Proteins
  • Fatty Acids, Nonesterified
  • Flavonoids
  • Interleukin-6
  • Isoquinolines
  • PPAR gamma
  • Perilipin-1
  • Phosphoproteins
  • Protein Kinase Inhibitors
  • Sulfonamides
  • Transcription Factors
  • peroxisome-proliferator-activated receptor-gamma coactivator-1
  • Cytokine Receptor gp130
  • Cyclic AMP-Dependent Protein Kinases
  • Extracellular Signal-Regulated MAP Kinases
  • N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide
  • 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one