Insulin causes fatty acid transport protein translocation and enhanced fatty acid uptake in adipocytes

Dev Cell. 2002 Apr;2(4):477-88. doi: 10.1016/s1534-5807(02)00143-0.

Abstract

Fatty acid uptake into 3T3 L1 adipocytes is predominantly transporter mediated. Here we show that, during 3T3 L1 adipocyte differentiation, expression of fatty acid transport proteins (FATPs) 1 and 4 is induced. Using subcellular membrane fractionation and immunofluorescence microscopy, we demonstrate that, in adipocytes, insulin induces plasma membrane translocation of FATPs from an intracellular perinuclear compartment to the plasma membrane. This translocation was observed within minutes of insulin treatment and was paralleled by an increase in long chain fatty acid (LCFA) uptake. In contrast, treatment with TNF-alpha inhibited basal and insulin-induced LCFA uptake and reduced FATP1 and -4 levels. Thus, hormonal regulation of FATP activity may play an important role in energy homeostasis and metabolic disorders such as type 2 diabetes.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 3T3 Cells / cytology
  • 3T3 Cells / metabolism
  • Adipocytes / drug effects
  • Adipocytes / metabolism*
  • Animals
  • Antineoplastic Agents / pharmacology
  • Carrier Proteins / metabolism*
  • Cell Differentiation / physiology
  • Cell Membrane / metabolism
  • Cell Nucleus / metabolism
  • Energy Metabolism / physiology
  • Fatty Acid Transport Proteins
  • Fatty Acids / pharmacokinetics*
  • Female
  • Hypoglycemic Agents / pharmacology*
  • Insulin / pharmacology*
  • Male
  • Membrane Transport Proteins*
  • Mice
  • Mice, Inbred BALB C
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Antineoplastic Agents
  • Carrier Proteins
  • Fatty Acid Transport Proteins
  • Fatty Acids
  • Hypoglycemic Agents
  • Insulin
  • Membrane Transport Proteins
  • Slc27a1 protein, mouse
  • Slc27a4 protein, mouse
  • Tumor Necrosis Factor-alpha