Adipocyte dysfunctions linking obesity to insulin resistance and type 2 diabetes

Nat Rev Mol Cell Biol. 2008 May;9(5):367-77. doi: 10.1038/nrm2391.


Acquired resistance to the action of insulin to stimulate glucose transport in skeletal muscle is associated with obesity and promotes the development of type 2 diabetes. In skeletal muscle, insulin resistance can result from high levels of circulating fatty acids that disrupt insulin signalling pathways. However, the severity of insulin resistance varies greatly among obese people. Here we postulate that this variability might reflect differences in levels of lipid-droplet proteins that promote the sequestration of fatty acids within adipocytes in the form of triglycerides, thereby lowering exposure of skeletal muscle to the inhibitory effects of fatty acids.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Adipocytes / cytology
  • Adipocytes / physiology*
  • Adipose Tissue / physiology
  • Animals
  • Diabetes Mellitus, Type 2 / physiopathology*
  • Humans
  • Inflammation / physiopathology
  • Insulin / metabolism
  • Insulin Resistance / physiology*
  • Lipolysis / physiology
  • Mitochondria / metabolism
  • Muscle, Skeletal / physiology
  • Obesity / physiopathology*
  • PPAR gamma / genetics
  • PPAR gamma / metabolism
  • Signal Transduction / physiology
  • Triglycerides / metabolism
  • Tumor Necrosis Factor-alpha / metabolism


  • Insulin
  • PPAR gamma
  • Triglycerides
  • Tumor Necrosis Factor-alpha