The adipocyte-myocyte axis in insulin resistance

Trends Endocrinol Metab. 2006 Dec;17(10):416-22. doi: 10.1016/j.tem.2006.10.010. Epub 2006 Nov 3.

Abstract

Insulin resistance in skeletal muscle is linked to an elevated adipose tissue mass, as is found in obesity, but can also be observed in lipodystrophy, in which adipose tissue is greatly reduced. Adipose tissue releases endocrine and metabolic mediators and is actively involved in crosstalk with skeletal muscle, a process that precedes and underlies the development of insulin resistance in muscles. Adipokines including tumor necrosis factor alpha, interleukin-6, leptin and adiponectin influence insulin signaling in skeletal muscle. Free fatty acids, their metabolites and ectopic fat in muscle also contribute to insulin resistance. Recent research indicates inflammation, endoplasmic reticulum stress and oxidative stress could be underlying mechanisms at the center of the development of insulin resistance. Insights into the role of macrophages in adipose tissue add to the complicated interplay between adipose tissue and skeletal muscle.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • AMP-Activated Protein Kinases
  • Adipocytes / physiology*
  • Adipose Tissue / cytology
  • Animals
  • Fatty Acids, Nonesterified / physiology
  • Humans
  • Insulin Resistance*
  • Lipodystrophy / complications
  • Macrophages / cytology
  • Macrophages / physiology
  • Models, Biological
  • Multienzyme Complexes / physiology
  • Muscle Cells / physiology*
  • Muscle, Skeletal / metabolism
  • Protein Serine-Threonine Kinases / physiology

Substances

  • Fatty Acids, Nonesterified
  • Multienzyme Complexes
  • Protein Serine-Threonine Kinases
  • AMP-Activated Protein Kinases