The adipocyte-myocyte axis in insulin resistance.
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.
Sell
Henrike
H
Institute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center, Düsseldorf, Germany.
Dietze-Schroeder
Daniela
D
Eckel
Jürgen
J
D055372:AMP-Activated Protein Kinases; D017667:Adipocytes / Q000502:physiology*; D000273:Adipose Tissue / Q000166:cytology; D000818:Animals; D005230:Fatty Acids, Nonesterified / Q000502:physiology; D006801:Humans; D007333:Insulin Resistance; D008060:Lipodystrophy / Q000150:complications; D008264:Macrophages / Q000166:cytology / Q000502:physiology; D008954:Models, Biological; D009097:Multienzyme Complexes / Q000502:physiology; D032342:Muscle Cells / Q000502:physiology*; D018482:Muscle, Skeletal / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000502:physiology
D005230:Fatty Acids, Nonesterified; D009097:Multienzyme Complexes; D017346:Protein Serine-Threonine Kinases; D055372:AMP-Activated Protein Kinases