The role of adipocytokines and neurohormonal dysregulation in metabolic syndrome

Curr Diabetes Rev. 2006 Nov;2(4):397-407. doi: 10.2174/1573399810602040397.


Metabolic syndrome, also known as the insulin resistance syndrome (IRS), dysmetabolic syndrome or syndrome X, is a burgeoning global epidemic. This constellation of risk factors, namely glucose intolerance, hypertension, dyslipidemia (high triglyceride and low HDL cholesterol), central obesity, pro-inflammatory and prothrombotic state, culminating to the development of premature cardiovascular and renal disease, has significant impact on life expectancy, societal productivity and quality of life. The underlying mechanism of this complex syndrome remains to be elucidated. In recent years, light has been shed on the roles of neuroendocrine system and adipocytokines on the pathogenesis of IRS. In this review, we summarize the possible links between insulin and various hormones (growth hormones (GH), catecholamines, glucocorticoids and sex hormones), partly mediated through visceral adiposity and adipocytokines (notably adiponectin, leptin, resistin, visfatin, tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6)) in the pathogenesis of this syndrome.

Publication types

  • Review

MeSH terms

  • Adipokines / physiology*
  • Adiponectin / physiology*
  • Aging
  • Animals
  • Diabetes Mellitus, Type 2 / physiopathology*
  • Glucose Intolerance / physiopathology
  • Growth Hormone / physiology
  • Human Growth Hormone / physiology
  • Humans
  • Insulin Resistance
  • Interleukin-6 / physiology
  • Metabolic Syndrome / physiopathology*
  • Models, Biological
  • Tumor Necrosis Factor-alpha / physiology


  • Adipokines
  • Adiponectin
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Human Growth Hormone
  • Growth Hormone