Neuroendocrinology of insulin resistance: Metabolic and endocrine aspects of adiposity

Gertjan Van Dijk, Koert De Vries, Lambertus Benthem, Csaba Nyakas, Bauke Buwalda, Anton J.W. Scheurink

Research output: Contribution to journalArticle

21 Citations (Scopus)


Abdominal obesity is a major risk factor to attract the insulin resistance syndrome. It is proposed that abdominal obesity exposes the liver to elevated levels of free fatty acids, which activate a neuroendocrine reflex, leading to increased circulating levels of glucocorticoids. Besides directly attenuating peripheral insulin signaling, glucocorticoids oppose the activity of central nervous regulatory systems that stimulate insulin action. Among the factors that promote insulin action is leptin. Leptin regulates peripheral fuel partitioning and insulin action mainly through hypothalamic neuronal networks, which in turn, regulate endocrine activity of adipose tissue in a way comparable to thiazolidinediones. These are a class of insulin-sensitizing drugs, which exert their antidiabetic effects through the gamma isoform of peroxisome proliferator-activated receptor (PPAR-γ). Since glucocorticoids oppose leptin action at several levels of control (including the central nervous system, CNS), it is argued that subjects easily develop obesity and associated metabolic disorders.

Original languageEnglish
Pages (from-to)31-42
Number of pages12
JournalEuropean Journal of Pharmacology
Issue number1-3
Publication statusPublished - Nov 7 2003


  • Adiponectin
  • Fatty acid
  • Glucocorticoid
  • Hypothalamus
  • Leptin
  • PPARγ (peroxisome proliferator-activated receptor)

ASJC Scopus subject areas

  • Pharmacology

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