title: Neuroendocrinology of insulin resistance: metabolic and endocrine aspects of adiposity.
abstract: 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-gamma). 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.
authors: Department of Neuroendocrinology, University of Groningen, P.O. Box 14, 9750 AA Haren, The Netherlands. g.van.dijk@biol.rug.nl
authors: Gertjan
authors: G
authors: van Dijk
authors: Koert
authors: K
authors: de Vries
authors: Lambertus
authors: L
authors: Benthem
authors: Csaba
authors: C
authors: Nyakas
authors: Bauke
authors: B
authors: Buwalda
authors: Anton J W
authors: AJ
authors: Scheurink
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism*; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D009765:Obesity / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified