title: Central nervous system mechanisms linking the consumption of palatable high-fat diets to the defense of greater adiposity.
abstract: The central nervous system (CNS) plays key role in the homeostatic regulation of body weight. Satiation and adiposity signals, providing acute and chronic information about available fuel, are produced in the periphery and act in the brain to influence energy intake and expenditure, resulting in the maintenance of stable adiposity. Diet-induced obesity (DIO) does not result from a failure of these central homeostatic circuits. Rather, the threshold for defended adiposity is increased in environments providing ubiquitous access to palatable, high-fat foods, making it difficult to achieve and maintain weight loss. Consequently, mechanisms by which nutritional environments interact with central homeostatic circuits to influence the threshold for defended adiposity represent critical targets for therapeutic intervention.
authors.affiliation: Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45237, USA.
authors.forename: Karen K
authors.initials: KK
authors.lastname: Ryan
authors.forename: Stephen C
authors.initials: SC
authors.lastname: Woods
authors.forename: Randy J
authors.initials: RJ
authors.lastname: Seeley
mesh_terms: D050154:Adiposity / Q000502:physiology*; D000818:Animals; D002490:Central Nervous System / Q000502:physiology*; D004041:Dietary Fats / Q000378:metabolism*; D059865:Endoplasmic Reticulum Stress / Q000502:physiology*; D005523:Food Supply; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D020738:Leptin / Q000378:metabolism; D008954:Models, Biological; D009765:Obesity / Q000453:epidemiology* / Q000503:physiopathology / Q000517:prevention & control*; D011493:Protein Kinase C / Q000378:metabolism
chemical_list: D004041:Dietary Fats; D020738:Leptin; D011493:Protein Kinase C