title: Diabetes, obesity, and the brain.
abstract: Recent evidence suggests a key role for the brain in the control of both body fat content and glucose metabolism. Neuronal systems that regulate energy intake, energy expenditure, and endogenous glucose production sense and respond to input from hormonal and nutrient-related signals that convey information regarding both body energy stores and current energy availability. In response to this input, adaptive changes occur that promote energy homeostasis and the maintenance of blood glucose levels in the normal range. Defects in this control system are implicated in the link between obesity and type 2 diabetes.
authors.affiliation: Division of Metabolism, Endocrinology and Nutrition, University of Washington, Seattle, WA 98110, USA. mschwart@u.washington.edu
authors.forename: Michael W
authors.initials: MW
authors.lastname: Schwartz
authors.forename: Daniel
authors.initials: D
authors.lastname: Porte
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism*; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D004435:Eating; D004734:Energy Metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D007031:Hypothalamus / Q000378:metabolism; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D020738:Leptin / Q000235:genetics / Q000378:metabolism; D008060:Lipodystrophy / Q000503:physiopathology; D008954:Models, Biological; D009474:Neurons / Q000502:physiology; D009765:Obesity / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D011972:Receptor, Insulin / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D005230:Fatty Acids, Nonesterified; D007328:Insulin; D020738:Leptin; D011972:Receptor, Insulin; D005947:Glucose