Document Detail


Sixteen years and counting: an update on leptin in energy balance.
MedLine Citation:
PMID:  21633176     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cloned in 1994, the ob gene encodes the protein hormone leptin, which is produced and secreted by white adipose tissue. Since its discovery, leptin has been found to have profound effects on behavior, metabolic rate, endocrine axes, and glucose fluxes. Leptin deficiency in mice and humans causes morbid obesity, diabetes, and various neuroendocrine anomalies, and replacement leads to decreased food intake, normalized glucose homeostasis, and increased energy expenditure. Here, we provide an update on the most current understanding of leptin-sensitive neural pathways in terms of both anatomical organization and physiological roles.
Authors:
Laurent Gautron; Joel K Elmquist
Related Documents :
12477046 - Fluorescence decay of singlet excited-state of safranine t and its interaction with gro...
9659936 - The inductive properties of mesoderm suggest that the neural crest cells are specified ...
11935176 - Microbial production of vitamin b12.
11746906 - Effect of impurities on the matrix-assisted laser desorption/ionization mass spectra of...
12789546 - Upregulation of glucose-dependent insulinotropic polypeptide and its receptor in the re...
6104626 - The dual effect of alloxan modulated by 3-o-methylglucose or somatostatin on insulin se...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2011-06-01
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  121     ISSN:  1558-8238     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-06-02     Completed Date:  2011-08-17     Revised Date:  2012-02-07    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2087-93     Citation Subset:  AIM; IM    
Affiliation:
Department of Internal Medicine, Division of Hypothalamic Research, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological
Adipose Tissue, White / secretion
Animals
Body Weight / physiology
Brain / physiology
Disease Models, Animal
Energy Metabolism / physiology*
Feeding Behavior / physiology
Glucose / metabolism
Humans
Hypothalamus / physiology
Leptin / deficiency,  genetics,  physiology*
Mice
Mice, Obese
Models, Biological
Overnutrition / physiopathology
Pro-Opiomelanocortin / physiology
Receptor, Melanocortin, Type 4 / physiology
Receptors, Leptin / deficiency,  genetics,  physiology*
Starvation / physiopathology
Sympathetic Nervous System / physiology
Chemical
Reg. No./Substance:
0/Leptin; 0/Receptor, Melanocortin, Type 4; 0/Receptors, Leptin; 50-99-7/Glucose; 66796-54-1/Pro-Opiomelanocortin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Genetic approaches to understanding human obesity.
Next Document:  Adipose tissue remodeling and obesity.