Document Detail


Why some of us get fat and what we can do about it.
MedLine Citation:
PMID:  17584845     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
There is a widespread obesity epidemic in the developed world which is having an adverse impact on the health of affected individuals. Many of the afflicted have a genetic predisposition to become obese. These individuals become obese when they over consume highly palatable, calorically dense foods which are readily available at low cost. Once obesity occurs, fewer than 10% of affected individuals can sustain significant weight loss permanently. The hypothesis of this review is that some obesity-prone individuals have an inborn reduction in their ability to sense and respond to inhibitory signals from adipose stores and other organs which should limit their intake of energy when it exceeds their metabolic needs. Furthermore, the physiological processes which drive all of us to seek and ingest food and limit energy expenditure during periods of negative energy balance provide an irresistible drive to regain lost adipose stores in weight-reduced obese individuals. For this reason, prevention of obesity and the identification factors which promote the development of neural pathways which enhance the negative feedback signals from the periphery should be a major focus of ongoing research in this field.
Authors:
Barry E Levin
Related Documents :
15527935 - Neural control of appetite: cross-talk between homeostatic and non-homeostatic systems.
20339365 - Food-related odor probes of brain reward circuits during hunger: a pilot fmri study.
12174325 - Molecular pathways to obesity.
16475415 - The brain and the biology of obesity.
10335365 - Consumer perceptions and concerns about food contaminants.
25251295 - Dairy food at the first occasion of eating is important for total dairy food intake for...
Publication Detail:
Type:  Journal Article; Review     Date:  2007-06-21
Journal Detail:
Title:  The Journal of physiology     Volume:  583     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-09-03     Completed Date:  2007-11-20     Revised Date:  2013-06-06    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  425-30     Citation Subset:  IM    
Affiliation:
Neurology Service, VA Medical Center, East Orange, NJ 07018-1095, USA. levin@umdnj.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adipose Tissue / metabolism
Animals
Energy Intake
Energy Metabolism / genetics*
Feeding Behavior
Genetic Predisposition to Disease
Homeostasis
Humans
Nervous System / metabolism*,  physiopathology
Obesity / genetics*,  metabolism,  physiopathology,  therapy
Risk Factors
Weight Gain / genetics*
Weight Loss / genetics
Comments/Corrections
Comment In:
J Physiol. 2007 Sep 1;583(Pt 2):423   [PMID:  17766646 ]

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


Previous Document:  Hypothalamic leptin regulation of energy homeostasis and glucose metabolism.
Next Document:  Influence of enhanced troponin C Ca2+-binding affinity on cooperative thin filament activation in ra...