Document Detail

Molecular pathways to obesity.
MedLine Citation:
PMID:  12174325     Owner:  NLM     Status:  MEDLINE    
Obesity results from a chronic imbalance between energy intake and energy expenditure. Environmental factors, such as the increased availability of high caloric food or the decreased need for physical activity, contribute to its development and their influence is amplified by genetic predisposition. In recent years remarkable progress has been made in the understanding of the pathophysiology of obesity. Although most of the insights into the regulation of energy balance have been obtained in rodent models, the rare clinical cases of monogenic obesity provided evidence for the importance of several of these mechanisms in humans. The identification of leptin as a factor originating from adipose tissue and informing the brain about the status of energy reserves firmly established the concept of long-term regulation of body fat stores. The disappointing therapeutic results with leptin in obese patients could be explained by the fact that during evolution this hormone developed rather as a starvation signal than as an adiposity signal. It is conceivable that the pharmacological interference with mechanisms downstream of leptin, for example with the melanocortin pathway, might be therapeutically more promising. The discovery of new molecular mechanisms involved in the regulation of the differentiation and proliferation of adipocytes and the elucidation of their paracrine and endocrine functions have changed the traditional view of adipose tissue as an inert depot for triglycerides. The identification of new uncoupling proteins could modify the current concepts of the regulation of thermogenesis in humans. The remarkable progress in the identification of novel targets involved in the regualtion of energy balance should have a positive impact on the search for new antiobesity agents.
K G Hofbauer
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity     Volume:  26 Suppl 2     ISSN:  -     ISO Abbreviation:  Int. J. Obes. Relat. Metab. Disord.     Publication Date:  2002 Sep 
Date Detail:
Created Date:  2002-08-13     Completed Date:  2002-11-12     Revised Date:  2014-06-03    
Medline Journal Info:
Nlm Unique ID:  9313169     Medline TA:  Int J Obes Relat Metab Disord     Country:  England    
Other Details:
Languages:  eng     Pagination:  S18-27     Citation Subset:  IM    
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MeSH Terms
Biological Evolution
Brain / physiology
Energy Metabolism
Leptin / physiology
Neuropeptide Y / physiology
Obesity / etiology*,  genetics
Reg. No./Substance:
0/Leptin; 0/Neuropeptide Y

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

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