Please use this identifier to cite or link to this item:
|Title:||The molecular pathogenesis of obesity: An unfinished jigsaw puzzle|
|Authors:||Lee, Y.S. |
|Source:||Lee, Y.S.,Loke, K.Y. (2000). The molecular pathogenesis of obesity: An unfinished jigsaw puzzle. Annals of the Academy of Medicine Singapore 29 (3) : 388-395. ScholarBank@NUS Repository.|
|Abstract:||Introduction: Obesity is a common but highly complex disease, which evolved from interactions of multiple genes and the environment. In the past decade, there have been major advances in our understanding of the molecular genetics and pathogenesis of obesity, especially with regards to the genetics and functions of chemical mediators and their receptors, such as leptin, the leptin receptor, neuropeptide Y, the melanocortin-4 receptor, agouti-related protein and the peroxisome-proliferator-activated receptor γ2. Methodology: Recent studies and reports on the obesity genes and chemical mediators were reviewed. Results: Despite exciting discoveries of single gene mutations with haplo-insufficiency in human subjects, and single-gene disorders resulting in obesity, most cases of obesity are likely the result of subtle interactions of several related genes with environmental factors, which favour the net deposition of calories as fat, culminating in the obese phenotype. Obesity is unlikely to be caused by a single gene defect unless it is extreme (body mass index >60), or present in an isolated population group. However, research has established that genes at multiple loci may interact centrally to determine satiety, and peripherally to influence the metabolic rate of obese individuals. Conclusion: The mechanisms of action of these genes in the development of obesity are now being examined, with the aim of eventually discovering a therapeutic intervention for obesity.|
|Source Title:||Annals of the Academy of Medicine Singapore|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Feb 23, 2018
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.