Friday, January 11, 2019

Genetics of Obesity



Obesity is a major risk factor for cardiovascular diseases, pulmonary diseases like sleep apnoea, metabolic disorders, osteoarticular diseases, for several of the Similar types of cancer and for serious psychiatric illness. Childhood obesity is associated with early-onset type 2 diabetes and with increased mortality risk for coronary heart disease in adulthood. If the escalating population prevalence of obesity and its serious implications for public health are generally accepted [with some notable exceptions], its causes and physiological consequences at the individual level are still elusive. 

Types:

Rare familial obesity:

Moreover a decade, obesity genetics has been predominantly driven by research into syndromic obesity. The cloning of the mouse gene and its human homologue, leptin, proved to be a paradigm for the field that resulted in the identification of many genes involved in the regulation of appetite via the leptin-melanocortin pathway. These variants account for 5% of morbid human obesity and include leptin and its receptor.

Common polygenic obesity:

The Human Obesity Gene Map summarizes the current situation in the field of common polygenic obesity. In any complex genetic disease, there are many unconfirmed genetic associations as some of these may be due to inadequate sample sizes for association studies of genes of modest effect or caused due to the inadequate examination of the genetic variation within these candidate genes.

GAD2:

The glutamic acid decarboxylase gene (GAD2) was first reported and recorded to be associated with obesity and feeding behaviors in morbidly obese adults, and this result was subsequently replicated in obese children. Moreover, an independent study failed to replicate these findings. These results illustrate the difficulty in determining whether a gene is truly associated with a complex genetic disease. 

Visfatin:

Pre-B cell colony-enhancing factor (PBEF1) was identified as the first protein secreted by lymphocytes over 10 years ago. This finding has now been replicated. The initial visfatin paper was also reported that visfatin had insulin mimetic activity. This was supported by a report where visfatin levels were altered in T2D patients. 

Ghrelin/ghrelin receptor/obestatin:

The growth hormone secretagogue receptor (GHSR) was identified in the year of 1996 and its endogenous ligand ghrelin in 1999. However, the evidence for ghrelin is not required as clear with initial positive results, but latterly, some negative results. 

Bardet–Biedl syndrome genes:

Bardet–Biedl syndrome genes are familial forms of obesity have been associated with common obesity, e.g. leptin, as well as the leptin receptor, were examined BBS gene variants for this possibility. Twelve SNPs along with BBS1, 2, 4 and 6 genes were selected and genotyped in adult and childhood obesity sample sets, with a total of 3242 subjects.

Contact details:
Alina Grace
Program Manager | Obesity Middle East 2019
Email Id: obesityendo@mehealthevents.org 

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