Abstract
In 2006, Rankinen et al. reported 127 candidate obesity-related genes, and since then more have been identified (http://www.genome.gov/gwastudies/). A lot of mutations in more than 7 genes, especially in the MC4-R gene, were reported as monogenic obesity (primarily related to the regulation of appetite). Many candidate genes related to polygenic obesity were reported in genome-wide association studies (GWAS) that compared the frequency of single-nucleotide polymorphisms (SNPs) between normal and obese individuals. There are numerous genes related to appetite control, glucose and lipid metabolism, as well as energy metabolism. Recently, it was reported that obesity and lifestyle-related diseases may be induced epigenetically. Specifically, the food intake and degree of exercise in childhood, together with the food intake of both parents, affect whether the offspring is likely to become obese in adulthood. Although the interplay between specific genes and molecules that are linked to obesity is gradually being elucidated, there is little evidence to suggest they are suitable targets for therapeutic intervention. Understanding obesity and lifestyle-related diseases at the molecular level will undoubtedly be helpful. Nonetheless, it is also important to confirm the nature of the disease for each individual. Adequate and timely intervention, by giving sound advice, will improve the health of individuals regardless of genetic risk factors.
