INSIG2 gene induced by insulin would inhibit the fatty acid and cholesterol synthesis. People with a sequence variation near the gene would exhibit more fat accumulation, as the normal functional gene could not complete its potential.

In three rare diseases of severe fat malabsorption, chylomicron retention disease (CMRD), Anderson disease and CMRD with Marinesco Sjogren syndrome, the Sar1b protein required for all dietary fat absorption could not work normally because of genetic mutation.

Gene variant FTO that is susceptible to type 2 diabetes can be found among over half of European population who is linked with obesity causes. If a person with two copies of FTO variant is likely to weigh 3 kilos more than a normal person, and person with only one copy there are more likely to weigh 1.2 kilos more.

The human lipin gene might be a candidate for obesity was excess levels in fat tissue or skeletal muscle will promote the condition. Deficiency in lipin levels would prevent normal development of mature fat cells.

Another mutant gene, ENPP1 which presents in 20% Caucasians and 50% of black people, will block insulin from binding in pancreas and the brain. Thus, the insulin resistance will store excess glucose production from liver as layers of fat and diminish insulin secretion that will lead to increased risk of type 2 diabetes.

GAD2, a gene found on chromosome 10 can speed up the production of a chemical transmitter in the brain, GABA, which stimulates appetite. One form of the gene appeared to protect some people against obesity, while another form increased the risk of the disorder.

About 20 genes maybe involved in causing common obesity, but genetics alone cannot fully account for a worldwide obesity trend in recent decades.