Obesity, becoming ever more common in modern societies, is often associated with serious health problems such as diabetes and heart disease. Obesity can be caused by a combination of too much food, too little exercise, and genetic susceptibility. Wikipedia Various genes are thought to affect susceptibility to obesity. The following are drawn primarily from genome wide association studies (GWAS), so are reports of variants often found in the general population that may (slightly) influence obesity predisposition. [See further below for obesity syndrome information.]
- FTO is also called the fatso gene. Wikipedia
- SCG3 may influence the risk of obesity through possible regulation of hypothalamic neuropeptide secretion. [PMID 17094264] In one study, two SNPs affected the transcriptional activity of SCG3, and subjects with the minor allele seemed to be resistant to obesity. 
- Adiponectin is a hormone produced by fat cells.
- The -11377 C > G adiponectin gene promoter variant is (i) associated with decreased serum adiponectin levels and therefore increased risk of obesity, (ii) correlated with the presence of coronary atherosclerosis, and (iii) significantly predictive of vascular events among men undergoing coronary angiography. [PMID 17334513]
- rs1851665 (risk allele A) [PMID 20876611]
- rs3865188 in the CDH13 gene (which encodes an adiponectin receptor) [PMID 20876611]
- rs864265 in the ADIPOQ gene [PMID 20876611]
- rs266717 in the ADIPOQ gene 
- rs11924390 near the KNG1 gene [PMID 20876611]
- rs7193788 [PMID 20887962]
- rs6444175 [PMID 20011104]
- rs4311394 in the ARL15 gene. The risk allele, G, is also associated with increased risk of coronary heart disease and type 2 diabetes. [PMID 20011104]
Other SNPs that affect obesity:
- rs6971091, in an uncharacterized gene on chromosome 7, is associated with more than doubled risk of obesity.
Obesity syndromes are quite different from the SNPs cited above, in which each SNP has quite modest effects. In contrast, obesity syndromes are monogenic, meaning a single gene inherited in a Mendelian fashion strongly influences the development of obesity. Syndromic forms of obesity are relatively rare, and in addition to obesity, include clinical characteristics such as intellectual disability, dysmorphic features and congenital abnormalities affecting specific organs. Examples of such syndromes are Prader-Willi and Bardet-Biedl syndrome. Non-syndromic forms of inherited obesity generally involve mutations in the leptin/melanocortin pathway, such as mutations in the leptin receptor, prohormone convertase 1, propiomelanocortin or melanocortin 4 receptor.[PMID 28346723]