"What specific types of genes are highly susceptible to suffer from obesity? In westernized countries especially, the accessibility of ample, energy-rich processed foods inthe last few decades has resulted in a sharp rise in the occurrence of obesity. Obesity is a keyrisk aspect for the various disease like pulmonary diseases, cardiovascular diseases,psychiatric illness metabolic related diseases (e.g. diabetes), osteoarticular diseases, somecancer also etc. In the 1960s, Neel gave the ‘thrifty gene’ hypothesis, explaining there are some genes whichenable individuals to competently collect and process food to store fat when there is anabundance of food. So, during starvation time stored fat can be decomposed to provideenergy to the body. People who possess these genes generally not becoming only slightlyoverweight, but exceptionally obese. According to USA studies, such kind of people can beseen in high-risk groups, like African-Americans, Pima Indians, Hispanic-Americans andPacific Islanders. Scientific studies demonstrate that genetics plays a significant role inobesity. Genes can be able to cause obesity directly in some of the syndromes like Bardet- Biedl syndrome, Prader-Willi syndrome etc. Obesity is a highly complex disease withconsequence of the interactions of an extensive variety of genetic and environmental factors. It is now investigated that overweight persons and their forms are related within a family.Obesity risk increased from two to eight folds for a person with a personal family history ascompared to those with no family history related to obesity. As the transfer of heredity, obesity gene may link to body fat from 5 to 40%, adipose tissue density, and occurrence ratefrom 40 to 55%. The increase in body weight and adipose gain upsurge with an increase inage, also affected by heredity that is ultimately linked to the gene. Incidences of monogenictypes of obesity are instigated by genetic mutations. The utmost common forms of obesity areundoubtedly the outcome of variations within a large and different amount of genes.Sequence variants inside a pool of 56 different genes were reported as being linked to obesityphenotypes, however, only a few showing positive results in different studies. Few genes associated with obesity due to monogenic effects and Mendelian disorderreported in previous years summarized below: a.Single-gene mutations with an obesity phenotype Gene Name1 Corticotropin-releasing hormone receptor CRHR12 Corticotropin-releasing hormone receptor CRHR23 G-protein-coupled receptor GPR244 Leptin (obesity homolog, mouse) LEP5 Leptin receptor LEPR6 Melanocortin 3 receptor MC3R7 Melanocortin 4 receptor MC4R8 Neurotrophic tyrosine kinase receptor type 2 NTRK29 Proopiomelanocortin POMC10 Proprotein convertase subtilisin/kexin type 1 PCSK111 Single-minded homolog 1 (Drosophila) SIM1b. Autosomal recessive12 Alstrom syndrome ALMS113 Bardet-Biedl syndrome 1 BBS1 14 Bardet-Biedl syndrome 2 BBS215 Bardet-Biedl syndrome 3 BBS316 Bardet-Biedl syndrome 4 BBS417 Bardet-Biedl syndrome 5 BBS518 Bardet-Biedl syndrome 6 MKKS19 Bardet-Biedl syndrome BBS720 Bardet-Biedl syndrome BBS821 Berardinelli-Seip congenital lipodystrophy AGPAT222 Berardinelli-Seip congenital lipodystrophy BSCL223 Carbohydrate-deficient glycoprotein syndrome type PMM224 Cohen syndrome COH125 Combined pituitary hormone deficiency PROP126 Fanconi-Bickel syndrome SLC2A227 Isolated growth hormone (GH) deficiency GHRHR28 Cortisone reductase deficiency H6PD29 Cortisone reductase deficiency HSD11B130 Severe insulin resistance with obesity PPARG, PPP1R3Ac. Autosomal dominant31 Achondroplasia FGFR332 AHO (Pseudopseudohypoparathyroidism) GNAS33 AHO 2 AHO234 Brachydactyly mental retardation syndrome STK2535 Angelman syndrome with obesity ANCR36 Anisomastia ANMA 37 Carney complex with primary pigmented nodular PRKAR1A38 Familial partial lipodystrophy, Dunnigan, type 3 PPARG39 Familial partial lipodystrophy, type 2 LMNA40 Insulin resistance syndromes INSR41 Isolated GH deficiency GH142 Multiple endocrine neoplasia, type 1 with Cushing’s disease MEN143 Posterior polymorphous corneal dystrophy (chromosome 1) COL8A244 Posterior polymorphous corneal dystrophy (chromosome 20) VSX145 Prader-Willi syndrome IPW46 Prader-Willi-like syndrome SIM147 Thyroid hormone resistance syndrome THRB48 Ulnar-Mammary (Schinzel) syndrome TBX349 WAGR syndrome with obesity WT1d. X linked50 Borjeson-Forssman-Lehmann syndrome PHF651 Choroideremia with deafness and obesity CHM52 Fragile X syndrome with Prader-Willi-like phenotype FMR153 Mental retardation X-linked, syndromic 7 MRXS754 Mental retardation X-linked, syndromic 16 MECP255 Mental retardation, X-linked, syndromic 11 MRXS1156 Prader-Willi-like syndrome, X-linked PWLSX57 Simpson-Golabi-Behmel 1 GPC358 Simpson-Golabi-Behmel 2 SGBS259 Wilson-Turner syndrome WTS There is presently 22 gene linked to five positive and confident studies (mentioned below).These genes comprise members of the various metabolic pathway like leptin–melanocortinpathway, pro-inflammatory cytokines, and various uncoupling proteins.Some genes related to obesity are as follows: S.No. Gene symbolFull name1 ACE Angiotensin I-converting enzyme (peptidyl-dipeptidase A) 2 ADIPOQ Adiponectin, C1Q and collagen domain containing3 ADRB2 Adrenergic, beta-2-, receptor, surface4 ADRB3 Adrenergic, beta-3-, receptor5 DRD2 Dopamine receptor D26 GNB3 Guanine nucleotide binding protein (G protein)7 HTR2C 5-hydroxytryptamine (serotonin) receptor 2C8 IL6 Interleukin 6 (interferon, beta 2)9 INS Insulin10 LDLR Low density lipoprotein receptor (familial hypercholesterolaemia)11 LEP Leptin (obesity homologue, mouse)12 LEPR Leptin receptor13 LIPE Lipase, hormone-sensitive14 MC4R Melanocortin 4 receptor15 NR3C1 Nuclear receptor sub-family 316 PLIN Perilipin17 PPARG Peroxisome proliferative activated receptor, gamma18 RETN Resistin19 TNF Tumor necrosis factor (TNF superfamily, member 2) 20 UCP1 Uncoupling protein 1 (mitochondrial, proton carrier)21 UCP2 Uncoupling protein 2 (mitochondrial, proton carrier)22 UCP3 Uncoupling protein 3 (mitochondrial, proton carrier)Beside these, it’s also needed to understand that environment factors also playing asignificant role in causing obesity. Environmental factors directly influence the activation anddeactivation of the mentioned gene. Significantly identification of those genes will surelyhelp in elucidating the etiology related to obesity and its metabolic significances. With thisknowledge further it will ease the identification of their risk factor in relations of their geneticprofile to develop their personalized treatment approaches.Conclusion:It is concluded that genes do not permanently predict future fitness. Genes and environmentalfactors both be required for a person to become overweight. In some cases multiple genesmay upsurge one’s vulnerability for obesity with required outside factors; such as lavish foodsupply with less physical movement. Scientists have found numerous obesity susceptibilitygenes and the mixture of an obesogenic atmosphere will obviously causing obesitydevelopment in any individual. Though, sometimes it is likely possible to be obese withouthaving any role of any candidate gene.Reference:1. Andrew, W. J., Alexandra, I.F., Blakemore, and Philippe F. (2006) Genetics ofobesity and the prediction of risk for health. Hum. Mol. Genet., 15 (suppl 2): R124- R130 doi:10.1093/hmg/ddl215.2. Rankinen, T., Zuberi, A., Chagnon, Y. C., Weisnagel, S. J., Argyropoulos, G., Walts,B., Pérusse, L. and Bouchard, C. (2006), The Human Obesity Gene Map: The 2005Update. Obesity, 14: 529–644. doi: 10.1038/oby.2006.71 "