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Obesity and genetics[edit]

Obesity is known as a disease when a person gains fat more than its body demands. BMI (body mass index) usually determines obesity in a person. BMI is the body mass ratio to the amount of fat in person's body according to their height. More than 25.9 of BMI could led to overweight and then progressed to obesity if not controlled.[1] Many people think the cause of obesity is by the external factors like poor lifestyle and malnutrition diet. Although these external factors plays role in obesity but genetics is an another hidden factor that could be number one cause of obesity too. Mutation or alteration in some of our genes can just change their function like totally opposite of what they are supposed to do. There are two types of obesity that are caused by genetics such as syndromic, monogenic and polygenic.[2] Polygenic is the gene that is control by many gene and located in different part of the body while, in contrast monogenic control by the single gene and found in one specific area of the human body and syndromic obesity triggers by the chromosomal deletion or insertion.[2] There are some genes as follow and their alteration can trigger obesity.

Genes that plays a major role in obesity[edit]

MC4R[edit]

MC4r is one of the polygenic gene that mostly likely to be mutated and is found in the hypothalamus part of the brain.[3] MC4r gene code for the protein Melanocortin receptor 4. The function of this gene is to let our brain know when we are full through the from of energy we get from food. This process happens when we consumes food which sends energy to the gene MC4r and this gene signals Melanocortin receptor 4 to signal our brain to suppressed the hunger signal. The hunger signal is accomplished by orexigenic neuron which trigger our appetite and the word “orexigenic” is derrived from the word appetite.[4] On the other hand, when we are hungry the MC4r gene attaches to Melanocortin receptor 4 again and now it signals to be full. and when we however, the mutated Mc4r lacks enough Melanocortin recptor 4. You might be thinking that if MC4r is just binding to melanocotrin receptor 4 to trigger both hunger and full signal, so what is the different. Well “health watcher” include that there is a difference in the types of hormone and protein. Weight watcher also mentioned that the “being full” is signaled by high energy that sent leptin or insulin to release the α MSH hormone which attaches to Melanocortin receptor 4 and as a result it decreases the hormone level that make us feel full.[5] Unlikeliness to full signal, hunger signals are triggered by low energy which sent ghrelin to trigger Agrp protein that attaches to Melanocortin receptor 4 and as a result the hormone are increased which led in the signal of hunger.[5]

Mutation in MCr4[edit]

If we look at the genetics of obesity perspective, MC4r gene could led to the major cause of obesity. A slightly difference in nucleotide of MC4r can change the whole function and oppose it. For example, not enough production of MC4r could cause less release of its receptor and which could be a cause of increase in hunger signal and decrease in full signals. This could also effect the production of neurons by increased in orexigenic neurons and decrease in anoriexigenic neuron and evetually this will be reason for increased hormone for craving like AGRP protein and decrease in α MSH which controls craving. A person who is diagnosed with this kind of genetic dysorder can"t control their hunger. Health watch article includes that these people crave for specific foods that are rich in fat.[5] “New study obesity” articles researched that the off springs of people who had high fat diet could have lower MC4r gene production which could led to obesity in them in future.[6] 

[7]

 Treatment[edit]

This disorder cannot be cured as it is a mutation in the gene. However, there are some lifestyle changes that can prevent diseases related to it. the person suffering from MC4r mutation can see a nutritionist or dietitian. A nutritionist or a dietitian could help make their diet plan and aware them on the restriction on some food. physical trainer can help to be active by make them eat specific food and types of exercise that would help to loose extra weight they are gaining. Yoga and meditation could also help them in clearing their mind from food and working on something else.

FTO gene[edit]

FTO (fat mass and obesity) gene is monogenic. FTO in mammals comes from the family of 2 oxyglturate Fe(II) 2 and dioxygenase which is similar to the gene found in E coli DNA repair enzyme AlkB[8]. The function of FTO is to absorb the energy mostly in the form of fat mostly Similarly to MCr4, FTO is also found in the hypothalamus which control the release and absorption of energy in the form of food. A study found that abundace of amino acid are need for FTO to work properly.[9] Additionally, Gulati P, Cheung included that a mice experiement illustrated that defect in FTP could lead to retardiness or slow in the growth of the mouse.[10] According to health watchers, a new study has suggested that FTO regulate the production Ghrelin m Rna and if we look back at MCR4, Ghrelin is a hormone that increases hunger level. furthermore, a defect in FTO would lead in the over expression of the gene for Ghrelin to produce which cause the person to feel hungry all the other and on the other hand it decreases the level of being full. The A Allele in the FTO that has abundance of SNP (single nucleotide polymorphism) which is direct correlated with your BMI and increases it to .04 or .05.[11] According to a study, children who carry this defective gene are way 4 kg more than the non carrier.[12] As we learned that FTO absorbed energy and mass, a study on mouse explained that deleting the whole FTO gene from the body made a great weight loss in the mice.[13] Although its still not enpugh research that how FTO, SNP and obesity are linked but its sure that BMI and FTO are positively realted.

Treatment[edit]

There are two types pf treatment for FTO genetic disorder such as drug treatment and change in their lifestyle. A diet enriched in protein and decrease in fat suggested by dietitians[5] Drug treatment is a future treatment that would include to get back the muscle that have been loosen up by FTO defect because as we learned that FTO defect could cause decrease in amino acid which are the building blocks of protein and increase fat absorption.

Prader Willi syndrome[edit]

PWS is a syndromic obesity disorder. The deletion on some gene on the chromosomal 15 causes PWS. Altogether, normal humans have 22 and one pair of sex chromosome.[14] When a child is born they get their 23 chromosome from their father and other 23 from their mother. Unfortunately, during the transfer of the DNA some gene might turned off in parents while transferring which is also called genetic imprinting disorder. This defective chromosome we get is from our paternal side. There are thousands of genes lined up in the chromosomal 15 but the specific gene name that becomes defective in PWS patient is 15q11-q13.[15] This happens due to mispaired of the nucleotide base pair. The gene 15q11-q13 from the paternal is usually defective. The gene 15q11-q13 has three breakpoints on the chromosome such as BP1, BP2 and BP3. BP1 and BP2 are located at the proximal part of the chromosome, while Bp3 is located to the distal part of the chromosome.[7] There are two types of deletion in the genes that causes PWS such as type I and II. Type I involves in the deletion of BP1 which is much bigger in size and type II involves deletion of BP2 which is much smaller compare to BP1.[15] BP1 is known to cause much behavioral problem in PWS patient compare to BP2 breakpoints deletion.[14] On the other hand, deletion on the breakpoints of BP3 causes the major disorder of PWS and the gene that are found at this breakpoints are MKRN3, MAGEL2 and NDN and are to control cardinal features.[15]

Treatment[edit]

Because PWS effect not just one part of the gene but many thats why there are dozens of treatment available for PWS patient. Some treatment included for PWS patients such as strict diet plan, growth hormone therapy, sleep treatment, eye treatment, spinal curvature treatment, behavioral therapy , some medication and sex hormone treatment.[16]

References[edit]

  1. ^ "Calculate Your BMI - Standard BMI Calculator". www.nhlbi.nih.gov. Retrieved 2017-04-23.
  2. ^ a b Raanan., Shamir,; Dominique., Turck,; Moshe., Phillip, (2013-01-01). Nutrition and growth. Karger. ISBN 9783318022650. OCLC 841303943.{{cite book}}: CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)
  3. ^ B., Reece, Jane; 1946-2004., Campbell, Neil A.,. Biology : a global approach. ISBN 9780321775658. OCLC 903099858. {{cite book}}: |last2= has numeric name (help)CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)
  4. ^ "Appetite-Enhancing Drugs". TheFreeDictionary.com. Retrieved 2017-04-23.
  5. ^ a b c d "Obesity and the MC4R Gene". www.gbhealthwatch.com. Retrieved 2017-04-23.
  6. ^ "New Obesity Study Results Reported from Bar-Ilan University (Thyroid hormone-dependent epigenetic regulation of melanocortin 4 receptor levels in female offspring of obese rats)." Obesity, Fitness & Wellness Week, 15 Apr. 2017, p. 7006. Academic OneFile, cod.idm.oclc.org/login?url=http://go.galegroup.com/ps/i.do?p=AONE&sw=w&u=cod_lrc&v=2.1&id=GALE%7CA488903935&it=r&asid=f55831329c0dc45e25576903bcde4228. Accessed 23 Apr. 2017.
  7. ^ a b Nicholls R D, Knepper J L. Genome organization, function, and imprinting in Prader-Willi and Angelman syndromes. Annu. Rev. Genomics Hum. Genet. 2001;2:153–175
  8. ^ Gulati, Pawan; Yeo, Giles S. H. (2013-10-01). "The biology of FTO: from nucleic acid demethylase to amino acid sensor". Diabetologia. 56 (10): 2113–2121. doi:10.1007/s00125-013-2999-5. ISSN 0012-186X. PMC 3764322. PMID 23896822.{{cite journal}}: CS1 maint: PMC format (link)
  9. ^ Cheung MK, Gulati P, O’Rahilly S, Yeo GS. FTO expression is regulated by availability of essential amino acids. Int J Obes (Lond) 2012;37:744–747. doi: 10.1038/ijo.2012.77.
  10. ^ Gulati P, Cheung MK, Antrobus R, et al. Role for the obesity-related FTO gene in the cellular sensing of amino acids. Proc Natl Acad Sci U S A. 2013;110:2557–2562. doi: 10.1073/pnas.1222796110.
  11. ^ Frayling TM, Timpson NJ, Weedon MN, Zeggini E, et al. 2007. A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science 316: 889–94. PMID 17434869
  12. ^ Sandholt CH, Hansen T, Pedersen O. 2012. Beyond the fourth wave of genome-wide obesity association studies. Nutr Diabetes. 2:e37. doi: 10.1038/nutd.2012.9. PMID 23168490
  13. ^ McMurray F, Church CD, Larder R, et al. Adult onset global loss of the fto gene alters body composition and metabolism in the mouse. PLoS Genet. 2013;9:e1003166. doi: 10.1371/journal.pgen.1003166.
  14. ^ a b Bittel D C, Butler M G. Prader-Willi syndrome: clinical genetics, cytogenetics and molecular biology. Expert. Rev. Mol. Med. 2005;7(14):1–20.
  15. ^ a b c G. Butler, Merlin. "Prader-Willi Syndrome: Obesity due to Genomic Imprinting". Current Genomics. 12 (3): 204–215. doi:10.2174/138920211795677877. PMC 3137005. PMID 22043168.{{cite journal}}: CS1 maint: PMC format (link)
  16. ^ "What are the treatments for Prader-Willi syndrome (PWS)?". www.nichd.nih.gov. Retrieved 2017-04-27.
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