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SPORTS MEDICINE : MEDICAL: CONDITIONS: OBESITY : MEDICAL RESEARCH : PHYSICAL EXERCISE AND FITNESS: Obesity Genetics: Genetic Switch Makes Fat Cells Burn Energy Rather Than Store It

David P. Dillard
 

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SPORTS MEDICINE :

MEDICAL: CONDITIONS: OBESITY :

MEDICAL RESEARCH :

PHYSICAL EXERCISE AND FITNESS:

Genetic Switch Makes Fat Cells Burn Energy Rather Than Store It


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Genetic Switch Makes Fat Cells Burn Energy Rather Than Store It

Daily news

20 August 2015

New Scientist

https://www.newscientist.com/article/ dn28076-genetic-switch-makes-fat-cells-burn-energy-rather-than-store-it/

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A shorter URL for the above link:

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http://tinyurl.com/qhzda3q

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A master gene that orders fat cells to burn energy rather than store it has been found. Tinkering with it made mice lose weight as their fat-storing cells were converted into fat-burning cells, raising the prospect of a gene therapy to treat obesity.

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snip

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Not all fat is created equal. Humans carry several different types. White fat is the insulating stuff that builds up around our middles, storing energy rather than burning it. Brown fat, which is found in small pockets around our neck and spinal cord, does the opposite burning calories to produce heat. Beige fat is somewhere in between. It has a different origin to classical brown fat and is dispersed within white fat cells but it also burns calories without us expending any effort.

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In the past few years, weve realised that it may be possible to turn peoples white fat cells into beige fat. But its not easy and involves doing things like exposing yourself to cold temperatures or doing strenuous exercise. Keliss teams work suggests that there might be an easier way just flip a genetic switch.

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snip

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Powerful cells

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Kelliss team was able to use gene editing techniques to adjust the functioning of the FTO gene in fat cells, converting fat-storing cells into fat-burning cells effectively turning white fat beige and vice versa.

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The IRX genes were twice as active in white fat cells from people that carry the risk variant as they were in cells from people without the variant, meaning that these cells were super-storers of energy.

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There was practically no difference just 1 per cent between brain cells in the different groups, suggesting that the impact of FTO on fat cells far outweighs that in the brain. This suggests that, for some people, the activity of their fat cells might play a greater role in dictating weight than exercise or diet.

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The complete article may be read at the URL above.

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FTO Obesity Variant Circuitry and Adipocyte Browning in Humans

Melina Claussnitzer, Ph.D., Simon N. Dankel, Ph.D., Kyoung-Han Kim, Ph.D., Gerald Quon, Ph.D., Wouter Meuleman, Ph.D., Christine Haugen, M.Sc., Viktoria Glunk, M.Sc., Isabel S. Sousa, M.Sc., Jacqueline L. Beaudry, Ph.D., Vijitha Puviindran, B.Sc., Nezar A. Abdennur, M.Sc., Jannel Liu, B.Sc., Per-Arne Svensson, Ph.D., Yi-Hsiang Hsu, Ph.D., Daniel J. Drucker, M.D., Gunnar Mellgren, M.D., Ph.D., Chi-Chung Hui, Ph.D., Hans Hauner, M.D., and Manolis Kellis, Ph.D.

August 19, 2015DOI: 10.1056/NEJMoa1502214

New England Journal of Medicine

http://www.nejm.org/doi/full/10.1056/NEJMoa1502214


Results

Our data indicate that the FTO allele associated with obesity represses mitochondrial thermogenesis in adipocyte precursor cells in a tissue-autonomous manner. The rs1421085 T-to-C single-nucleotide variant disrupts a conserved motif for the ARID5B repressor, which leads to derepression of a potent preadipocyte enhancer and a doubling of IRX3 and IRX5 expression during early adipocyte differentiation. This results in a cell-autonomous developmental shift from energy-dissipating beige (brite) adipocytes to energy-storing white adipocytes, with a reduction in mitochondrial thermogenesis by a factor of 5, as well as an increase in lipid storage. Inhibition of Irx3 in adipose tissue in mice reduced body weight and increased energy dissipation without a change in physical activity or appetite. Knockdown of IRX3 or IRX5 in primary adipocytes from participants with the risk allele restored thermogenesis, increasing it by a factor of 7, and overexpression of these genes had the opposite effect in adipocytes from nonrisk-allele carriers. Repair of the ARID5B motif by CRISPRCas9 editing of rs1421085 in primary adipocytes from a patient with the risk allele restored IRX3 and IRX5 repression, activated browning expression programs, and restored thermogenesis, increasing it by a factor of 7.

Full Text of Results...

Conclusions

Our results point to a pathway for adipocyte thermogenesis regulation involving ARID5B, rs1421085, IRX3, and IRX5, which, when manipulated, had pronounced pro-obesity and anti-obesity effects. (Funded by the German Research Center for Environmental Health and others.)

http://www.nejm.org/doi/full/10.1056/NEJMoa1502214#t=articleDiscussion


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