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Gene that Lets You Eat As Much As You Like Holds Promise Against Obesity

Summary: Removing the RCAN1 gene in mice reduced weight gain, even when the animals were fed high fat diets for prolonged periods of time. Researchers say the findings could help develop new treatments to help prevent obesity in humans.

Source: Flinders University.

It sounds too good to be true, but a novel approach that might allow you to eat as much food as you want without gaining weight could be a reality in the near future.

When a single gene known as RCAN1 was removed in mice and they were fed a high fat diet, they failed to gain weight, even after gorging on high fat foods for prolonged periods.

The international team behind the study are hopeful a similar approach that inhibits this gene will also be effective with humans to combat obesity and serious diseases like diabetes.

Led by Professor Damien Keating at Flinders University, the study used a huge genetic screen in rodents to identify novel genetic candidates that may cause obesity, potentially paving the way for new drug therapies.

“We know a lot of people struggle to lose weight or even control their weight for a number of different reasons. The findings in this study could mean developing a pill which would target the function of RCAN1 and may result in weight loss,” Professor Keating says.

Obesity is a major global health epidemic, resulting in increased risk of serious diseases like type 2 diabetes, and heart disease, but avenues for effective therapeutic treatments are lacking.

There are two types of fat in the human body- brown fat burns energy, while white fat stores energy.

Professor Keating says blocking RCAN1 helps to transform unhealthy white fat into healthy brown fat, presenting a potential treatment method in the fight against obesity.

“We have already developed a series of drugs that target the protein that this gene makes, and we are now in the process of testing them to see if they inhibit RCAN1 and whether they might represent potential new anti-obesity drugs,”

“In light of our results, the drugs we are developing to target RCAN1 would burn more calories while people are resting. It means the body would store less fat without the need for a person to reduce food consumption or exercise more.”

a person

When a single gene known as RCAN1 was removed in mice and they were fed a high fat diet, they failed to gain weight, even after gorging on high fat foods for prolonged periods. The international team behind the study are hopeful a similar approach that inhibits this gene will also be effective with humans. NeuroscienceNews.com image is adapted from the Flinders University news release.

Two thirds of Australian adults and a quarter of children are either overweight or obese, and the statistics are just as concerning in Britain and the US.

“We looked at a variety of different diets with various timespans from eight weeks up to six months, and in every case we saw health improvements in the absence of the RCAN1 gene.”

The researchers say these findings open up a potentially simple treatment but further studies are required to determine if they translate the same results to humans.

“Our research is focused on understanding how cells send signals to each other and how this impacts health and the spread of disease”.

“We really want to pursue this, it’s exciting and we have research funding from the Australian government through the National Health and Medical Research Council to continue to explore viable options. These results show we can potentially make a real difference in the fight again obesity.”

About this neuroscience research article

Source: Damien Keating – Flinders University
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is adapted from the Flinders University news release.
Original Research: Abstract for “Regulator of Calcineurin 1 helps coordinate whole‐body metabolism and thermogenesis” by David Rotter, Heshan Peiris, D Bennett Grinsfelder, Alyce M Martin, Jana Burchfield, Valentina Parra, Christi Hull, Cyndi R Morales, Claire F Jessup, Dusan Matusica, Brian W Parks, Aldons J Lusis, Ngoc Uyen Nhi Nguyen, Misook Oh, Israel Iyoke, Tanvi Jakkampudi, D Randy McMillan, Hesham A Sadek, Matthew J Watt, Rana K Gupta, Melanie A Pritchard,Damien J Keating, and Beverly A Rothermel in EMBO Reports. Published November 1 2018.
doi:10.15252/embr.201744706

Cite This NeuroscienceNews.com Article
Flinders University”Gene that Lets You Eat As Much As You Like Holds Promise Against Obesity.” NeuroscienceNews. NeuroscienceNews, 4 December 2018.
<http://neurosciencenews.com/obesity-genetics-eatingi-120201/>.
Flinders University(2018, December 4). Gene that Lets You Eat As Much As You Like Holds Promise Against Obesity. NeuroscienceNews. Retrieved December 4, 2018 from http://neurosciencenews.com/obesity-genetics-eatingi-120201/
Flinders University”Gene that Lets You Eat As Much As You Like Holds Promise Against Obesity.” http://neurosciencenews.com/obesity-genetics-eatingi-120201/ (accessed December 4, 2018).

Abstract

Regulator of Calcineurin 1 helps coordinate whole‐body metabolism and thermogenesis

Increasing non‐shivering thermogenesis (NST), which expends calories as heat rather than storing them as fat, is championed as an effective way to combat obesity and metabolic disease. Innate mechanisms constraining the capacity for NST present a fundamental limitation to this approach, yet are not well understood. Here, we provide evidence that Regulator of Calcineurin 1 (RCAN1), a feedback inhibitor of the calcium‐activated protein phosphatase calcineurin (CN), acts to suppress two distinctly different mechanisms of non‐shivering thermogenesis (NST): one involving the activation of UCP1 expression in white adipose tissue, the other mediated by sarcolipin (SLN) in skeletal muscle. UCP1 generates heat at the expense of reducing ATP production, whereas SLN increases ATP consumption to generate heat. Gene expression profiles demonstrate a high correlation between Rcan1 expression and metabolic syndrome. On an evolutionary timescale, in the context of limited food resources, systemic suppression of prolonged NST by RCAN1 might have been beneficial; however, in the face of caloric abundance, RCAN1‐mediated suppression of these adaptive avenues of energy expenditure may now contribute to the growing epidemic of obesity.

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