Sugar Craving Gene That Lowers Body Fat Identified

Sugar Craving Gene That Lowers Body Fat Identified

by Adeline Dorcas on Apr 11 2018 5:40 PM
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  • A common version of the gene FGF21 is linked with increased sugar and alcohol consumption
  • The gene lowers body fat and redistributes fat in the upper body which may increase blood pressure
  • The gene is associated with higher waist-to-hip ratio and raised blood pressure levels
Scientists have previously mentioned that a common version of the gene FGF21 makes a person eat a lot of carbohydrates. For the first time, a team of researchers found that this gene variant decreases fat in the body. The results of the study were published in the journal Cell Reports.//
Gene: Increases Sugar Consumption and Lowers Body Fat
It was surprising that the version of the gene has an association between increased sugar consumption and lower body fat, said Timothy Frayling, a molecular geneticist at the University of Exeter Medical School in the UK and the study's first author.

"This goes against the current perception that eating sugar is bad for health. It may reduce body fat because the same allele also results in lower consumption of protein and fat in the diet. But while this version of the gene lowers body fat, it also redistributes fat to the upper body, where it's more likely to cause harm, including higher blood pressure," said Timothy Frayling.

The UK Biobank aims at improving the prevention, diagnosis, and treatment of many diseases by providing information for population-based research.

The bank contains biological samples such as blood, urine, and saliva samples from 500,000 people living in the UK that can be used for analysis. Participants agreed to give a detailed health report, and health follow up.

Details of the Study

The research team collected data from the Biobank to link the associations between different versions of the FGF21 gene, diet, body composition, and blood pressure.

The analysis of the study made use of more than 450,000 study participants, and this provided relevant data needed for the study, said Niels Grarup, an associate professor at the University of Copenhagen and one of the paper's co-authors.

The data also included a food frequency questionnaire from 175,000 people. The blood pressure levels of every participant involved in the study were measured.

Findings of the Study

The FGF21 hormone present in the liver has various functions. It suppresses sugar and alcohol intake by acting on the hypothalamus in the brain, stimulates glucose update by fat cells, and also serves as an insulin sensitizer.

The findings of the study show that the "A version" of the FGF21 gene leads to increased sugar and alcohol intake, it is linked to a lower percentage of total body fat, higher waist-to-hip ratio and raised blood pressure levels.

The author suggests that analyzing different variants of FGF21 can help to find some genetic and biological aspects related to obesity.

The A version of the gene was found to be more common. About 20 percent of the European population were found to have maximum two copies of it.

People having this gene version need not worry because the effect on individuals was quite small. Only a slight increase in the blood pressure (i.e., less than a third of one millimeter of mercury) on the blood pressure scale was obtained, said Frayling.

The team of researchers was not able to describe the mechanism by which FGF21 alters the amount and distribution of body fat, and this was the limitation of the study. The team suggests further study in this aspect.

Pharmaceutical companies are currently researching to find ways to produce drugs that replace FGF21, mainly in the treatment of diabetes.

"Our studies could refocus those efforts by revealing potential benefits and unintended side effects of manipulating this hormone," said Frayling.

  1. Timothy M. Frayling, et al. A Common Allele in FGF21 Associated with Sugar Intake Is Associated with Body Shape, Lower Total Body-Fat Percentage, and Higher Blood Pressure, Cell Reports (2018)DOI: 10.1016/j.celrep.2018.03.070


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