A genetic variant has been found that predisposes to thinness and is carried by 60% of Europeans.

Nov 10, 2022 | Current affairs, Featured, Post, Revista Lloseta, Thursday Daily Bulletin, Tradition, Uncategorized


Researchers at the CNIO and the IMDEA Food Institute have discovered that those with a certain version of a gene involved in cell nutrition tend to accumulate less fat.

TDB keeps you informed. Follow us on FacebookTwitter and Instagram.

How much do genes influence our body weight? For the general population, this influence is around 20%, according to studies that in recent years have analysed the complete genome of tens of thousands of people. In other words, “lifestyle, such as eating habits and exercise, have a big impact, but genetic factors also play a role,” explains researcher Nerea Deleyto Seldas, from the Spanish National Cancer Research Centre (CNIO).

Some of these genetic factors are already known. Nearly a hundred genetic variants have already been identified that moderately increase the probability of having a high Body Mass Index – the BMI, a common indicator of overweight and obesity. CNIO and IMDEA Food researchers have just identified a new one. Their work is published in the journal Genome Biology, with Nerea Deleyto Seldas (CNIO) and Lara P. Fernández, from the IMDEA Food Institute, as the first authors.

This variant affects the amount of fat accumulated in the body, and the authors of the new study show that it is particularly prevalent in Europe. It is estimated to be present in almost 60% of the European population.

Variants of a gene are slightly different versions of that gene, which often do not translate into visible changes in the body. But in this case, they do. This variant affects the amount of fat the body stores, and the authors of the new study show that it is particularly prevalent in Europe. It is estimated to be present in almost 60% of the European population.

For Alejo Efeyan, head of the CNIO’s Metabolism and Cell Signalling Group, “the finding is another step forward in understanding the genetic components of obesity”. Ana Ramírez de Molina, director of the IMDEA Food Institute, believes that “knowledge of the involvement of the cellular nutrient sensing pathway in obesity may have implications for the development and application of personalised strategies in the prevention and treatment of obesity”.

Genetics and body measurements of 790 volunteers
Overweight and obesity are defined as an abnormal or excessive accumulation of fat that affects health. To search for genetic variants that influence the phenomenon, and the associated metabolic alterations, a team from IMDEA Alimentación collected genetic material and data such as weight; Body Mass Index; amounts of total and visceral fat; the amount of muscle mass; and waist and hip circumferences, among others, from 790 healthy volunteers.

The authors of the study analysed the possible associations of these parameters with 48 specific genetic variants, selected for their possible functional relevance. They found a “significant correlation between one of these variants in the FNIP2 gene and many of these obesity-related parameters,” they say.

Demonstration in animal models
The effect of this variant was then studied in mice – which had previously been genetically modified to express it – “We found that mice with this variant, which is associated with people with a slim build, have 10-15% less fat than their non-carrier counterparts,” explains the researcher.

In humans, the effect of this variant cannot be isolated from that of the many other genetic and environmental variables that influence physique, so it is impossible to calculate the precise strength of its effect. But given that the influence of genetics on obesity is no more than 20%, the contribution of the variant now identified is necessarily small.

That’s why the researchers use terms like predisposition or tendency: “It’s not at all the case that people with this version can overeat without getting fat,” Efeyan says.

The animals genetically modified for this study showed no other alterations or differences. “This result is very striking because many of these studies tend to report associations; in this paper, we show that a single letter change in the entire mouse genome is enough to replicate what was observed in the human variant,” Efeyan continues.

A genetic variant has been found that predisposes to thinness and is carried by 60% of Europeans.
Researchers at the CNIO and the IMDEA Food Institute have discovered that those with a certain version of a gene involved in cell nutrition tend to accumulate less fat.

How much do genes influence our body weight? For the general population, this influence is around 20%, according to studies that in recent years have analysed the complete genome of tens of thousands of people. In other words, “lifestyle, such as eating habits and exercise, have a big impact, but genetic factors also play a role,” explains researcher Nerea Deleyto Seldas, from the Spanish National Cancer Research Centre (CNIO).

Some of these genetic factors are already known. Nearly a hundred genetic variants have already been identified that moderately increase the probability of having a high Body Mass Index – BMI, a common indicator of overweight and obesity. CNIO and IMDEA Food researchers have just identified a new one. Their work is published in the journal Genome Biology, with Nerea Deleyto Seldas (CNIO) and Lara P. Fernández, from the IMDEA Food Institute, as the first authors.

This variant affects the amount of fat accumulated in the body, and the authors of the new study show that it is particularly prevalent in Europe. It is estimated to be present in almost 60% of the European population.

Variants of a gene are slightly different versions of that gene, which often do not translate into visible changes in the body. But in this case, they do. This variant affects the amount of fat the body stores, and the authors of the new study show that it is particularly prevalent in Europe. It is estimated to be present in almost 60% of the European population.

For Alejo Efeyan, head of the CNIO’s Metabolism and Cell Signalling Group, “the finding is another step forward in understanding the genetic components of obesity”. Ana Ramírez de Molina, director of the IMDEA Food Institute, believes that “knowledge of the involvement of the cellular nutrient sensing pathway in obesity may have implications for the development and application of personalised strategies in the prevention and treatment of obesity”.

Genetics and body measurements of 790 volunteers
Overweight and obesity are defined as an abnormal or excessive accumulation of fat that affects health. To search for genetic variants that influence the phenomenon, and the associated metabolic alterations, a team from IMDEA Alimentación collected genetic material and data such as weight; Body Mass Index; amounts of total and visceral fat; the amount of muscle mass; and waist and hip circumferences, among others, from 790 healthy volunteers.

The authors of the study analysed the possible associations of these parameters with 48 specific genetic variants, selected for their possible functional relevance. They found a “significant correlation between one of these variants in the FNIP2 gene and many of these obesity-related parameters,” they say.

Demonstration in animal models
The effect of this variant was then studied in mice – which had previously been genetically modified to express it – “We found that mice with this variant, which is associated with people with a slim build, have 10-15% less fat than their non-carrier counterparts,” explains the researcher.

In humans, the effect of this variant cannot be isolated from that of the many other genetic and environmental variables that influence physique, so it is impossible to calculate the precise strength of its effect. But given that the influence of genetics on obesity is no more than 20%, the contribution of the variant now identified is necessarily small.

That’s why the researchers use terms like predisposition or tendency: “It’s not at all the case that people with this version can overeat without getting fat,” Efeyan says.

The animals genetically modified for this study showed no other alterations or differences. “This result is very striking because many of these studies tend to report associations; in this paper, we show that a single letter change in the entire mouse genome is enough to replicate what was observed in the human variant,” Efeyan continues.

The goal for the future is to “better understand the molecular basis of what this genetic variant does, i.e. what is happening biochemically to the cell,” adds Nerea Deleyto. “We need to improve the genetic tools to dissect when the functional consequences of this variant become important in the organism, for example, during the fat formation process,” she stresses.

The finding also opens up questions that concern other areas of science, such as what evolutionary pressures favoured the selection of this variant and when it occurred.