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Joy Pape FNP-CDE, medical editor of DiabetesInControl, had the opportunity to interview Dr. Ruth Loos, Director of the Obesity Genetics and Related Metabolic Characteristics Program, at the Charles R. Bronfman Institute of Personalized Medicine, lead author of the study: The variants coding for proteins involve new genes related to lipid homeostasis contributing to the distribution of body fats. Posted 18 February 2019 online: Nature Genetics.
What is the background of this study?
Obesity usually includes two components; [1] there is a global body size (badessed with the help of a BMI) and [2] there is a breakdown of fats (badessed using the ratio of waist / hips (WHR). Both are "heritable", which means that they are partly determined by our genome (and the l 39; another part by our way of life.) Over the past 15 years, geneticists have used an approach to badyze the entire genome of thousands of people to identify genetic variations that differ, for example, from obese people compared to non-obese people.
We have applied this approach to the two components of obesity and have found until now that the genes of "overall body size" seem to act in the brain, probably controlling hunger, satiety, reward , etc., while the genes that determine
When excess fat will be stored when you gain weight (that is, the breakdown of fat) seems to act more "locally" at the level of fat cells, thus determining the storage and the release of fat. (Published February 18 in Nature Genetics.)
What were the main results of the study?
Our new study differs from those we did before. The genome of people is very large and all our genetic material does not encode genes; a large part of our genetic material "links" the genes. In the past, we looked at the entire genome and many identified genetic variations, located between genes – and it was very difficult to determine which gene was the "causal" gene.
To meet this challenge, in our new study, we focused only on genetic variations that localize "in" genes and thus have the potential to alter the function of the gene and its protein. As such, it becomes easier to "locate" the causative gene.
In this study, we combined data from more than 400,000 people from more than 70 research institutes around the world and identified 24 new genetic variants involved in determining where fat is stored. Follow-up badyzes show that
Many of these variants also affect the risk of diseases such as diabetes, cardiovascular disease, etc.
What is the takeaway message?
We have known for a long time that storing fat at the waist (apple) is more harmful than storing fat at the hips (pear). With our study,
we have identified genes that could help elucidate the biology that links the distribution of fat to disease. Knowing the biology that links the distribution of fat with the disease can eventually help us to "dissociate" the disease from the distribution of fat, possibly by means of drugs targeting the identified genes.
This is not a science fiction idea, because there are cholesterol-lowering drugs (TZDs) that target a gene (PPARG) that influences the distribution of fat; that is, this drug reduces glucose by at least partially redistributing the fat (i.e., reducing intra-abdominal fat storage).
What are the future studies needed?
Identifying genes for fat distribution is just the beginning of a long, extra search path. Follow-up studies will need to look at how genes work, in which pathways, which tissues, and whether they would be good targets, for example. drug development.
Learn more by reading the newspaper at https://rdcu.be/bnkK0
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