Is Obesity Genetic? Study Highlights New Link Between DNA And Body Fat
Connie K. Ho for redOrbit.com — Your Universe Online
If you´re thinking of eating a burger and have the right DNA, you might just get away with eating this fatty culinary delight without doing too much damage to your waistline. Researchers from the Health Sciences Department at the University of California, Los Angeles (UCLA) recently found that genetics can affect the way a person´s body-fat levels react to a fast-food diet. The researchers found a number of genes that they believe manage those reactions, adding further fuel to the debate over whether genes or environment are the main culprit in obesity, and providing at least a partial answer to the question: Is obesity genetic?
The findings of the study were recently featured in the online edition of the journal Cell Metabolism. The scientists believe that the study is unique in its observation of metabolic responses in regards to a diet high in sugar and fat content.
The team studied a diverse mouse population in specific environmental conditions, allowing them to create a model that resembled the diversity of natural human populations. What they found is that the risk of obesity was only partially affected by the amount and type of food consumed.
“Our research demonstrates that body-fat responses to high-fat, high-sugar diets have a very strong genetic component, and we have identified several genetic factors potentially regulating these responses,” explained the study´s first author Brian Parks, a postdoctoral researcher at UCLA, in a prepared statement.
“We found that obesity has similar genetic signatures in mice and humans, indicating the mice are a highly relevant model system to study obesity. Overall, our work has broad implications concerning the genetic nature of obesity and weight gain.”
The project shows that while fatty diets and a sedentary lifestyle can definitely impact an individual´s chances of becoming obese, people´s body-fat reactions may also be a large part attributed to their inherited DNA. The study was conducted over a period of two years, during which scientists tracked adipose (fat) tissue, global gene expression, intestinal flora (normal intestinal bacteria), and obesity traits in regards to a diet high in sugar and fat.
The team experimented with a group of over 100 inbred strains of mice that were first placed on a normal diet for eight weeks and then given a diet high in fat and sugar the following eight weeks. The researchers determined 11 genome-wide “regions” that were linked to fat gain and obesity that were affected by diets high in fat and sugar.
“We measured the change in fat dynamically, at five different points following a high-fat, high-sugar feeding, providing strong evidence for a genetically controlled body-fat set-point,” continued Parks in the statement. “Our use of inbred mice strains also enabled detailed analysis of the relationship between obesity traits, gene expression, intestinal flora and diet.”
There was a range of dietary responses from the different strains of mice, with increase of body-fat percentage between zero to over 600 percent. During the first four weeks of the high-fat, high-sugar diet, many of the strains of the mice responded to the diet. However, following this initial period, there was no more accumulation of extra fat. Researchers believe that this shows that there is a certain set-point at which the body stops gaining fat due to genetic factors.
“We observed high heritability of about 80 percent for body-fat percentage across the study timeline,” commented the study´s principal investigator Jake Lusis, a UCLA professor of medicine and human genetics. “Changes in body-fat percentage after high-fat, high-sugar feeding were also highly heritable, suggesting that dietary responses are strongly controlled by genetics.”
Furthermore, the researchers noted that while diets high in sugar and calories can contribute to obesity, other environmental factors are also at play.
“Our results emphasize the importance of gene-by-environment interactions, with important implications for an understanding of the overall genetic architecture of obesity,” noted Lusis in the statement. “In particular, it will be of interest to examine behavioral and neurological differences among the strains as they relate to obesity traits.”
To better understand energy expenditure versus body-fat percentage, the scientists believe that it is necessary to further study those mice strains that have faster and slower metabolisms. As obesity has steadily risen in the U.S. population in the last few decades, the team of investigators believes that the study is of profound importance. Obesity can heighten the risk of cancer, heart disease and type 2 diabetes.
“Our future studies will investigate the development of metabolic syndrome and diabetes after high-fat, high-sugar feeding,” concluded Parks. “We will also begin to focus on specific, identified genetic factors and their role in dietary interactions and obesity.”