Washington, Apr 17 : It's long been thought that obesity is the trigger to a collection of heath risk factors called metabolic syndrome. However, a new study states that the actual culprit may be overeating.
The finding is based on a study on mice carried out by researchers at the UT Southwestern Medical Center.
Metabolic syndrome raises a person's chances of developing insulin resistance, fatty liver, heart disease and type 2 diabetes
"Most people today think that obesity itself causes metabolic syndrome when in fact it is the spillover of fat into organs other than fat cells that damages these organs, such as the heart and the liver. Depositing fatty molecules in fat cells where they belong actually delays that harmful spillover," said Dr. Roger Unger, professor of internal medicine at UT Southwestern and senior author of the study.
"Obesity delays the onset of metabolic syndrome, but it doesn't prevent it. People who are obese or overweight are on the road to developing metabolic syndrome unless they stop overeating. Sooner or later, it will happen," he added.
The researchers carried out the study to determine whether a person's capacity to store fat in fat cells plays a role in whether they develop metabolic syndrome and type 2 diabetes and at what point that occurs.
As a part of the research, the boffins compared mice genetically altered to prevent their fat cells from expanding when overfed to mice with no protections against obesity.
They noted that overeating made normal mice fat, but they didn't develop signs of metabolic syndrome until about 7 weeks into the experiment, at about 12 weeks of age.
Some of the genetically engineered mice however became seriously ill at 4 to 5 weeks of age and displayed evidence of severe heart problems and marked hyperglycemia by 10 weeks of age, a full 8 weeks before the normal mice displayed even minimal heart problems.
The rodents also suffered devastating damage to heart cells and to the insulin-secreting cells in their pancreas.
Dr. May-yun Wang, assistant professor of internal medicine at and lead author of the study said the genetically engineered mice got sick quicker because the extra calories were not stored in the fat cells, the one place in the body equipped to store fat.
Instead, fat was stored in other tissues.
The study, available online, is to be published in a future issue of the Proceedings of the National Academy of Sciences.