Exceeding ‘cell fat storage capacity’ might trigger type-2 diabetes

WASHINGTON - A new study has found that fat cells and tissues of acutely obese people and animals have a limit of storing fat after which further expansion may trigger other health problems.

Research funded by the Biotechnology and Biological Sciences Research Council (BBSRC), the Medical Research Council (MRC) and the European Union Sixth Framework Programme,

The new research has shown that a protein called secreted frizzled-related protein 1 (SFRP1) is produced by fat cells and may be involved in changes to our metabolism that could increase the risk of diabetes and cardiovascular disease.

Antonio Vidal-Puig from the University of Cambridge said, “We have known for some time that many obese individuals are at greater risk of developing diabetes, cardiovascular disease and also cancer. But this is not true for all obese people.”

Jaswinder Sethi, also from the Institute of Metabolic Sciences, University of Cambridge added “What we still do not fully understand, is how the expansion of fat tissue is regulated in healthy people and how this process of regulation might be different in those obese people who have health problems such as the metabolic syndrome.”

“To investigate this we have been using a combination of molecular cell biology, human gene profiling and mouse genetics as tools to understand what is happening as fat cells and tissues develop and then, in some very obese people, lose their normal process of regulation,” he said.

The researchers have found that the level of SFRP1 increases as fat cells and tissues increase in volume until it peaks at about the point of mild obesity.

“SFRP1 seems to be very closely linked to some sort of tipping point, after which the way in which our fat tissue is regulated changes significantly and there are knock-on consequences to our wider metabolism. We think that in very obese people this may be an early event that triggers metabolic syndrome and the chronic health problems associated with it, such as diabetes and cardiovascular disease,” said Sethi.

In this tissue, the researchers also found the levels of SFRP1 begin to fall so as to prevent further expansion of the tissue. It is this fall in SFRP1 that has knock-on effects on metabolism that may in part explain the link between morbid obesity and metabolic syndrome.

The findings will be published in the International Journal of Obesity. (ANI)