14 DAY TRIAL // A new research found that once fat cells and tissues of morbidly obese people and animals no longer can store fat appropriately, they trigger changes within the body, that are linked to type 2 diabetes and other obesity-related diseases.
This work was funded by the Biotechnology and Biological Sciences Research Council (BBSRC), the Medical Research Council (MRC) and the European Union Sixth Framework Program, and was carried out at the University of Cambridge.
The results of the research show that a protein called secreted frizzled-related protein 1 – SFRP1, which is produced by fat cells, can change the body's metabolism and lead to an increased risk of diabetes and cardiovascular disease.
The SFRP1 recruits new fat cells and its level keeps rising at the same rate as the fat cells and tissue, until it reaches its peak – the point of mild obesity.
Dr Jaswinder Sethi, from the Institute of Metabolic Sciences said that “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.”
The researchers noticed that in the case of obese people who also suffer from diabetes, fat tissue is not properly regulated and SFRP1 levels start to decrease, stopping the tissue from expanding any further.
It is this fall that affects the metabolism and which could be a plausible explanation for the link between the metabolic syndrome and morbid obesity.
The team think that SFRP1 is not working alone and that there are other molecules that help it respond to the availability, or lack, of energy, the same molecules that establish just how much our fat tissue can expand when the calorie intake is higher than the burning.
"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,” said Professor Antonio Vidal-Puig from the Institute of Metabolic Science, University of Cambridge.
Dr Sethi added that “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.”
There is however a hypothesis that storing extra fat is not necessarily a cause of the metabolic syndrome; in this case, once the body passes the fat limit it can safely store, its natural responses lead to the chronic health problems often linked with obesity.
“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,” said Dr Sethi.
Professor Douglas Kell, BBSRC Chief Executive added that “research such as this leads to better understanding of the biochemistry that drives normal human physiology.
“In particular we can see how we usually respond to extremes brought on by the various onslaughts of our lifestyles and environments.
“Increasing our understanding of the fundamentals of metabolic signaling is an important part of working towards an increase in health span to match our increasing life spans.”
The study will be published in a future edition of the International Journal of Obesity Research.