Health problems if the fat cells reach their limit
The fat cells of obese people seem to have a limit on the amount of fat that are capable of storing.
According to new research funded in part by the EU, the fat cells of obese people seem to have a limit on the amount of fat that are capable of storing. Once this limit is reached, will trigger a series of biological processes that stop the further expansion of adipose tissue and could be the cause of some of the health problems associated with obesity such as type 2 diabetes and cardiovascular disease.
The study is published in the International Journal of Obesity and was supported by the EU through a Marie Curie grant and the project HEPADIP (hepatic and adipose tissue and functions in the metabolic syndrome “), which was funded as part of ‘ thematic area ‘Life sciences, genomics and biotechnology for health in the Sixth Framework Programme (FP6). These findings could help explain why some obese people develop diabetes, cardiovascular disease and cancer, while others do not.
“What we still do not understand at all, as is the expansion of adipose tissue is regulated in healthy people and how this adjustment process may be different in those obese individuals who have health problems like metabolic syndrome,” explained Dr . Jaswinder Sethi Institute of Metabolic Science, University of Cambridge in the UK.
Some scientists believe that storing too much fat does not lead directly to metabolic syndrome, there is indeed a limitation with regard to how much fat can be stored safely before the body reacts, triggering the many health problems often associated with obesity.
It appears that a protein called protein 1 secretion frizzled-related (SFRP1), which is produced by fat cells, is essential for this process. While increasing the volume of cells and adipose tissue, also increases the level of SFRP1. According to the team, there is evidence that the SFRP1 helps to promote the expansion of adipose tissue.
However, the levels of SFRP1 not continue to increase indefinitely, but reach a peak when the subject is moderately obese. In fact, the levels of SFRP1 gradually decreased in severe obesity. The researchers suggest that the SFRP1 could work together with other molecules to react to the availability of energy, if there is a surplus of energy, these molecules determine the extent to which we can expand the adipose tissue.
The decreasing levels of SFRP1 could be the basis of metabolic problems suffered by obese. In particular, the adipose tissue of obese subjects with diabetes to show a decline in the levels of SFRP1.
“The SFRP1 seems to be closely connected to some kind of tipping point, beyond which the way that our fat tissue is set to change significantly and there are consequences for our chain metabolism in general,” said Dr. . Sethi. “We believe that in subjects with severe obesity this might be an early event that triggers the metabolic syndrome and chronic health problems associated with it, such as diabetes and cardiovascular disease.”
Understanding these complex pathways may also contribute to the development of treatments for metabolic diseases associated with obesity. As pointed out by researchers, obesity levels are increasing despite efforts to promote changes in lifestyle that lower the risk of putting on too much weight. The researchers concluded that these new findings could have “potential therapeutic uses in the treatment of metabolic complications associated with obesity.”
The team arrived at these conclusions after conducting the profiling of human genes and genetic studies of mice to find out what happens during the development of cells and adipose tissue.
Additional research funding was provided by the Biotechnology and Biological Sciences Research Council (BBSRC) and the Medical Research Council (MRC) of the United Kingdom. The study also involved scientists in Spain and Finland.
