New research offers hope of treatments for obesity
A Franco-American team of researchers has identified the genetic 'master switch' that triggers the production of brown fat, a finding the scientists hope will lead to new treatments for obesity. The work, which was partly funded by the EU, is published in the journal Cell Metabolism. There are two types of fatty tissue: white fat and brown fat. White fat cells store energy primarily in the form of triglycerides; it is this kind of fat that is causing increasing numbers of waistlines to bulge. In contrast brown fat cells dissipate energy in the form of heat. 'Brown fat is present in mice and in human infants, where it keeps them warm by dissipating food energy as heat, instead of storing it as white fat,' explains Professor Bruce Spiegelman of Harvard Medical School in the US, who led the research. 'Human adults don't have much brown fat, but there is some, and from a therapeutic perspective the question is whether that pathway can be reactivated.' Currently little is known about the developmental origins of brown and white fat cells. In this latest piece of research, Professor Spiegelman and his team identified a gene called PRDM16 which is found in brown fat cells but not in white fat cells. Analyses revealed that PRDM16 triggers the formation of brown fat cells by activating genes which allow cells to release large amounts of energy as heat. The researchers also inserted PRDM16 genes into white fat precursor cells and injected these under the skin of mice. The PRDM16 gene subsequently caused these precursor cells to generate brown fat cells. 'These results illustrate that the gene we identified can turn on a broad programme of brown fat cell development when we insert it into precursors that otherwise would produce white fat,' explains Professor Spiegelman. The scientists believe that inducing PRDM16 activity in white fat precursors could constitute a strategy to boost whole body energy expenditure and prevent the accumulation of excess fat. This could be achieved by drugs to raise PRDM16 levels in fat cells, or by engineering fat precursor cells with PRDM16 in the lab and injecting these into patients. 'You might not have to implant a large amount of engineered precursors in people who are at risk for being obese,' said Professor Spiegelman. 'In theory, you would only have to reduce the accumulation of white fat by one per cent or so to have an effect.' The next step for the researchers is to test these theories further in animals, for example by boosting PRDM16 levels in mice and overfeeding them to see if they are resistant to becoming obese. EU funding for the work came from the Sixth Framework Programme HEPADIP (Hepatic and Adipose Tissue and Functions in the Metabolic Syndrome) project.
Countries
France, United States