Scientists at the University of Michigan led by physiologist Ormond MacDougald have discovered thatfat-storing cells get fat and burn fat more slowly as the body increases obesity levels. If their conclusions, obtained in experiments with mice, are confirmed to apply equally to humans, the research could provide a new target for drugs that fight excess weight. In analyzing the signals that fat-storing cells exchange with each other, the team demonstrated the crucial – and previously unknown – role played by amolecule called Sfrp5. The results will be published in the July issue of the magazine Journal of Clinical Investigation.
Previous studies had already shown that the amounts ofSfrp5produced within fat tissue are higher in obese animals. The researchers created mice that couldn’t make the molecule, and they hoped they would resist obesity because they couldn’t convert more cells into adipocytes that would store excess fat from their high-fat diet. Instead they found thatmice without Sfrp5 had as many fat cells as other mice, but these cells did not accumulate fat or grow in size. As a result, the mice did not independently gain fat content in their diet.
On closer observation of mice deficient inSfrp5, the researchers saw increased activity in the expression of genes related to the mitochondria – the “furnaces” inside the cell that burn fat and other fuels for energy.as if dry wood were added to the ovens when the Sfrp5 was not present, so that fat was consumed at a higher rate than normal.? From our results we believe that fatSfrp5is it an important moderator of mitochondrial activity ?, the authors explain.
