FGF21, in turn, stimulates the use of stored fats as energy and causes torpor. In properly fed mice, FGF21 is not normally active; however, when the researchers introduced FGF21 into these mice, the animals’ metabolism changed.
“When mice were given this hormone, their metabolism appeared as if they were starved, even after they had just eaten,” said Dr. Kliewer.
Because limiting food consumption is known to have a range of beneficial effects, such as lowering blood pressure, cholesterol and glucose levels in the blood, Dr. Kliewer is interested in understanding how FGF21 impacts these processes.
“We want to see if we can get some benefits of eating less without actually eating less,” he said.
Manipulating the PPAR-alpha-FGF21 signaling pathway might ultimately prove to be a vital part of the ongoing search for new therapies for human obesity and other metabolic conditions, Dr. Kliewer said.
“Given that the PPAR-alpha receptor already is the target of drugs that work to boost high-density lipoproteins, or the ‘good’ cholesterol, and reduce the amount of fat in the blood, we believe this new pathway may lead to a new class of drugs that will impact many human conditions,” he said.
Source:UT Southwestern Medical Center