Good news for people who wish to eat fat and lose weight at the same time, as team of researchers has identified a pathway to prevent fat cells from growing larger that leads to weight gain and obesity.
According to researchers from Washington University in St. Louis U.S., by activating Hedgehog pathway in fat cells in mice they could feed the animals a high-fat diet without making them obese.
Senior investigator Fanxin Long said this could lead them to a new therapeutic target for treating obesity.
"What's particularly important is that the animals in our study ate a high-fat diet but didn't gain weight, and in people, too much fat in the diet is a common cause of obesity," Long added.
They explained that fat gain is due mainly to increased fat cell size and each fat cell grows bigger so that it can hold larger fat droplets. A person gains weight mainly because fat cells get bigger, as opposed to having more fat cells.
He focused on the so-called Hedgehog protein pathway that is active in many tissues in the body.
His team engineered mice with genes that activated the Hedgehog pathway in fat cells when those animals ate a high-fat diet.
The results suggested that after eight weeks of eating the high-fat diet, control animals whose Hedgehog pathways had not been activated became obese.
But the mice that had been engineered with genes to activate the pathway did not gain any more weight than did control animals that consumed normal diets.
The Hedgehog pathway prevented obesity by inhibiting the size of the fat cells, Long said.
By stimulating Hedgehog and related proteins in fat cells, Long's team kept the animals' fat cells from collecting and storing fat droplets.
"If we can come up with strategies to carefully target fat cells, then I think activating this pathway could be effective in the fight against obesity," he said.
People with obesity have an increased risk for stroke, heart attack, diabetes and cancer.
The research appears in the journal eLife.
Disclaimer: No Business Standard Journalist was involved in creation of this content
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