Are some people born to make more fat cells?

By Mark Prigg

Researchers have uncovered a protein they say controls how the body produces fat cells.

Called Thy1 it has a fundamental role in controlling whether a primitive cell decides to become a fat cell.

Experts say it could be harnessed in obesity treatments.

Called Thy1, the protein has a fundamental role in controlling whether a primitive cell decides to become a fat cell. Experts say it could be harnessed in obesity treatments.

‘We believe that weight gain is not necessarily just a result of eating more and exercising less,’ said lead author Richard Phipps of the University of Rochester.

‘Our focus is on the intricate network involved in fat cell development.’

The Rochester teram discovered that a protein, Thy1, has a fundamental role in controlling whether a primitive cell decides to become a fat cell, making Thy1 a possible therapeutic target, according to a study published online this month by the FASEB Journal.

Although Thy1 was discovered 40 years ago and has been studied in other contexts, its true molecular function has never been known.

Phipps’ laboratory reported for the first time that expression of Thy1 is lost during the development of fat cells, suggesting obesity could be treated by restoring Thy1.

They’re also working towards developing an anti-obesity drug, a Thy1-peptide, and have applied for an international patent to protect the invention.

Phipps has been investigating Thy1 since 1989; The UR is trying to identify a company to help with commercializing the patent asset and bring a new obesity treatment to the marketplace.

‘Our goal is to prevent or reduce obesity and in this paper we’ve shown how to do this in principle,’ said Phipps.

Researchers studied mice and human cell lines to confirm that a loss of Thy1 function promotes more fat cells.

Mice lacking the Thy1 protein and fed a high-fat diet gained more weight and faster, compared to normal mice in a control group that also ate the same high-fat diet.

In addition, the fatter mice without Thy1 had greater than twice the levels of resistin in their blood, a biomarker for severe obesity and insulin-resistance or diabetes.

‘Our goal is to prevent or reduce obesity and in this paper we’ve shown how to do this in principle,’ said Phipps.

Experiments using human fatty tissue from the abdomen and eyes showed similar results.

Phipps and colleagues, including key researcher Collynn Woeller, Ph.D., research assistant professor of Environmental Medicine, are continuing to investigate why cells with the potential to turn into fat cells lose the Thy1 protein, and why fat accumulates faster when Thy1 shuts off.

It’s not clear whether Thy1 levels are different in people at birth, or whether they change with time and exposure to various environmental agents.

To address the latter question, Phipps’ laboratory is separately studying whether chemicals known as obesogens – such as bisphenol A (BPA), flame retardants, and phthalates – reduce Thy1 expression in human cells and promote obesity.

Source: Dailymail.co.uk