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Obesity research wins Fernström Prize

This year's Fernstrm Foundation Nordic Prize, worth SEK 1 million, goes to Professor Peter Arner from Karolinska Institutet, Sweden, who conducts research on fat. His team was the first to show that fat cells are formed throughout one's lifetime, not just in childhood. He has also discovered certain genes that provide protection against the negative effects of fat cells and shown how fat cells are affected by abdominal obesity, which is more dangerous than fat in other parts of the body.

Shipowner Eric K. Fernstrm's foundation is based at the Faculty of Medicine at Lund University. The Foundation awards an annual Nordic prize of SEK 1 million and local prizes of SEK 100 000 each to promising young researchers at Sweden's six university medical faculties.

The Nordic Prize has prize money of SEK 1 million. This year's prize recognises Peter Arner's work to "increase understanding of the function and regulation of human fat tissue and its major significance in health and disease".

The old understanding in the research community was that the human body stopped forming fat cells in adolescence. Now, however, thanks to the work of Peter Arner and others, we know that roughly ten per cent of all fat cells are renewed each year. The fat in the fat cells is also replaced several times during the lifetime of the cells. The turnover of both fat cells and fat content in the cells can change with certain common conditions.

"With such a rapid rate of renewal, it should be possible to influence the fat cells to increase or reduce fat production", says Peter Arner. A fat cell moderating substance would of course be a huge hit on the dieting market. However, Peter Arner is not really interested in the cosmetic possibilities.

"Obesity in itself is not usually a hereditary disease, but rather a condition that is best countered with exercise and the right diet!" he stresses.

As a doctor, he wants to focus on fat-related diseases, for example cachexia, or wasting syndrome, the opposite of obesity. This is a condition that affects some cancer patients and that can prove fatal. Another dangerous condition is a hereditary lipid disorder that gives patients dramatically raised cholesterol without them being obese. Another area of interest is of course the conditions associated with obesity, such as high blood pressure and diabetes.

However, a third of all obese individuals turn out to have completely normal blood pressure and no insulin resistance (a preliminary stage of diabetes). For these people, the most likely health problem resulting from their obesity is joint problems caused by their weight.

Why do a third of obese individuals experience so few problems? This is a question which Peter Arner's team is now going to address. Perhaps these individuals have protective genes. One such gene, called cidea, was discovered by the team almost ten years ago. The gene stops the fat producing any waste products that can harm other cells.

Waste products from the fat around our intestines are one possible reason why abdominal obesity is more harmful to our health than obesity on the thighs and buttocks, for example, as Peter Arner and his team have shown. Another reason could be that fatty acids from the central fat can travel directly into the liver and affect blood lipids and sugar metabolism.

Waist measurement is in fact more strongly associated with insulin sensitivity than blood lipids, blood pressure or body weight, as Peter Arner has shown in another study. A waist measurement of less than 100 cm entails almost no risk of insulin resistance, whereas the risk increases strongly with greater abdominal obesity.

"People who carry a small amount of excess weight around the abdomen but are otherwise slim have a particular problem. They cannot diet, because they become too thin. We could do with a way to influence only the central fat", says Peter Arner.

He is hopeful that this will become possible in the future. The team will shortly publish new results on where fat cells are formed and on the genes and proteins that influence the renewal of fat cells and their fat content. The latter is an area in which work will continue, and there are likely to be plenty of ideas for possible treatments.

Contact: Peter Arner
Lund University

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