NEWS |
TO FIGHTING AND PREVENTING OBESITY Findings could lead to ideal pharmacological intervention for weight problems
U
NIVERSITY OF FLORIDA researchers and colleagues have identified a protein that, when absent, helps the body burn fat and prevents insulin resistance and obesity.
The findings from the study have been
published in Nature Medicine, and could aid development of drugs that not only prevent obesity, but also spur weight loss in people who are already overweight, said Stephen Hsu, one of the study's corresponding authors and a principal investigator with the UF Sid Martin Biotechnology Development Institute. Although unrelated studies have shown that
lifestyle changes such as choosing healthy food and increasing exercise can help reduce obesity, people are often unable to maintain these changes over time, Hsu said. 'The problem is when these studies end and
the people go off the protocols, they almost always return to old habits and end up eating the same processed foods they did before, and gain back the weight they lost during the study,' he said. Developing drugs that target the protein, called TRIP-Br2, and mimic its absence may allow for the prevention of obesity without relying solely on lifestyle modifications. First identified by Hsu, TRIP-Br2 helps
regulate how fat is stored in and released from cells. To understand its role, the researchers compared mice that lacked the gene responsible
for production of the protein, with normal mice that had the gene. Mice missing the
TRIP-Br2 gene did not gain weight no matter what they ate, and were otherwise normal and healthy. However, the mice that still made TRIP- Br2 gained weight and developed associa t ed problems such as insulin resistance, type 2 diabetes and high cholesterol when placed on a high-fat diet. The normal and fat-resistant mice ate the same amount of food, ruling out differences in food intake as a reason why the mice lacking TRIP-Br2 were leaner. When functioning normally, TRIP-Br2
restricts the amount of fat that cells burn as energy. But when TRIP-Br2 is absent, a fat-burning fury seems to occur in fat cells. Although other proteins have been linked to the storage and release of fat in cells, TRIP-Br2 is unique in that it regulates how cells burn fat in a few different ways, Hsu said. When TRIP-Br2 is absent, fat cells dramatically increase the
DISCOVERY OF PROTEIN THAT COULD BE KEY
release of free fatty acids and also burn fat to produce the molecular fuel called ATP that powers mitochondria. In addition, cells free from the influence of TRIP-Br2 start using free fatty acids to
generate thermal energy, which protects the body from exposure
to cold. As the studies were done
mostly in mice, additional studies are still needed to see if the findings translate
to humans. 'We are very optimistic about
the translational promise of our
findings because we showed that only human subjects who had the kind of fat (visceral) that becomes insulin-resistant also had high protein levels of TRIP-Br2,' said Hsu. 'Imagine you are able to develop drugs that
pharmacologically mimic the complete absence of TRIP-Br2. If a patient started off fat, he or she would burn the weight off. If people are at risk of obesity and it's associated conditions, it would help keep them lean regardless of how much fat they ate. That is the ideal anti-obesity drug, one that prevents obesity and helps people burn off excess weight.'
IMPROVEMENTS IN SIGHT FOR THOSE SUFFERING FROM AMD
A tiny ‘telescope’ or implant in the eye, fitted in less than 30 minutes, is set to revolutionise the lives of many over-60s as it offers a massive improvement in treatment options for the ‘dry’ form of age-related macular degeneration (AMD).
AMD is a degenerative
condition of the centre of the retina associated with ageing. It is the most common cause of blindness in people over 60 years in the UK and usually affects both eyes.
The new IOL Revolution lens
offers a significant improvement to the central vision of those
10 ❚
suffering from both the ‘dry’ and ‘wet’ forms of AMD. Wet AMD has been treatable for some years with injections, but these have not been effective in those suffering from dry AMD. Previous treatment options have been through implants that offer limited improvements in vision, especially as the disease progresses. Dry AMD is caused by an accumulation of waste products from the light-sensitive cells of the retina, causing a gradual degeneration of vision. Until now it has been untreatable. The new implant procedure to fit the IOL-Revolution involves two
January/February 2013 |
prime-journal.com
small lenses being inserted into the eye, which together act like a miniature telescope, slightly magnifying the image seen by the eye and moving it to a healthier part of the retina. The healthy retina takes over the role of the macula and can give significantly improved vision.
Implanting the IOL-Revolution
Lens takes approximately 30 minutes and does not require an overnight stay in hospital. Recipients are given simple exercises to undertake after the operation to help reinforce the improvement achieved. Both eyes are treated separately, usually
2–3 weeks apart. If the AMD progresses in the
years following the implant, the lens can be easily rotated to move the image to a healthier part of the retina. An earlier generation of IOL lenses were used to treat a range of other conditions such as macular holes, myopic degeneration, diabetic retinopathy and hereditary retinal diseases. These lenses carried a small risk of corneal damage or developing glaucoma, but the new IOL-Revolution is much safer as it is implanted within the capsular bag in the eye, away from the cornea.
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