Being overweight greatly increases the risk of developing diabetes but the reasons why this is so have remained difficult to find. Now researchers in the US report the discovery of at least one potential link, a discovery that could lead to new treatments.
A team from the University of Pennsylvania School of Medicine led by Dr Mitchell Lazar identified a new hormone released by fat cells that interferes with the uptake of insulin. The findings are reported today in the journal Nature.
The discovery relates to Type II diabetes, the most common form of the disease which accounts for 90 per cent of all cases. This form mostly occurs in people over 40, but its incidence is increasing rapidly in industrialised countries and is beginning to occur in much younger age groups. The risk is particularly high if the person is overweight with about 80 per cent of sufferers medically classed as obese.
It is usually controlled by a careful diet and tablets, unlike Type I which requires insulin injections. However, the risk to health with Type II diabetes is not trivial. It can lead to serious circulatory problems and recurring infections which are difficult to treat.
Researchers have long sought the connection between being overweight and the Type II disease, the hope being that once found the link could be used to develop new treatments. The University of Pennsylvania team believe they have at least part of the answer, a hormone released by fat cells which they have christened "resistin".
Diabetes is caused when the body is unable to supply enough insulin, a protein that enables muscle and other tissues to make use of sugars in the blood. Without insulin these sugars build up to the point where tissue damage is possible and the person's life can be put at risk.
Obesity causes certain tissues including muscle and liver to be less sensitive to insulin. Being overweight increases the risk that tissues will not be able to make full use of whatever insulin is available. Obesity occurs when the body stores excess fat in cells known as adipocytes. Dr Lazar and his team discovered that the fat cells released resistin, a substance found to promote insulin resistance. The more fat cells the greater the potential for insulin resistance.
The team tested the link using mice models bred to have both diet-induced and hereditary diabetes. The heightened resistin levels in these mice were reduced when the researchers used new anti-diabetes drugs that worked against resistin. They also attempted to reduce resistin levels by using an anti-resistin antibody. In both cases the treatments improved blood sugar and insulin action in mice.
While the discovery of the role played by resistin is important, it is only part of the biochemical story. Yet to be discovered is how resistin interrupts the normal effects of insulin and what role resistin plays in healthy individuals.
It does open up new treatment opportunities targeted at the protein. It may also provide new ways of assessing the development of Type II diabetes in at-risk patients who show no signs of the disease.