Fresh data released this week show in excess of 200 million adults across the EU may be overweight or obese.
And the number of overweight European kids is rising by a hefty 400,000 a year, according to the data from the International Obesity Task Force (IOFT), one of the stakeholders contributing to the new EU platform.
Obesity, defined as a Body Mass Index over 30, is a risk factor for a host of (expensive) illnesses including heart disease, diabetes and respiratory disease. According to the Commission, obesity accounts for between 2 to 8 per cent of healthcare costs in Europe.
But scientists are still trying to determine how the obesity and diabetes conditions are linked, and what it takes to turn an obese person into a person with diabetes. New findings suggest the influences could be much more than food.
Yesterday researchers at the University of Michigan and Harvard University reported on new evidence in mice that may help explain that link - and may help them understand why some obese people never develop diabetes while many others do.
"Taken together, our findings show there's more to the obesity-diabetes link than the classic thinking that if you eat too much sugar, you'll get fat and get diabetes," says senior author Martin Myers. "There's something else contributing. Now the challenge is to find out what that is."
The study, published in Cell Metabolism, suggests that the hormone leptin regulates blood sugar through two different brain-body pathways: one that controls appetite and fat storage; and another that tells the liver what to do with its glucose reserves.
It is already known that disrupting leptin's appetite-controlling role leads to obesity, and that obesity is known to significantly raise the risk of diabetes.
But more than ten years after influential obesity researcher Jeffrey Friedman and colleagues discovered leptin, these latest results suggest it may take disruptions to both pathways to bring on full-blown diabetes and overwhelm the body's ability to control blood glucose levels via the action of insulin.
The new research is based on mice that the researchers genetically modified to disable the leptin-STAT3 cell-signaling pathway that leads from the brain to the body.
The mice, called the s/s strain, could still produce both leptin and the receptor it binds to when sending STAT3 signals to the body.
The s/s mice ate too much and became obese, but they did not develop diabetes even after six months, a long time for a mouse, say the researchers. Meanwhile, other strains of mice that made no leptin, or have no leptin receptors, all became obese and died of diabetes.
"The blood sugar of the s/s mice was high, but it was much more in control than mice that had no leptin receptors at all, and was not because of differences in their insulin production," says Myers.
"And when the s/s mice were put on calorie-restricted diets, their blood sugar normalised.
These findings suggest that since the leptin-STAT3 signal was disrupted, some other signal must have been keeping glucose in check," he adds.
The other signaling pathway, though still unknown, likely controls the release of stored glucose from the liver, since that is the only other major source in the body, the scientists add.
This brain-liver leptin signal pathway, for which the U-M/Harvard team is already searching, is involved in glucose homeostasis, or the regulation of blood sugar by feedback loops, says Myers.