Obesity could be treated with a slimming pill that targets the immune system, according to new research.
Experiments showed mice lacking a particular type of white blood cell remained as lean as their peers – even when fed a junk food style diet.
Scientists believe the same would apply to humans. It offers hope of burning off the flab with an immunosuppressant tablet.
In a series of tests the Japanese team showed lab rodents lacking immune cells called ILC2s could gorge – without gaining any extra weight.
What is more, they did not suffer from any of the physiological symptoms of a poor diet that affect health – and can lead to type 2 diabetes and other illnesses.
The discovery may lead to the development of a medication that allows couch potatoes to shed the pounds – while watching TV.
First author Dr Takaharu Sasaki, of the University of Tokyo in Japan, said: “Now we know that despite a high-fat diet, diet-induced obesity can be prevented by eliminating small intestinal ILC2s.”
A ‘Holy Grail’ diet pill could help millions of overweight Britons beat middle age spread.
The UK has been dubbed the ‘Fat Man’ of Europe with almost two in three adults overweight or obese.
Immunosuppressants are a class of drugs that suppress, or reduce, the body’s immune cells.
Everyone knows eating too many burgers, pizzas, chips and cakes is a recipe for a bulging waistline. But the reasons have never been fully understood.
The findings, published in the journal Cell Reports, suggests the answer lies in the activity of ILC2s (group-2 innate lymphoid cells) that live in the small intestine.
Many factors can contribute to obesity including an individual’s genes, gut bacteria and diet.
Recent studies have shown the immune system can also have an effect – but the details are still unclear.
Dr Sasaki’s team analysed genetically engineered mice to determine the role of innate lymphoid cells – a type of white blood cell.
They examined two groups – one lacking only highly specialised immune cells, called acquired immune cells, and the other having no ILCs.
They then fed the mice either a normal or high-fat diet for 8 weeks, after which they were compared with a third set of unmodified mice that acted as a control.
All the animals showed mild weight gain on a normal diet. When fed the high fat diet, both the control mice and those missing acquired immune cells, as expected, gained a tremendous amount.
But those lacking ILCs did not. In fact, they stayed as slim as those who received the normal diet – despite consuming the same amount of high-fat food as the other two groups of mice.
Subsequent testing showed mice lacking ILCs also failed to show other signs of obesity such as more white fat, larger livers, raised blood sugar and impaired insulin resistance.
To back up the results the researchers reintroduced ILCs into the deficient mice through a bone marrow transplant.
After two months on a high-fat diet, they found these same mice now showed all the symptoms of obesity. This made the team sure it was the lack of ILCs that had prevented diet-induced obesity.
There are actually three types of ILCs but – after specific tests – the group-2 set were identified as being key to weight gain.
Dr Sasaki said: “This was surprising. In the past, ILC2s from white adipose tissue were shown to help prevent obesity.
“However, here we found that when they come from the small intestines, they actually promote obesity.”
The researchers confirmed this finding by transferring white fat-ILC2s into the mice lacking all immune cells.
They found only those that received ILC2s from the small intestine became obese after eating the high-fat diet.
Dr Sasaki added: “This means that aside from controlling our diets, some function of these cells could be a potential target for obesity treatment.
“Our next step is therefore to determine how small intestinal ILC2s induce obesity.”
ENDS