Our body's fat-storing mechanisms - called adipose tissues - are very good at the job of taking our excess calories and storing them in the form of high-energy molecules called lipids.

But new research suggests their cells can expand to a size that literally suffocates them, triggering inflammation and making the adipose tissues less efficient. Not only is this bad news for losing weight, it also puts other organs at risk of critical damage.

Research led by the University of Exeter in the UK found that levels of an enzyme called lysyl oxidase increase in adipose tissues as an individual's body mass index goes up, indicating the cells were being scarred as they expanded in size.

Lysyl oxidase – or LOX – crosslinks fibres of collagen, a tough protein that builds structures inside cells and helps connect tissue. Excess LOX can mean there's too much fibrous structure surrounding cells, making the tissue rigid.

All of this adds up to fat cells that can no longer expand to fit more lipids, and change how fat is distributed around the body.

Scarred adipose tissue can see more fat distributed around organs and less under the skin, giving people an 'apple' shape with larger bodies and thinner limbs.

Since this visceral fat is more of a concern for our health than subcutaneous fat, it's a serious problem that warrants addressing.

"One could have very little fat below the skin and still be at risk of diabetes due to a lot of fat within the abdomen and inner organs," says physician Katarina Kos from the University of Exeter's Medical School.

It also means there's less room for fat to be stored inside the adipose tissue itself.

While you might imagine this to be a good thing, that fat doesn't disappear – instead, it can be diverted into other tissues such as the liver and the heart, raising the risk of cardiovascular disease.

And if all that isn't bad enough, stiffer adipose tissues also make it hard for the cells to release their stores of fat.

"Scarring of fat tissue may make weight loss more difficult," says Kos.

Much of the problem starts with the cells in adipose tissue becoming starved of oxygen.

The researchers compared the levels of messenger RNA expressed for the LOX enzyme in adipose tissues from patients undergoing bariatric surgery, and again in samples collected over nine months later.

They also analysed LOX expression in response to mild inflammation in the fat tissues of healthy male volunteers, and compared levels in diabetic patients.

While having diabetes didn't affect the levels of LOX, and therefore the scarring of the tissues, low levels of oxygen and inflammation had a significant impact on its expression.

This was taken to suggest that as the cells fill and expand, they're deprived of the oxygen they need to survive. This triggers and inflammation process, increasing LOX levels and making the cells more fibrous.

Unfortunately weight loss surgery didn't see the LOX levels decrease, making it unlikely that the tissues would become less scarred even with radical interventions.

The take-home message is to keep our adipose tissue in check before it gets to that stage.

"There is evidence that once fat tissue becomes scarred, despite weight loss, it may not recover fully," says Kos.

"We need to look after our fat tissue which can cease to cope if it is overworked when being forced to absorb more and more calories."

Kos's advice is to exercise or at least take a walk after a meal. Weight loss is hard, and while a few people have the ability to keep at it, others face an uphill battle thanks to a mix of biology and habit.

But if knowing it could only get harder later gives some people that incentive to cut a few calories and walk after a meal, then this is one study to pay close attention to.

This research was published in Metabolism.