Our body’s fat storing mechanisms – known as adipose tissues – are very good at taking our excess calories and storing them in the form of high-energy molecules called lipids.
However, new research suggests that 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 weight loss, but it also puts other organs at risk of critical damage.
Research led by the University of Exeter in the United Kingdom found that levels of an enzyme called lysyl oxidase increase in adipose tissues as an individual’s body mass index increased, indicating the cells were being scarred as they expanded.
Lysyl oxidase – or LOX – crosslinks fibers of collagen, a strong protein that builds structures inside cells and helps to connect tissue. Excessive LOX can mean that there’s too much fibrous structure surrounding the cells, making the tissue rigid.
All this means fat cells that can no longer expand to fit more lipids, and change how fat is distributed around the body. Scarred adipose tissue could mean more fat distributed around organs and less under the skin, giving people an ‘apple’ shape with large bodies and thinner limbs.
Since this visceral fat is much more of a concern for our health than subcutaneous fat, it’s a serious issue that needs addressing.
Katrina Kos, a physician from the University of Exeter’s Medical School, says that “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.”
It also means that there’s less room for fat to be stored inside the adipose tissue itself. While you might think this is a good thing that fat doesn’t disappear, it could be diverted into other tissues such as the heart and liver, raising the risk of cardiovascular disease. If this wasn’t bad enough, stiffer adipose tissues also make it difficult 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 who were undergoing bariatric surgery, and again in samples collected nine months later. They also analyzed LOX expression in response to mild inflammation in the fat tissues of male volunteers, and compared levels in diabetic patients.
While being diabetic didn’t affect the levels of LOX, and therefore the scarring of the tissues, low levels of oxygen and inflammation had a significant effect on its expression.
This was taken to mean that as the cells fill and expand, they’re deprived of the oxygen that they need to survive. This triggers an inflammation process, increasing LOX levels and making the cells more fibrous.
Unfortunately, weight loss surgery did not see a decrease in LOX levels, making it unlikely that the tissues would become less scarred even with radical interventions. The message to take home here is to keep our adipose tissues in check before it gets to this stage.
Kos goes on to say that “there is evidence that once fat tissue becomes scarred, despite weight loss, it may not fully recover. We need to look after our fat tissue which can cease to cope if it’s overworked when being forced to absorb more and more calories.”
Kos’s advice is to exercise after a meal. Weight loss is hard, and while a few of us have the ability to keep at it, others face an uphill battle thanks to a mixture of ability and habit.
But if knowing that it could only get harder later in life gives some people that incentive to cut out a few calories and exercise after a meal, then this study has been worth it.
Source: sciencealert
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