How Aging Fat Cells Make You Sick(er)
By: Gunnar De Winter
Tags: Biology, Health, Disease, Science, Aging

How Aging Fat Cells Make You Sick(er)

Fully developed fat cells (Wikimedia commons, M. Oktar Guloglu)

Age, age, everywhere

When we reach adulthood, our individual biological time does not stop. The biological clock keeps ticking. We age. Over our entire body, things start to go wrong.

Our skin loses its tight smoothness, our body shape and fat distribution change, muscle tone decreases. The immune function starts to sputter, the risk for cancer goes up, joints creak, memory falters, and even our microbiome might give us trouble.

Of course, the extent of these changes differs between individuals and there are lifestyle factors that can speed up or slow down the process. Still, no one escapes it (not even centenarians).

One of the reasons why aging affects so many parts of our bodies is that — within our own body — aging is contagious. Cells that turn senescent stop dividing and start slacking off. They also tend to develop what is called the senescence-associated secretory phenotype or SASP. Senescence-associated = related to aging, secretory phenotype = stage in which cells excrete stuff.

Unfortunately, when it comes to SASP, the excreted stuff is bad news. Inflammatory molecules, protein chompers… A lot of molecules that have a negative effect on neighboring cells. Aging spreads.

(Removing some of the SASP-associated molecules might be a reason why blood dilution or exchange is being studied to mitigate the effects of aging.)

Old fat

The bright spots are telomeres capping human chromosomes. (Wikimedia commons, U.S. Department of Energy Human Genome Program)

Another reason why aging is everywhere might be telomeres. Telomeres are protective ‘caps’ on the end of chromosomes that comprise the DNA in cells.

With each cell division, a small bit of those caps is chipped off. Enough divisions, and the caps are gone, exposing coding DNA to the ravages of time.

A new study looks in detail at what happens in fat cells when the telomeres shorten.

To do this, the scientists overfed mice. Why overfeeding? Obesity has been linked to premature aging in adipose tissue (fat).

In the mice, overfeeding and aging delivered a one-two punch that resulted in telomere attrition (DNA caps getting smaller) and apidocyte hypertrophy (growing fat cells). The fat cells also showed signs of inflammation and fibrosis (tissue stiffening). This, in turn, led to higher insulin resistance (interestingly, only in male mice, female mice are thought to be protected by estrogen).

But, as you should know by now, we need to be cautious. Mice are not human.

However, the scientists also looked at fat tissue biopsies of obese humans. They found that:

… telomere shortening was observed in SAT [subcutaneous adipose tissue, ‘fat’] of obese humans with metabolic disease who were also less sensitive to the anti-obesity effects of bariatric surgery.

In other words, people who are obese have short telomeres in fat tissue (shorter than people who are either old or obese). This ‘old fat’ tissue also increases the chance of developing insulin resistance, which could be why some people still have metabolic disease (in the form of type two diabetes) after weight loss surgery.

They conclude that:

… over-proliferation of APCs, which is expedited by over-nutrition, leads to their premature exhaustion, providing a mechanistic link between obesity, diabetes and ageing.

So, don’t accumulate too much body fat (of course, you need body fat to survive, but try to keep it under control).

Also, don’t age.