The Amazing Life of a Fat Cell

[Guest guest]

The Amazing Life of a Fat Cell

The intriguing story of adipose tissue

By John McIntosh; illustrations by David Cutler

REMEDY Spring 2008

 

 

 

 

“My name is Adi: Adipose Tissue. I have been called many things in my

life, from ‘inert tissue’ to ‘a chunk of useless slime.’ Most people look

at me with disdain, but I’m really here to help them! I protect vital

organs, store fuel and energy in case food gets scarce, make hormones

work and control chemicals that regulate brain function, the immune

system and metabolism. Without me, life would be impossible. But what

thanks do I get? So often, I’m lipo’d out and thrown away­just when there

is so much good left for me to do.”

Fast Fat Facts

Fortunately, scientists are delving ever-deeper into the mysteries of fat

cells and discovering more and more about the functions these expandable

little lipid suitcases serve­and why some good fat cells go bad.

 

Adipose tissue is active and complex.

It comes in a variety of sizes and types: small, medium, large,

extra-large, predeveloped, young and old.

Fat cells transmit signals to the brain; they also have receptors

that get switched on and off. These receptors may tell the cell to store

more fat, release more fat or trigger secretion of various chemicals that

influence appetite and the body’s use of insulin.

Fat cells are seriously opinionated: They even seem to have a gender

preference when it comes to where they congregate and multiply.

They are also always in the process of evolving and

growing.

 

“If you take a glob of fat and look at it under a microscope, you are

going to see cells in various stages of maturity,” says Matthew Kaufman,

M.D., a plastic and reconstructive surgeon who practices at the Institute

for Advanced Reconstruction and the Plastic Surgery Center in New Jersey

and Manhattan. Recent research shows, he notes, that a glob of fat

contains not only adipocytes (mature, or adult, fat cells) but also

preadipocytes (immature fat cells), and is a source of adult stem cells

(precursor cells that have the potential to develop into various cells

and tissues).

This stew of not-yet, almost and full-blown fat cells may play an

important role in determining many aspects of overall health, from body

weight to insulin resistance, from sex hormones to emotional

well-being.

Our current understanding of the life stages of a fat cell is a far cry

from the days when scientists believed that fat cells neither died nor

reproduced.

“We think preadipocytes may be used to replace old fat cells when they

die out,” Dr. Kaufman says. “And the preadipocytes may come from stem

cells in fat that are somehow prompted to emerge.

 

“There is also evidence that fat is stimulated by certain chemicals in

the body. One of these is insulin growth factor, or IGF. There is an

intimate relationship between fat tissue in the body and insulin

production.”

Researchers have observed that as fatty tissue increases, insulin levels

increase, perhaps with a corresponding elevation in IGF. Fat cells, Dr.

Kaufman explains, are in turn stimulated by IGF; both insulin and IGF are

likely to stimulate cell growth and inhibit cell death. In other words,

you produce more fat cells, and they hang around longer.

The ever-increasing number of fat cells also produces hormones called

adipocytokines. These speed up cell growth and play a role in

inflammatory processes. And that, Dr. Kaufman says, is the beginning of a

cycle of weight gain and increasing difficulty in losing weight:

“Individual fat cells expand, storing more lipids within their walls.

This stimulates the maturation of preadipocytes into additional fat

cells, and these mature fat cells get bigger, just like the ones before

them.”

A Fat Virus?

Given all the concern about our growing national waistline and the

epidemic of type 2 diabetes that threatens to swamp our health-care

system over coming decades, it’s no surprise that researchers are trying

to figure out just why Americans are so stubbornly fat and getting fatter

all the time. Granted, we eat an enormous amount of fast food and watch

far too much TV, but it doesn’t seem possible that those factors alone

could account for all the excess weight we have put on.

While we now have some knowledge of what happens in adipose tissue that

makes fat cells fatter and more plentiful, we are just beginning to

discover what sets off that process.

In 2007, Magdalena Pasarica, M.D., Ph.D., principal researcher at the

Pennington Biomedical Research Center in Baton Rouge, LA, presented a

paper at the International Applied Fat Technology Society meeting about

her research on the human adenovirus 36 (AD-36) and its effect on the

various fat cells found in fatty tissue. Adenoviruses, the common viruses

that cause colds and flu, usually produce conjunctivitis, respiratory

tract infections or diarrhea. “But when we infected chickens, rats,

marmosets and mice with AD-36,” says Dr. Pasarica, “after three to six

months, they all became obese, even though they consumed similar amounts

of food as the control group did.”

 

Dr. Pasarica’s group then studied the effect of AD-36 in animal

preadipocyte cell lines and found that the virus caused these cells to

accumulate fat. “Then,” she explains, “a study was done in humans.

Researchers tested for the presence of AD-36 antibodies in the blood of

500 subjects from New York, Wisconsin and Florida; they were testing for

people who had been infected with the virus at one point. What they found

was that the people who were antibody positive were significantly heavier

than the ones that were antibody negative.”

The next step for Dr. Pasarica was to see what effect AD-36 had on adult

stem cells found in fat. These stem cells, she notes, can become any type

of cell­bone cells, fat cells, muscle cells. It all depends on the

induction that you use for them; as Dr. Pasarica puts it, “They are like

blank cells.”

After isolating the cells from liposuction aspirate, Dr. Pasarica’s team

performed a Petri dish experiment that showed that once the stem cells

extracted from fat were infected with the virus, they became fat

cells.

“The virus tells them to become fat cells,” she says. “You can

extrapolate this to humans: Suppose that a human is infected with this

virus. The virus could go to the adipose tissue and induce the

development of new fat cells. Also, existing fat cells will be fatter

after infection.

 

“We’ve shown that AD-36 could act in three ways to make people become

fatter and fatter,” conjectures Dr. Pasarica. “The virus makes existing

fat cells bigger and fatter. It makes pre-fat cells turn into fat cells

that in turn get fatter and fatter. And it influences stem cells in

adipose tissue to turn into fat cells. It appears this is how we get more

fat cells and fatter fat cells.”

But the doctor knows that AD-36 is not the only cause of obesity in

humans: “We are not claiming that all obesity is caused by this

infection,” she stresses, “but we do believe that a certain percent might

be caused by it.”

This line of research may eventually help provide the answer to the

age-old question: “Why, given two people with comparable diets and

exercise routines, may one person become obese while the other person

does not?”

Clearly, we have yet to reveal all the mysteries surrounding the life of

adipose tissue. But at least we now realize that it deserves our

attention and respect.