News and Research
Immune System
Fat Cells Fight Disease, Purdue University Researchers
Find
Purdue
researchers have determined that fat cells in humans defend
against biochemical processes involved in illnesses such
as diabetes and cancer. The research team is headed by
Michael Spurlock (left), professor of animal sciences,
and Kolapo Ajuwon, a doctoral student. (Purdue Agricultural
Communications photo/Tom Campbell).
1-21-2004
WEST LAFAYETTE, Ind. - Fat cells, commonly blamed for a
number of diseases, also may aid in the body's defense against
illnesses such as diabetes and cancer, according to Purdue
University researchers.
Rather
than contributing to disease, fat cells, or adipocytes (pronounced
ah-dip-poe-sights), normally function as part of the immune
system and help control lipid accumulation, so they actually
may benefit human health, said Michael Spurlock, animal
sciences professor.
"Adipocytes
[fat cells] can be functional and beneficial without creating
obesity," Spurlock said. "The key is that we want
plenty of adipocytes to meet whatever immunological and
endocrinological needs they fulfill, but we don't want them
to overaccumulate lipid."
In
the January issue of The American Journal of Physiology,
Spurlock and Kolapo Ajuwon, both of the Department of Animal
Sciences and the Comparative Medicine Program, report that
pig fat cells respond to infections by producing hormone-like
proteins that regulate certain aspects of the body's immune
response.
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"This
is additional evidence that fat cells behave in many ways as immune
cells," Spurlock said. "It also is the first evidence that
adipocyte cells [fat cells] respond directly to bacterial toxins like
classical immune cells."
To produce
this infection-fighting response, Ajuwon, a doctoral student, performed
experiments exposing fat cells to interferon-gamma, a small protein
produced by infection-fighting T-cells. This caused the adipocytes
to produce hormone-like proteins, called cytokines.
"Our
research documents a pathway by which the adipocytes participate in
the immune response," Spurlock said. "We have very clearly
shown that interferon-gamma is increasing expression of cytokines
in pig fat cells."
In another
part of the study, the researchers found that a molecule, or ligand,
binds to molecules on the outside of pig fat cells incubated in a
laboratory dish. In this case the ligand is an inflammatory molecule
called LPS. This binding with the receptor molecule on pig fat cells,
like a key in a lock, signals fat cells to produce more of another
hormone-like cytokine.
The researchers
believe that this is similar to what happens in humans since some
pig breeds show marked similarity in cardiovascular disease, hyperglycemia
and insulin resistance, Spurlock said. The study's findings that the
LPS ligand and interferon-gamma regulate production of cytokines that
impact both energy metabolism and immune function are significant
in studying human diseases, including cancer and diabetes.
The factor
in the fat tissue that is linked to diseases is the amount of lipid,
also known as fatty acid or tricylglycerol, in the adipocytes, he
said. As adipocytes accumulate excess lipid, their normal function
is distorted and they produce too much of some biochemicals and not
enough of others. These abnormalities can culminate in disease.
"For
a long time, we have looked for the link between the immune system,
obesity and insulin resistance," Spurlock said. "The fact
that fat cells actually promote or secrete factors, such as the cytokine
interleukin-6, may be fundamentally linked to insulin resistance in
diabetes. This makes adipocytes very important cells."
People
with Type II diabetes produce insulin in their pancreas, but the insulin
can't control their glucose levels. Fat cells normally produce factors
that promote insulin regulation of glucose levels, but these factors
don't function properly when obesity is involved.
Spurlock
and his research team now want to determine other factors, such as
certain classes of fatty acids, that will activate or suppress the
LPS receptor.
"We
know there are non-infectious ligands that activate the receptor,
so we want to know what they are," he said. "If we can discover
these regulators, then we might be able to find a way to manipulate
the receptors and immune pathways to regulate the body's energy metabolism
and apply that to diabetes and cancer."
The other
researchers involved in the study are doctoral student Sheila Jacobi
and research associate Joanne Kuske, both of the Purdue Department
of Animal Sciences and the Comparative Medicine Program. The program
is a collaboration of Purdue's Department of Animal Sciences, School
of Veterinary Medicine and Indiana University School of Medicine with
initial funding from the Indiana 21st Century Research and Technology
Fund.
This
article has been adapted from a news release about fat cells issued
by Purdue University, www.purdue.edu.
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