FOR IMMEDIATE RELEASE
October 16, 2008
Contact: Christine Guilfoy
Office: (301) 634-7253
cguilfoy@the-aps.org
Fructose Sets Table For Weight
Gain Without Warning
Common
sweetener found in many foods leads to leptin resistance and exacerbates
obesity when paired with high-calorie, high-fat diet
BETHESDA, Md. (Oct. 16, 2008) − Eating too much fructose can
induce leptin resistance, a condition that can easily lead to becoming
overweight when combined with a high-fat, high-calorie diet, according to a
new study with rats.
Although previous studies have shown that being leptin resistant can lead
to rapid weight gain on a high-fat, high-calorie diet, this is the first
study to show that leptin resistance can develop as a result of high
fructose consumption. The study also showed for the first time that leptin
resistance can develop silently, that is, with little indication that it is
happening.
The study, “Fructose-induced leptin resistance exacerbates weight gain in
response to subsequent high-fat feeding,” was carried out by Alexandra
Shapiro, Wei Mu, Carlos Roncal, Kit-Yan Cheng, Richard J. Johnson and Philip
J. Scarpace, all at the University of Florida College of Medicine in
Gainesville. The study appears in the American Journal of Physiology –
Regulatory, Integrative and Comparative Physiology, published by The
American Physiological Society.
Leptin as regulator
Leptin is a hormone that plays a role in helping the
body to balance food intake with energy expenditure. When leptin isn’t
working -- that is, when the body no longer responds to the leptin it
produces -- it’s called leptin resistance. Leptin resistance is associated
with weight gain and obesity in the face of a high-fat, high-calorie diet.
Obesity has been a growing problem in the U.S. and in
other parts of the world and fructose has been suspected of playing a role.
Fructose is the sugar found in fruit, but it’s not the normal consumption of
fruit that is the problem. Table sugar and high-fructose corn syrup are
about 50% fructose and these ingredients have become increasingly common in
many foods and beverages. With sugar and high-fructose corn syrup being
added to many foods, people now eat much more fructose than ever before.
The University of Florida researchers hypothesized that
a high-fructose diet could lead to leptin resistance, which in turn could
lead to exacerbated weight gain in the face of a high-fat, high-calorie
diet, a typical diet in industrialized countries. To test their hypothesis,
the research team performed a study with two groups of rats. They fed both
groups the same diet, with one important exception: one group consumed a lot
of fructose while the other received no fructose.
Two groups similar over
six months
During these six months, there were no differences in
food intake, body weight, and body fat between rats on the high-fructose and
the rats on the fructose-free diets. In addition, there was no difference
between the two groups in the levels of leptin, glucose, cholesterol or
insulin found in their blood. There was only one difference at the end of
the six months: The rats on the high-fructose diet had higher levels of
triglycerides in their blood.
The researchers next tested the animals to see if they
were leptin resistant. They injected all the animals with leptin, to see if
they would respond by eating less. Animals whose leptin response is
functioning normally will lower their food intake. The researchers
discovered that the rats on the high-fructose diet were leptin resistant,
that is, they did not lower their food intake when given leptin. The
no-fructose animals responded normally to leptin by eating less.
This first six months of the study showed that leptin
resistance can develop silently. “Usually, leptin resistance is associated
with obesity, but in this case, leptin resistance developed without
obesity,” Shapiro said. “This was very surprising.”
Role of diet
Having seen that leptin resistance could develop
silently, the researchers next wanted to find out what would happen if they
switched the rats to a high-fat, high-calorie diet -- the kind many
Americans eat. They found that the animals exposed to the high-fructose
diet, the leptin resistant rats, ate more and gained much more weight and
fat than the leptin responsive animals on the fructose-free diet. All told,
this study showed that leptin resistance can:
-
develop by eating a lot of fructose
-
develop silently, that is, with very little indication it
is happening
-
result in weight gain when paired with a high fat, calorie
dense diet
Scarpace said the study suggests it is the interaction
between consumption of large amounts of fructose-containing foods and eating
a high-fat, high-calorie diet that produces the weight gain. “This study may
explain how the global increase in fructose consumption is related to the
current obesity epidemic,” Shapiro said.
How it happens
Other studies have shown that elevated triglycerides
impair the transport of leptin across the blood brain barrier. The
researchers hypothesize that the elevation in triglycerides produced by
fructose prevented leptin from reaching the brain. If leptin does not reach
the brain, the brain will not send out the signal to stop eating.
“The presence of high fructose alters the way leptin
works, fooling the brain so that it ignores leptin,” Scarpace said.
Consumers should be cautious about what they eat, checking labels to see how
much sugar the items contain, Shapiro said.
The researchers hope to perform future studies to find
out if leptin resistance can be reversed by removing or reducing the
fructose content of the diet.
Editor’s Notes: To arrange an interview with Dr.
Shapiro or Dr. Scarpace, please contact Christine Guilfoy at
cguilfoy@the-aps.org or (301) 634-7253.
A fuller audio interview with Drs. Shapiro and Scarpace
is available in Episode 14 of the APS podcast, Life Lines, at
www.lifelines.tv.
Funding: The National Institutes of Health
Physiology
is the study of how molecules, cells, tissues and organs function to create
health or disease. The American Physiological Society (APS) has been an
integral part of this scientific discovery process since it was established
in 1887.
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