A new University of
Illinois study suggests that we may pay a price for ingesting too much
fructose. According to lead author Manabu Nakamura, dietary fructose
affects a wide range of genes in the liver that had not previously been
identified.

Chances are you consume quite a bit of fructose. Most Americans do–in
refined sugars such as sucrose or table sugar (which is half fructose)
and in high-fructose corn syrup, used in products as diverse as soft
drinks, protein bars, and fruit juice.

But many scientists believe that high dietary fructose contributes to
the development of metabolic syndrome, a group of risk factors that
predict heart disease and Type 2 diabetes.

“For this reason, its important for scientists to understand exactly
how consuming high amounts of fructose affects human health,” said
Nakamura, a U of I associate professor of food science and human
nutrition.

Nakamuras lab is continuing to study the metabolism of fructose with
an eye to making recommendations about its dietary use.

His study shows that the metabolism of fructose is more complex than
the data had indicated. “Our gene-expression analysis showed that both
insulin-responsive and insulin-repressive genes are induced during this
process. Our bodies can do this, but its complicated, and we may pay a
price for it,” he said.

According to the scientist, most carbohydrates are handled fairly
simply by our bodies. They are converted quickly to glucose and used
for energy or stored as fat. “When we are eating, blood sugar–and
insulin production–goes up. When we sleep or fast, it goes down,” he
said.

The process is not so simple with fructose, he noted. “In order for
fructose to be metabolized, the body has to create both fasted and fed
conditions. The liver is really busy when you eat a lot of fructose.”

Because, unlike glucose, fructose metabolism occurs mainly in the
liver, Nakamura wanted to gain a complete picture of gene expression in
the liver during fructose metabolism.

In Nakamuras study, 24 rats were fed either a 63 percent glucose or
fructose diet four hours a day for two weeks; at the end of this
period, half the animals fasted for 24 hours before the scientists
performed a gene expression analysis; the other half were examined at
the end of a four-hour feeding.

Fructose feeding not only induced a broader range of genes than had
previously been identified, there were simultaneous increases in
glycogen (stored glucose) and triglycerides in the liver.

“To our surprise, a key regulatory enzyme involved in the breakdown of
glucose was about two times higher in the fructose-fed group than in
the glucose-fed group,” Nakamura said.

The study also suggests that a protein called carbohydrate response
element binding protein is responsible for the fructose effect on
certain genes that trigger the production of fat, he said.

“We’re continuing to assess the risk of fructose insulin resistance and
the consequent risk for development of diabetes,” he said.

Co-authors of the study, published in a recent issue of Biochimica et
Biophysica Acta, are Hyun-Young Koo, Matthew A. Wallig, Takayuki Y.
Nara, and B. H. Simon Cho of the University of Illinois and Byung Hong
Chung of the University of Alabama at Birmingham.

Source: University of Illinois