A new study relates liquid fructose intake to fatty liver disease

Date:
March 4, 2022
Source:
University of Barcelona
Summary:
A high-fat diet is not enough to cause short-term fatty liver
disease.

However, if this diet is combined with the intake of beverages
sweetened with liquid fructose, the accumulation of fats in the
liver accelerates and hypertriglyceridemia -- a cardiovascular
risk factor -- can appear, according to researchers.



FULL STORY ==========================================================================
A high-fat diet is not enough to cause short-term fatty liver
disease. However, if this diet is combined with the intake of beverages sweetened with liquid fructose, the accumulation of fats in the liver accelerates and hypertriglyceridemia -- a cardiovascular risk factor --
can appear.


==========================================================================
This is explained in a study on a mouse experimental model, published in
the journal Molecular Nutrition and Food Researchand led by Professor
Juan Carlos Laguna, from the Faculty of Pharmacy and Food Sciences,
the Institute of Biomedicine of the University of Barcelona (IBUB)
and the Physiopathology of Obesity and Nutrition Networking Biomedical
Research Centre (CIBEROBN).

The study counts on the collaboration of the researchers Aleix Sala-Vila
and Iolanda La'zaro, from the Hospital del Mar Medical Research Institute (IMIM), and Jose' Rodri'guez-Morato', from IMIM-Hospital del Mar and MELIS-Pompeu Fabra University, among other experts.

Fructose and lipid metabolism Fructose is one of the most common
sweeteners in the food industry. This simple sugar (monosaccharide)
is industrially obtained from corn syrup, a product derived from this gramineae. With a great sweetener power and low production costs, fructose
is used by the food industry to sweeten beverages, sauces and processed
foods, despite the scientific evidence that associates it with metabolic diseases which are risk factors of cardiovascular pathologies.

According to the new study, the effect caused by fructose in the increase
in the synthesis of fatty acids in the liver is more decisive than the
external introduction of fats through the diet. "In high-fat diets which
are supplemented with liquid fructose, this monosaccharide is able to
induce an increase in the de novo lipogenesis -- that is, the formation
of fats through sugar -- and an inhibition of the lipid oxidation in
the liver," says Professor Juan Carlos Laguna, from the Department of Pharmacology, Toxicology and Therapeutical Chemistry.



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"In particular, fructose intake affects directly the expression and
activity of the nuclear factor ChREBP. Once activated, this factor
causes an increase in the expression of enzymes that control the hepatic synthesis of fatty acids," he continues. "Parallelly, fructose intake
reduces the activity of the nuclear receptor PPARalfa, which is the
main responsible for the controlling of the expression of genes that
code the enzymes involved in the fatty acid oxidation (mitochondrial
and peroxisome) in the liver." As stated in the preclinical study, the combination of the saturated fat from dietary origin and the induction
of the endogen synthesis of fatty acids is what causes the emergence of
the fatty liver. "Moreover, we are describing for the first time that
fructose -- unlike high-fat diets -- increases the expression of the
PNPLA3 protein, associated with the appearance of hypertriglyceridemia,
a risk factor for cardiovascular diseases," notes Nu'ria Roglans,
co-author of the study and member of the mentioned Department.

Fatty liver disease in humans Several epidemiologic studies related
the consumption of drinks that are sweetened with fructose to the
non-alcoholic fatty liver disease (NAFLD), a pathology for which there
is no specific pharmacological therapy. In these patients, de novo
lipogenesis contributes up to a 30% of the lipids accumulated in the
liver, while in healthy people, this synthesis brings only the 5% of
hepatic lipids.

The animal model characterized by the team will be of potential interest
to study future drugs to treat the non-alcoholic fatty liver disease
(NAFLD).

"People with this pathology have a higher endogenous synthesis of lipids
in the liver than healthy people. Therefore, the effects described in
this study might appear in humans as well," note the experts.

"Unfortunately, -- they continue -- the fatty liver is the starting point
for more serious pathologies, such as steatohepatitis and cirrhosis. It
is a practically asymptomatic pathology, although in some cases, some
mild unspecific digestive disorders can appear. Apart from following
a healthy diet and physical activity, there is no efficient treatment
against this pathology for now." The effects described in the study
are only observable if fructose is taken in its liquid form. "Regarding sweetened beverages, fructose is quickly absorbed and it reaches the
liver massively, producing the described metabolic alterations. To find
a comparison, we could talk about the appearance of a fructose overdose
when this is taken in sweetened drinks," notes the team.

"However, when we eat fruit, the amount of taken fructose is a lot
lower compared to a sweetened drink. Also, the process of chewing it
and the presence of other elements in the fruit, such as fiber, slows
down the absorption of fructose and its arrival to the liver," conclude
the authors.

========================================================================== Story Source: Materials provided by University_of_Barcelona. Note:
Content may be edited for style and length.


========================================================================== Journal Reference:
1. Ana Magdalena Vela'zquez, Roger Bentanachs, Aleix Sala‐Vila,
Iolanda La'zaro, Jose Rodri'guez‐Morato', Rosa
M. Sa'nchez, Marta Alegret, Nu'ria Roglans, Juan Carlos
Laguna. ChREBP‐driven DNL and PNPLA3 Expression Induced by
Liquid Fructose are Essential in the Production of Fatty Liver
and Hypertriglyceridemia in a High‐Fat Diet‐Fed Rat
Model. Molecular Nutrition & Food Research, 2022; 2101115 DOI:
10.1002/mnfr.202101115 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2022/03/220304112024.htm

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