Sugar overload can cause heart damage?
Eating too much sugar can set people down a pathway to heart
failure, a new study has warned.
A single small molecule, the glucose metabolite glucose
6-phosphate (G6P), causes stress to the heart that changes the muscle proteins
and induces poor pump function leading to heart failure, according to the
researchers at The University of Texas Health Science Center at Houston
(UTHealth).
G6P can accumulate from eating too much starch and/or sugar,
researchers said.
"Treatment is difficult. Physicians can give diuretics
to control the fluid, and beta-blockers and ACE inhibitors to lower the stress
on the heart and allow it to pump more economically," said Heinrich
Taegtmeyer, principal investigator and professor of cardiology at the UTHealth
Medical School.
"But we still have these terrible statistics and no new
treatment for the past 20 years," said Taegtmeyer.
Taegtmeyer performed preclinical trials in animal models, as
well as tests on tissue taken from patients at the Texas Heart Institute, who
had a piece of the heart muscle removed in order to implant a left ventricle
assist device. Both led to the discovery of the damage caused by G6P.
"When the heart muscle is already stressed from high
blood pressure or other diseases, and then takes in too much glucose, it adds
insult to injury," Taegtmeyer said.
Researchers said the study has opened doors to possible new
treatments. Two drugs, rapamycin (an immunosuppressant) and metformin (a
diabetes medication) disrupt signalling of G6P and improved cardiac power in
small animal studies, they said.
"These drugs have a potential for treatment and this
has now cleared a path to future studies with patients," Taegtmeyer said.
The study was published in the Journal of the American heart
Association.
Researchers are using advanced mathematical models to
engineer viruses that can infect and destroy cancer cells without affecting
healthy tissue.
The technique predicts how different treatments and genetic
modifications might allow cancer-killing, oncolytic viruses to overcome the
natural defences that cancer cells use to stave off viral infection.
"Oncolytic viruses are special in that they
specifically target cancer cells," said Dr Bell, a senior scientist at the
Ottawa Hospital Research Institute and professor at the University of Ottawa's
Faculty of Medicine.
"Unfortunately, cancer is a very complicated and
diverse disease, and some viruses work well in some circumstances and not well
in others. As a result, there has been a lot of effort in trying to modify the
viruses to make them safe, so they don't target healthy tissue and yet are more
efficient in eliminating cancer cells," said Bell.
Bell and co-author Mads Kaern, an assistant professor in the
University of Ottawa's Faculty of Medicine led a team that used mathematical
modelling to devise strategies for making cancer cells exquisitely sensitive to
virus infection - killing them without affecting normal, healthy cells.
"By using these mathematical models to predict how
viral modifications would actually impact cancer cells and normal cells, we are
able to accelerate the pace of research," said Kaern. Bell and Kaern have
established a mathematical model that described an infection cycle, including
the way a virusreplicated, spread and activated cellular defence mechanisms.
They used knowledge about key physiological differences between normal cells
and cancer cells to identify how modifying the genome of the virus might
counter the anti-viral defences of cancer cells.
Model simulations were remarkably accurate, with the
identified viral modifications efficiently eradicating cancer nin a mouse model
of the disease "What is remarkable is how well we could actually predict
the experimental outcome based on computational analysis. This work creates a
useful framework for developing similar types of mathematical models in the
fight against cancer," said Bell. The study was published in the journal
Nature Communications.
There is no such thing in anyone's life as an unimportant day
Alexander Woollcott
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