The SA Journal Diabetes & Vascular Disease Vol 12 No 1 (July 2015)

43 / 48

VOLUME 12 NUMBER 1 • JULY 2015 41
SA JOURNAL OF DIABETES & VASCULAR DISEASE NEWS
Diabetes News
Anew study suggests uric acid may play a
role in causing the metabolic syndrome,
a cluster of risk factors that increases the risk
of heart disease and type 2 diabetes.
Uric acid is a normal waste product that is
removed from the body by the kidneys and
intestines and is released in the urine and
stools. Elevated levels of uric acid are known
to cause gout, an accumulation of the acid in
the joints. High levels are also associated with
markers of the metabolic syndrome, which is
characterised by obesity, high blood pressure,
and elevated blood sugar and cholesterol
levels. But it has been unclear whether uric
acid itself is causing the damage or it is simply
a by-product of other processes that lead to
the dysfunctional metabolism.
New research from the Washington
University suggests that excess uric acid in
the blood is no innocent bystander. Rather, it
appears to be a culprit in disrupting normal
metabolism. The research team states
that uric acid may play a direct, causative
role in the development of the metabolic
syndrome. The work showed that the gut
is an important clearance mechanism for
uric acid, opening the door to new potential
therapies for preventing or treating type 2
New culprit identified in metabolic syndrome
diabetes and the metabolic syndrome.
Recent research by the senior author,
Kelle H Moley, the James P Crane professor
of obstetrics and gynecology, and her
collaborators has shown that a protein called
GLUT9 is an important transporter of uric
acid. The team studied mice to learn what
happens when GLUT9 stops working in the
gut, essentially blocking the body’s ability to
remove uric acid from the intestine. In this
study, the kidney’s ability to remove uric acid
remained normal.
Eating regularly, mice missing GLUT9
only in the gut quickly developed elevated
uric acid in the blood and urine compared
with control mice. And at only six to eight
weeks of age, they developed the hallmarks
of the metabolic syndrome: high blood
pressure, elevated cholesterol and blood
insulin levels, and fatty liver deposits, among
other symptoms.
The researchers also found that the
drug allopurinol, which reduces uric acid
production in the body and has long been
used to treat gout, improved some but not
all of the measures of metabolic health.
Treatment with the drug lowered blood
pressure and total cholesterol levels.
Exposure to uric acid is impossible to
avoid because it is a normal byproduct
of cell turnover in the body. But there is
evidence that diet may contribute to uric
acid levels. Many foods contain compounds
called purines that break down into uric
acid. Adding to growing concerns about
fructose in the diet, evidence suggests that
fructose metabolism in the liver also drives
uric acid production.
Switching to foods heavy-laden with
fructose over the past 30 years has been
devastating, according to Moley. ‘There’s a
growing feeling that uric acid is a cause, not
a consequence, of the metabolic syndrome.
The medical community now knows that
fructose directly makes uric acid in the liver.
With that in mind, the laboratory is doing
further research to study what happens to
these mice on a high-fructose diet.’
Source
1.
culprit-identified-in-metabolic-syndrome/https://
2. DeBosch BJ, Kluth O, Fujiwara H, Schurmann A,
Moley KH. Early-onset metabolic syndrome in mice
lacking the intestinal uric acid transporter SLC2A9.
Nature Commun Aug 7, 2014.
Low-density lipoprotein cholesterol
(LDL-C) level wasn’t a good predictor
of cardiovascular disease in type 1
diabetes, but the total cholesterol-to-
high-density lipoprotein cholesterol
(HDL-C) ratio appeared more reliable,
an observational study has shown. Dr
Christel Hero, of Sahlgrenska University
Hospital in Gothenburg, Sweden, and
colleagues reported that LDL-C had
modest associations with the development
of cardiovascular disease but no consistent
dose response above the 100-mg/dl
threshold for statin treatment in this
population (American Diabetes Association
2014; Abstract 301-OR).
In type 1 diabetes patients already on
statins, LDL-C levels didn’t have any significant
link to subsequent cardiovascular disease in
the Swedish National Diabetes Registry data.
The total cholesterol-to-HDL-C ratio had
Low-density lipoprotein cholesterol does not predict cardiac risk in diabetes
similarlymodest links to cardiovascular disease
in patients on or off lipid medications, but
with a consistent rise in risk across categories.
Hero added, ‘The ratio of total cholesterol to
HDL-C is a more reliable marker for risk when
considering primary prevention.’
Dr Fernando Ovalle, director of the
Comprehensive Diabetes Centre of the
University of Alabama in Birmingham,
commented, ‘The findings emphasised
how much remains unknown about
cardiovascular disease in type 1 diabetes.
We made a lot of assumptions and jumped
to a lot of conclusions that the markers of
cardiovascular disease and treatments for
prevention of cardiovascular diseases will
be the same in type 1 diabetes as in type 2,
and that just may not be the case. This could
potentially change how we see the use of
statins and the assessment of cardiovascular
risk in general.’
Dr Elizabeth Seaquist, president for
medicine and science and a moderator at
the session, cautioned, ‘Don’t toss out LDL-C
in clinical practice just yet.’ Dr Seaquist
continued by saying that LDL-C may not
be as strong a predictor for cardiovascular
disease as in type 2 diabetes, as has been
suspected from prior studies, but further
research is needed to determine what to use
in the clinic. ‘These patients are still at great
risk for cardiovascular events, and we need
to make certain that we’re doing the right
things to prevent that’, she said. ‘It will help
us if we were to do a trial to determine the
benefits of lipid-lowering in type 1 patients.’
This studywas published as an abstract and
presented at a conference. These data and
conclusions should be considered preliminary
until published in a peer-reviewed journal.
Source:
/16480-ada-ldl-doesnt-predict-heart-risk-in-diabetes