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

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NEWS SA JOURNAL OF DIABETES & VASCULAR DISEASE
44 VOLUME 12 NUMBER 1 • JULY 2015
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Consuming low-carbohydrate diets can reduce inflammation in
patients with type 2 diabetes, which may decrease the risk of
patients developing cardiovascular disease (CVD). According to a
Swedish study [Diabetologia 2012; 55(8): 2118–2127], eating a
low-carbohydrate diet can reduce inflammation in patients with
type 2 diabetes.
People with type 2 diabetes have a higher level of inflammation
than those without diabetes, and this may play a role in the increased
risk of CVD associated with diabetes. The Linkoping University study
included 61 participants with type 2 diabetes. The participants were
randomly divided up and given either a low-carbohydrate or low-fat
diet. The study method was a retrospective follow-up study.
The low-carbohydrate and the low-fat diet participants were
compared over the course of two years. Additionally, the researchers
studied how the diets impacted on inflammation by checking the
inflammation levels in the blood of each patient.
The results showed that both the low-carbohydrate and low-
fat diets helped participants lose weight, roughly around nine
pounds (4 kg), but when it came to which diet produced reduced
inflammatory markers in the blood, the low-carbohydrate diet
succeeded. Additionally, glucose levels dropped more in the low-
carbohydrate diet groups.
In respect of cardiovascular risk, the researchers recommended
aiming for a carbohydrate energy intake of 20% as a treatment
alternative for at-risk patients.
Source:
of-low-carbohydrate-diets-to-reduce-cvd-risk.
The potential of low-carbohydrate
diets to reduce cardiovascular risk
Vanderbilt University scientists have found evidence that the
insulin-secreting beta-cells of the pancreas, which are either
killed or become dysfunctional in the two main forms of diabetes,
have the capacity to regenerate. The surprising finding, posted
online by Cell Metabolism earlier this year, suggests that by
understanding how regeneration occurs, scientists may one day
be able to stop or reverse the rising tide of diabetes. ‘The study
provides clues to how we might learn what signals promote beta-
cell regeneration in type 1 and type 2 diabetes’, said Dr Alvin
Powers, the senior author and director of the Vanderbilt Diabetes
Center.
In the past three months, the Powers group at Vanderbilt,
in four separate articles, has reported important findings about
the ‘microenvironment’ of the insulin-secreting beta-cells and
glucagon-secreting alpha-cells, which are among four types
of cells clustered in islets in the pancreas. Both hormones are
important in regulating blood glucose levels and ensuring that
glucose is delivered to the muscles and brain to be used as fuel,
and stored in the liver. Powers called the islets a ‘mini-organ’
because they are highly vascularised and innervated, and exist
within a specialised environment.
In type 1 diabetes, the beta-cells are destroyed and glucose levels
rise in the blood because not enough insulin is being produced. In
type 2 diabetes, a frequent consequence of obesity, tissues become
resistant to insulin, again causing blood glucose to rise. Beta-cell
function also becomes abnormal.
In two articles in the journal Diabetes and one each in
Development and Cell Metabolism, the researchers described
four main findings about islet vascularisation and innervation.
First, vascular endothelial growth factor A (VEGF-A) is important
for development of the islets’ blood supply and for beta-cell
proliferation. Blocking the growth factor early in development in a
mouse model ultimately reduced beta-cell mass and insulin release
and impaired glucose clearance from the bloodstream.
Second, VEGF and other ‘signals’ released by the endothelial
cells lining the islet blood vessels consequently stimulated growth
of islet nerves in mice that connected to the brain. ‘If the islets
don’t become vascularised properly, they don’t become innervated
properly’, Dr Marcela Brissova, who was co-author on three of the
four articles, said. ‘These signals also promote beta-cell growth.’
Third, VEGF-A was not involved when the beta-cell mass
increased in an obese mouse model of type 2 diabetes in response
to rising glucose levels. Unlike tumours, which sprout new blood
vessels as they grow, the beta-cell tissue increased its blood supply
by dilating existing vessels.
Finally, too much VEGF-A can lead to beta-cell death. But that
sets up a regenerative micro-environment involving an interaction
of vascular endothelial cells and macrophages, which, in turn, leads
to beta-cell proliferation both in mice and human islets. ‘That’s very
unusual because islet cells are like neurons; once they’re dead, they
don’t usually regrow’, Brissova said. ‘We think that the endothelial
cells and macrophages that are recruited from bone marrow create
an environment that promotes the proliferation and regeneration
of those beta-cells.’
Source:
regenerate.html
Diabetes researchers track cells’
ability to regenerate