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VOLUME 11 NUMBER 3 • SEPTEMBER 2014
DIABETES PERSONALITY
SA JOURNAL OF DIABETES & VASCULAR DISEASE
difference for that one!” And that’s what drives me, making a difference
one patient at a time.’
‘It’s important to see each patient as an individual and not only the
diabetes’, she says. ‘This requires genuine interest in who they are, the
whole person, and to help them see the light within.’ She knows she’s
succeeding when a patient smiles when she enters a room or unexpect-
edly gives her a hug.
There is an emotional component to diabetes that Hester thinks is
often under-recognised. Diabetes patients and their families face many
challenges – there are lots of ups and downs and a lot of pain. These
emotional aspects can sometimes seem overwhelming.
Hester understands this at a deeply personal level. Several years ago
she took Gareth in, a teenager with type 1 diabetes, becoming, as she
puts it, an ‘instant mom’. ‘So I live with the reality every day myself. I
see his fears of hypoglycaemic episodes and of long-term complica-
tions – and have experienced first-hand the challenges of dealing with
medical schemes to ensure that my “pot of gold at the end of the
rainbow” gets the best treatment possible. Today he is an awesome,
responsible young man who shares our vision of creating a better place
for those living with diabetes. He sees his diabetes as a gift rather than
a disadvantage.’
Concluding, she underscores that it’s a great honour to work at the
CDE with a team of colleagues she considers mentors. ‘I learn more and
more from them every day. And despite the challenges, I can honestly say
that there has never been a day when I’ve hated my job. I’ve never been
bored. I love what I do!’
P Wagenaar
I
n mice with diet-induced diabetes, the equivalent of type 2
diabetes in humans, a single injection of the protein FGF1 was
enough to restore blood glucose levels to a healthy range for
more than two days. The discovery by Salk scientists, published
recently in the journal Nature, could lead to a new generation of
safer, more effective diabetes drugs.
The team found that sustained treatment with the protein
doesn’t merely keep blood glucose under control, it also
reverses insulin insensitivity, the underlying physiological cause
of diabetes. Equally exciting is that it doesn’t result in the side
effects common to most current diabetes treatments.
‘Controlling glucose is a dominant problem in our society’, says
Ronald M Evans, director of Salk’s Gene Expression Laboratory
and corresponding author of the article. ‘And FGF1 offers a new
method to control glucose in a powerful and unexpected way.’
Diabetes drugs currently on the market aim to boost insulin
levels and reverse insulin resistance by changing expression
levels of genes to lower glucose levels in the blood. But many of
these drugs, which increase the body’s production of insulin, can
cause glucose levels to dip too low and lead to life-threatening
hypoglycaemia, as well as other side effects.
In 2012, Evans and his colleagues discovered that FGF1, a
long-ignored growth factor, has a hidden function: it helps the
body respond to insulin. Unexpectedly, mice lacking FGF1 quickly
develop diabetes when placed on a high-fat diet, which suggests
that FGF1 plays a key role in managing blood glucose levels. This
led the researchers to wonder whether providing extra FGF1 to
diabetic mice could affect symptoms of the disease.
Evans’ team injected doses of FGF1 into obese mice with
diabetes to assess the protein’s potential impact on metabolism.
The researchers were stunned by what happened: they found
that with a single dose, blood glucose levels quickly returned to
normal.
‘Many previous studies that had injected FGF1 showed no
effect on healthy mice’, says Michael Downes, a senior staff
A single injection of FGF1 arrests type 2 diabetes in mice
scientist and co-corresponding author of the study. ‘However,
when we injected it into a diabetic mouse, we saw a dramatic
improvement in glucose levels.’
Importantly, FGF1, even at high doses, did not cause glucose
to drop to dangerously low levels, a risk factor associated
with many glucose-lowering agents. Instead, the injections
restored the body’s own ability to regulate insulin and blood
sugar naturally, keeping glucose levels within a safe range and
effectively reversing the core symptoms of diabetes.
‘With FGF1, we really haven’t seen hypoglycaemia or other
common side effects’, says Salk postdoctoral research fellow
Jae Myoung Suh, a member of Evans’ laboratory. ‘It may be
that FGF1 leads to a more “normal” type of response compared
to other drugs because it metabolises quickly in the body and
targets certain cell types.’
The mechanism of FGF1 still isn’t fully understood; neither is
the mechanism of insulin resistance, but Evans’ group discovered
that the protein’s ability to stimulate growth is independent
of its effect on glucose, bringing the protein a step closer to
therapeutic use.
‘There are many questions that emerge from this work and
the avenues for investigating FGF1 in diabetes and metabolism
are now wide open’, Evans says. Identifying the signalling
pathways and receptors that FGF1 interacts with is one of the
first issues he would like to address. He is also planning human
trials of FGF1 with collaborators, but it will take time to fine-
tune the protein into a therapeutic drug.
‘We want to move this to people by developing a new
generation of FGF1 variants that solely affect glucose and not
cell growth’, he says. ‘If we can find the perfect variation, I
think we will have found a new, very effective tool for glucose
control.’
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