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Block brain enzyme to reduce waistline
JUST by blocking a brain enzyme, medical scientists
reduced appetite and prompted weight loss, even as the blockage
improved the body’s ability to handle blood sugar levels.
“We believe we have identified an important drug development target
(enzyme CaMKK2) that could potentially turn into a metabolic triple
play: appetite control, weight loss and blood sugar management,”
said Tony Means of Duke University, who led the research.
For many years, scientists have been testing every step of appetite
stimulation and suppression pathways, to help people control weight
and minimise risk of diabetes, heart disease and other conditions.
An empty stomach releases the hormone ghrelin, which launches a
cascade of signals. Then CaMKK2 in the ghrelin pathway activates
AMPK, an enzyme that stimulates animals to eat and gain weight.
When scientists blocked CaMKK2 in mice with a specialised molecule
inhibitor, they found the rodents ate significantly less than
untreated mice during a six-day trial, and also lost body weight,
which looked encouraging for scientists.
“The fact that blocking CaMKK2 worked in normal mice to make them
eat less and lose weight, but not in mice missing the enzyme,
provides compelling evidence that CaMKK2 signalling is a requirement
for appetite control,” Means said.
They also studied both normal mice and mice missing CaMKK2 to learn
how these types responded to low-fat and high-fat diets.
After nearly 30 weeks on the specific diets, the normal mice on the
high-fat diet became diabetic - they were unable to respond to
insulin and weren’t able to manage blood sugar levels well. Normal
mice on a low-fat diet stayed healthy.
“Remarkably, we find that blocking CaMKK2 prevents deposits of fat
in liver and skeletal muscle that are characteristic of obese,
diabetic patients,” Means said.
These results were published in the May issue of Cell Metabolism.
Another research shows that activated vitamin D administered to
patients with moderate to severe chronic kidney disease (CKD)
reduces mortality by a fourth, according to the latest findings. The
findings are based on a study of 1,418 patients with moderate to
severely impaired kidney function. They also had high parathyroid
hormone levels (hyperparathyroidism), which can contribute to
weakening of the bones in CKD patients.
Researchers identified a group that was being treated with
calcitriol to lower parathyroid hormone levels, and another group
that was not receiving calcitriol.
Patients with advanced CKD take calcitriol, an oral form of
activated vitamin D, to treat elevated levels of parathyroid
hormone, explained Bryan Kestenbaum of the University of Washington,
one of the co-authors of the study.
During a two-year follow-up period, mortality rates were compared
for patients who were and were not taking calcitriol. “We then
adjusted for differences in age, kidney function, parathyroid
hormone levels, other illnesses, and other medications,” says
Kestenbaum.
In the adjusted analysis, the overall risk of death was about 26
percent lower for patients taking calcitriol. Patients on calcitriol
were also less likely to develop end-stage renal disease, requiring
dialysis to replace lost kidney function.
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