(This is an excerpt of the Health Rounds newsletter, where we present latest medical studies on Tuesdays and Thursdays.)
Feb 20 (Reuters) – Diabetes is less common among people living at high altitudes, where oxygen levels are low, than at sea level, and researchers who have discovered why that happens say the reason may lead to new treatments.
In low-oxygen conditions, like those on high mountains, red blood cells can shift their metabolism to soak up sugar from the bloodstream, acting as “glucose sponges,” they reported on Thursday in Cell Metabolism.
At high altitudes, being able to carry more glucose gives the red blood cells extra energy to deliver oxygen throughout the body more efficiently. It also has the beneficial side effect of lowering blood sugar levels, according to the report.
In previous experiments, the researchers had seen that mice breathing low-oxygen air had dramatically lower blood glucose levels than normal. That meant the animals were quickly using up glucose after they ate, putting them at lower risk for diabetes.
“When we gave sugar to (these mice), it disappeared from their bloodstream almost instantly,” study author Yolanda Martí-Mateos of the Gladstone Institutes in San Francisco said in a statement.
“We looked at muscle, brain, liver… but nothing in these organs could explain what was happening.”
Ultimately, her team found that red blood cells were the “glucose sink” — a term used to describe anything that pulls in and uses a lot of glucose from the bloodstream.
In low-oxygen conditions, mice not only produced significantly more red blood cells, but each cell took up more glucose than red blood cells produced under normal oxygen levels.
The researchers then tested a drug they developed, called HypoxyStat, that mimics the effects of low-oxygen air by making hemoglobin in red blood cells grab onto oxygen more tightly, keeping it from reaching tissues.
The drug completely reversed high blood sugar in diabetic mice, working even better than existing medications, they said.
The discovery “opens the door to thinking about diabetes treatment in a fundamentally different way, by recruiting red blood cells as glucose sinks,” study co-author Isha Jain, also of the Gladstone Institutes, said in a statement.
IMPROVING MUSCLE ENDURANCE REQUIRES HELP FROM BRAIN CELLS
Improving stamina via exercise depends not only on hard-working muscle cells but on brain-cell activity, too, new research in mice that challenges conventional wisdom reveals.
Without the activity of certain brain cells called neurons, mice fail to show endurance gains no matter how hard they sprint on a treadmill, researchers found.
But when researchers artificially activated the neurons after exercise, the animals gained even more endurance than usual, according to a report in Neuron.
“The idea that muscle remodeling requires the output of these brain neurons is a pretty big surprise,” study leader Erik Bloss of The Jackson Laboratory in Bar Harbor, Maine said in a statement.
“It really challenges conventional thinking” that exercise benefits come solely from muscles, he said.
Tracking brain activity in mice during and after running, the researchers found that a particular cluster of neurons in the hypothalamus that express a protein called steroidogenic factor-1 became active for about an hour after mice finished running.
As the mice trained over weeks, more and more SF1 neurons became activated after each exercise session, and connections between the SF1 neurons became stronger and more numerous, the researchers reported.
Animals that exercised had about twice as many connections between these neurons as animals that did not, the researchers also found.
When SF1 neurons were “turned off” for 15 minutes after each training session, the mice stopped improving their endurance and began to fare worse on voluntary run tests.
“If you give a normal mouse access to a running wheel, they will run kilometers at a time,” said Bloss. “When we silence these neurons, they effectively don’t run at all. They hop on briefly but can’t sustain it.”
When researchers stimulated SF1 neurons for an hour after treadmill sessions, mice showed enhanced endurance gains and reached higher maximum speeds.
“There’s the very real possibility that we can eventually take advantage of this circuit to boost the effects of moderate exercise,” said Bloss.
“If we can mimic or enhance exercise-like patterns in the brain, that could be particularly valuable for older adults or people with mobility limitations who can’t engage in intensive physical activity but could still benefit from exercise’s protective effects on the brain and body.”
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(Reporting by Nancy Lapid; Editing by Bill Berkrot)
