DIABETES CAN REVERSE
In a ray of hope for
diabetes patients, scientists have discovered the cellular sequence that leads
to the trigger of the disease.
They also found
potential molecular targets for preventing or reversing the process.
“We have described the
etiology of obesity-related diabetes. We have pinpointed the steps, the way the
whole thing happens,” said Jerrold M. Olefsky, a distinguished professor of
medicine at University of California, San Diego.
“The research on mice
suggests that the processes are comparable in humans and these findings are
important to not just understanding how diabetes begins, but how better to
treat and prevent it,” he added.
During the study, the
researchers fed mice a high-fat diet.
They observed that the
abundant saturated fatty acids in the diet activated adenine nucleotide
translocase 2 (ANT2) – a mitochondrial protein in fat cell membranes that is
involved in cellular energy metabolism.
Activation of ANT2
caused increased oxygen consumption, which meant less was available for the
rest of the cell.
The result was a
relative state of hypoxia or inadequate oxygen supply.
It subsequently
induced production of a protective transcription factor in fat cells called
HIF-1alpha.
In turn, HIF-1alpha
triggered release of chemokines, proteins that signal cellular distress,
launching the immune system’s inflammatory response.
A sustained high-fat
diet ensured that the process continued unabated, leading to obesity, chronic
low-grade tissue inflammation and eventually, insulin resistance in the mice.
The elucidation of
this sequence also revealed two potential therapeutic targets: ANT2 and
HIF-1alpha.
The researchers
suggest that inhibiting either could blunt, or even reverse, the damaging
cellular sequence.
Diabetes is
characterised by high blood sugar levels poorly regulated by either inadequate
insulin production or because cells to not respond properly to the regulating
hormone.
The findings were
published in the journal Cell.
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