Mitochondria size vital to keeping blood sugar levels in check

A new study has found that changes in the size of mitochondria in brain cells can affect blood sugar levels.
By Amy Wallace  |  Feb. 15, 2017 at 12:35 PM
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Feb. 15 (UPI) -- Researchers at Yale University School of Medicine have discovered that changes in mitochondria size in brain cells plays a vital role in maintaining safe blood sugar levels.

Keeping blood sugar levels in a safe range is crucial for the management of type 1 and type 2 diabetes.

"Low blood sugar can be as dangerous as high blood sugar," Sabrina Diano, professor in the Departments of Obstetrics, Gynecology & Reproductive Sciences, Neuroscience and Comparative Medicine at Yale and senior author of the study, said in a press release. "We've found that changes in the size of mitochondria -- small intracellular organelles responsible for energy production -- in certain cells in the brain, could be key to maintaining the blood sugar within a safe range. This new finding adds to our understanding of how the body keeps blood sugar levels within a safe range when sugar levels drop, like during fasting, or when they spike after a meal."

Researchers studied mice with a specific mitochondrial protein, dynamin-related protein 1, or DRP1, that was missing or present in varying amounts in the brain cells that sense circulating sugar levels. They found that when the mouse was hungry or not, mitochondria showed dynamic changes in size and shape driven by the DRP1 protein.

"We found that when DRP1 activity in the neurons was missing, these neurons were more sensitive to changes in glucose levels," Diano said. "What surprised our research team was that these intracellular changes in this small subset of neurons were specifically important to increase blood sugar levels during a fasting period by activating the so-called counter-regulatory responses to hypoglycemia, in which the brain senses lower glucose levels and sends signals to peripheral organs such as the liver to increase glucose production."

The results show that changes in this mechanism may be crucial for the development of hypoglycemia-associated autonomic failure, a complication of diabetes treatments that happen in type 1 diabetes patients who take insulin daily for survival.

The study was {link:published in Cell Metabolism.:"" target="_blank"}

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