Tiny Brain Organelles Influence Glucose Levels
Scientists have discovered something relevant to people with type 1 or 2 diabetes, and it may lead to less diabetes related complications.
The discovery involves mitochondria in brain cells. Mitochondria are cell organelles involved in respiration and energy production. Researchers at the Yale School of Medicine determined that alterations in the size of specific brain mitochondria play an essential role in maintaining safe blood glucose levels.
“Low blood sugar can be as dangerous as high blood sugar,” said researcher and Yale professor Sabrina Diano. “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.”
The Yale investigators were interested in understanding how the brain’s appetite regulating neurons influence the body’s sugar levels. Their study involved mice where the mitochondria protein called dynamin-related protein 1 (DRP1) was either missing, or was present in differing amounts in brain cells that detect circulating glucose.
It was discovered that, driven by the DRP1 protein, the mitochondria changed its shape and size depending on whether a mouse was, or was not hungry. “We found that when DRP1 activity in neurons was missing, these neurons were more sensitive to changes in glucose levels,” said Diano.
The researchers were surprised that the observed intracellular changes in such a small group of neurons were important for raising blood sugar levels during fasting periods by activating a brain response signaling organs such as the liver to step-up glucose production.
The study’s findings, according to Diano, imply that changes in this mechanism may be involved in the development of hypoglycemia-associated autonomic failure (HAAF), a diabetes complication that more often occurs in those with type 1 diabetes.
HAAF is characterized by decreased symptom perception, or hypoglycemia unawareness, and a diminished counter-regulatory hormone response to low blood sugar. The Yale team plans to continue their investigation by focusing on the role of mitochondria changes in the development of HAAF.