<p>To manage any type of diabetes be it Type 1 or Type 2, we need to keep blood sugar levels within a safe range. In a new research that could lead make the way simpler for diabetes patients, researchers have found that changes in the size of mitochondria in a small subset of brain cells play a crucial role in safely maintaining blood sugar levels. </p>rnrn<p>According to the researcher Sabria Diano, "low blood sugar can be as dangerous as high blood sugar&rdquo;. "We&#039;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." </p><p>"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," Diano added. </p><p>The study was designed in a way to help understand how neurons in the brain that regulate appetite affect systemic glucose levels. The team used mouse models in which a specific mitochondrial protein, dynamin-related protein 1 (DRP1), was either missing or present in varying amounts in the subset of brain cells that sense circulating sugar levels. </p><p>The researchers found that depending on whether the mouse was hungry or not, mitochondria displayed dynamic changes in size and shape, driven by the DRP1 protein. </p><p>"We found that when DRP1 activity in the neurons was missing, these neurons were more sensitive to changes in glucose levels," said Diano, who is also a member of the Program in Integrative Cell Signaling and Neurobiology of Metabolism and the director of the Reproductive Neuroscience Group at Yale University School of Medicine. </p><p> "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." </p><p> “The research findings suggest that alterations in this mechanism may be critical for the development of hypoglycemia-associated autonomic failure (HAAF), a complication of several diabetes treatments occurring most often in people with type 1 diabetes who must take insulin for survival,&rdquo; said Diano. </p><p>The study has been published in the journal Cell Metabolism. </p><p>Story source / Credit:  Yale University </p><p>Journal References: </p><p>Anna Santoro, Michela Campolo, Chen Liu, Hiromi Sesaki, Rosaria Meli, Zhong-Wu Liu, Jung Dae Kim, Sabrina Diano. DRP1 Suppresses Leptin and Glucose Sensing of POMC Neurons. Cell Metabolism, 2017; DOI: 10.1016/j.cmet.2017.01.003</p>