{"id":765077,"date":"2026-05-01T03:42:13","date_gmt":"2026-05-01T03:42:13","guid":{"rendered":"https:\/\/www.europesays.com\/us\/765077\/"},"modified":"2026-05-01T03:42:13","modified_gmt":"2026-05-01T03:42:13","slug":"glucose-levels-signal-the-growth-of-myelin","status":"publish","type":"post","link":"https:\/\/www.europesays.com\/us\/765077\/","title":{"rendered":"Glucose Levels Signal the Growth of Myelin"},"content":{"rendered":"<p><strong>Summary: <\/strong>Scientists have long wondered why myelin, the brain\u2019s essential insulation, develops at different speeds in different regions. A new study reveals that glucose isn\u2019t just fuel; it\u2019s a traffic signal.<\/p>\n<p>High sugar levels tell stem-like cells to multiply, while low sugar levels signal them to stop dividing and start maturing into myelin-forming cells. This metabolic \u201cgear shift\u201d ensures the brain\u2019s wiring is built at exactly the right time and place.<\/p>\n<p><strong>Key Facts<\/strong><\/p>\n<ul class=\"wp-block-list\">\n<li><strong>The Glucose Signal:<\/strong> In the developing brain, regions with high glucose levels act as nurseries for <strong>Oligodendrocyte Progenitor Cells (OPCs)<\/strong>, causing them to divide rapidly. When glucose levels drop, these cells receive the signal to mature into myelin-producing oligodendrocytes.<\/li>\n<li><strong>The ACLY Enzyme:<\/strong> The researchers identified an enzyme called <strong>ATP-citrate lyase (ACLY)<\/strong> as the key translator. It turns glucose into a molecule (acetyl-CoA) that enters the cell nucleus to \u201cturn on\u201d the genes needed for multiplication.<\/li>\n<li><strong>Metabolic Switch:<\/strong> Once the cells mature, they stop relying on glucose for development. Instead, they switch to alternative fuels like <strong>ketone bodies<\/strong> to actually build the myelin membrane.<\/li>\n<li><strong>Ketogenic Rescue:<\/strong> In mice lacking the ACLY enzyme, myelin production was stunted. However, when these mice were placed on a <strong>ketogenic diet<\/strong>, the alternative fuel source bypassed the glucose bottleneck and improved the myelin deficits.<\/li>\n<li><strong>Critical Windows:<\/strong> The developmental stage studied (32\u201340 weeks in human gestation) is a high-risk period for premature babies. Understanding this metabolic signal could lead to new ways to protect the white matter of preemies.<\/li>\n<\/ul>\n<p><strong>Source: <\/strong>CUNY<\/p>\n<p><strong>Researchers at the\u00a0Advanced Science Research Center at the CUNY Graduate Center\u00a0(CUNY ASRC) have uncovered a surprising link between low brain sugar levels and the development of myelin \u2014 the protective coating that allows nerve cells to communicate rapidly and efficiently. <\/strong><\/p>\n<p>The study, set for publication in\u00a0Nature Neuroscience, reveals that the glucose-sensing ability of stem-like cells during early development helps them determine whether they should multiply and remain undifferentiated or mature into myelin-forming cells, thereby shaping brain development.<\/p>\n<p>Myelin is the membrane of specialized cells called oligodendrocytes, which arise from progenitor cells, called oligodendrocyte progenitor cells (OPCs). Myelination begins before birth and continues into adulthood, supporting critical milestones such as sitting, crawling, walking, and talking.<\/p>\n<p>Scientists have long puzzled over why myelin forms at different times in different brain regions. The CUNY ASRC team discovered that local changes in glucose (the brain\u2019s main energy source) act as a signal that directs behavior during development.<\/p>\n<p>Using advanced technology at the CUNY ASRC MALDI Imaging Core Facility (co-directed by professors Rinat Abzalimov and Ye He), the researchers mapped glucose levels across developing mouse brains. They found that glucose levels vary by region and over time. Areas with higher glucose levels had more actively dividing OPCs while areas with lower glucose levels contained cells beginning to mature into myelin-producing oligodendrocytes.<\/p>\n<p>\u201cOur findings show that glucose is not just fuel for the brain, it\u2019s also a signal for the cells to divide,\u201d said lead author\u00a0Sami Sauma, a postdoctoral researcher with the CUNY ASRC Neuroscience Initiative who received his Ph.D. from Graduate Center.<\/p>\n<p>\u201cWe found that when glucose levels are high in a particular brain region, progenitors use it to drive proliferation. As glucose levels shift, the same cells switch gears and begin maturing. It\u2019s a beautifully coordinated metabolic system that helps shape brain development.\u201d<\/p>\n<p>At the center of this process is an enzyme called ATP-citrate lyase (ACLY). ACLY converts glucose-derived molecules into acetyl-CoA in the cell nucleus, enabling chemical changes to DNA-associated proteins that activate genes required for cell proliferation.<\/p>\n<p>When the researchers genetically deleted ACLY in OPCs, those cells could no longer multiply effectively. As a result, mice showed a temporary reduction in myelin due to a smaller pool of progenitor cells. Remarkably, however, the cells were still able to mature into myelin-producing oligodendrocytes by switching to alternative metabolic sources.<\/p>\n<p>The team discovered that while progenitor cells depend on glucose-derived acetyl-CoA to multiply, mature oligodendrocytes rely on acetyl-CoA generated outside the nucleus from other fuels, such as ketone bodies, to produce myelin.<\/p>\n<p>In fact, when transgenic mice lacking the ACLY enzyme in OPCs were placed on a ketogenic diet, which increases ketone levels in the blood, their myelin deficits improved.<\/p>\n<p>\u201cThis study reveals that the same cell lineage interprets different metabolic signals at distinct stages of development,\u201d said\u00a0Patrizia Casaccia, founding director of the CUNY ASRC Neuroscience Initiative and Einstein Professor of Biology at the\u00a0CUNY Graduate Center.<\/p>\n<p>\u201cBy understanding how glucose and alternative energy sources regulate proliferation and myelin formation, we are uncovering new metabolic strategies that could be harnessed to protect myelin in the developing brain and even promote repair in disease states.\u201d<\/p>\n<p>The developmental window studied in mouse models corresponds to approximately 32 to 40 weeks of human gestation, which is a critical period when premature birth can result in white matter injury. The findings suggest that metabolic support during this vulnerable stage could help protect progenitor cells responsible for building myelin.<\/p>\n<p>The implications may also extend to neurological disorders characterized by myelin loss in children and adults, including multiple sclerosis. By targeting the metabolic pathways that regulate progenitor cell proliferation and oligodendrocyte maturation, researchers may be able to design new therapies to enhance myelin repair.<\/p>\n<p>As scientists continue to uncover how metabolism shapes brain development, this research highlights a powerful and potentially modifiable influence on how the brain builds its essential wiring.<\/p>\n<p><strong>Funding: <\/strong>The study was supported by the National Institute of Neurological Disorders and Stroke at the National Institutes of Health.<\/p>\n<p>Key Questions Answered:<strong class=\"schema-faq-question\">Q: Does \u201clow brain sugar\u201d mean I should avoid sugar during pregnancy?<\/strong><\/p>\n<p class=\"schema-faq-answer\"><strong>A:<\/strong> No. \u201cLow sugar\u201d in this context refers to localized, natural metabolic shifts within specific brain regions as they develop. This study is about how cells sense sugar, not a recommendation to change dietary intake. The brain always requires a steady supply of glucose to function.<\/p>\n<p><strong class=\"schema-faq-question\">Q: Could a ketogenic diet help treat myelin-related diseases like MS?<\/strong><\/p>\n<p class=\"schema-faq-answer\"><strong>A:<\/strong> The study found that ketones can provide an alternative \u201cfuel\u201d for myelin formation when the primary glucose pathway is broken. While this is promising for neonatal brain injury and potentially Multiple Sclerosis, more research is needed before the ketogenic diet can be prescribed as a standardized clinical treatment for myelin repair.<\/p>\n<p><strong class=\"schema-faq-question\">Q: Why do different parts of the brain develop myelin at different times?<\/strong><\/p>\n<p class=\"schema-faq-answer\"><strong>A:<\/strong> This study provides a major clue: glucose levels vary across the brain in a timed sequence. By mapping these \u201cglucose gradients,\u201d researchers showed that the brain essentially uses sugar levels to orchestrate the construction of its electrical wiring in a specific, prioritized order.<\/p>\n<p>Editorial Notes:<\/p>\n<ul style=\"background-color:#ffffe8\" class=\"wp-block-list has-background\">\n<li>This article was edited by a Neuroscience News editor.<\/li>\n<li>Journal paper reviewed in full.<\/li>\n<li>Additional context added by our staff.<\/li>\n<\/ul>\n<p>About this neuroscience research news<\/p>\n<p class=\"has-background\" style=\"background-color:#ffffe8\"><strong>Author:\u00a0<\/strong><a href=\"https:\/\/www.utoronto.ca\/news\/authors-reporters\/don-campbell\" target=\"_blank\" rel=\"noreferrer noopener nofollow\"><a href=\"http:\/\/neurosciencenews.com\/cdn-cgi\/l\/email-protection#c5b6b7ada0a485a2a6eba6b0abbceba0a1b0\" target=\"_blank\" rel=\"noreferrer noopener nofollow\">Shawn Rhea<\/a><br \/><strong>Source:\u00a0<\/strong><a href=\"https:\/\/cuny.edu\" target=\"_blank\" rel=\"noreferrer noopener nofollow\">CUNY<\/a><br \/><strong>Contact:\u00a0<\/strong>Shawn Rhea \u2013 CUNY<br \/><strong>Image:\u00a0<\/strong>The image is credited to Sami Sauma<\/p>\n<p class=\"has-background\" style=\"background-color:#ffffe8\"><strong>Original Research:\u00a0<\/strong>Closed access.<br \/>\u201c<a href=\"https:\/\/doi.org\/10.1038\/s41593-026-02263-7\" target=\"_blank\" rel=\"noreferrer noopener nofollow\">Glucose-dependent spatial and temporal modulation of oligodendrocyte progenitor cell proliferation via ACLY-regulated histone acetylation<\/a>\u201d by Sami Sauma,\u00a0Stephanie Stransky,\u00a0Ipek Selcen,\u00a0Simone Sidoli,\u00a0Rinat Abzalimov,\u00a0Ye He\u00a0&amp;\u00a0Patrizia Casaccia.\u00a0Nature Neuroscience<br \/><strong>DOI:10.1038\/s41593-026-02263-7<\/strong><\/p>\n<p><strong>Abstract<\/strong><\/p>\n<p><strong>Glucose-dependent spatial and temporal modulation of oligodendrocyte progenitor cell proliferation via ACLY-regulated histone acetylation<\/strong><\/p>\n<p>How it is determined whether postnatal oligodendrocyte progenitor cells (OPCs) will survive, proliferate or differentiate remains unclear.<\/p>\n<p>Here we suggest that temporal and brain regional fluctuations of glucose, concomitant with changes in vascularization, modulate OPC population dynamics.<\/p>\n<p>We found that regions with high glucose levels exhibited greater OPC proliferation and histone acetylation than regions with low glucose and that this was mediated by the enzyme ATP-citrate lyase (ACLY), which converts glucose-derived citrate to acetyl-CoA.<\/p>\n<p>Mice with\u00a0Acly\u00a0deletion in OPCs showed a transient hypomyelination phenotype resulting from decreased OPC numbers, whereas their differentiation into oligodendrocytes (OLs) proceeded due to compensatory upregulation of enzymes responsible for extranuclear generation of acetyl-CoA from alternative metabolic substrates.<\/p>\n<p>Therefore, OPCs rely on ACLY-dependent nuclear acetyl-CoA from glucose-derived citrate, to regulate proliferation, whereas OLs rely on extranuclear acetyl-CoA from other sources for myelin formation.<\/p>\n<p>This suggests a metabolic regulation of OL lineage cell population dynamics.<\/p>\n","protected":false},"excerpt":{"rendered":"Summary: Scientists have long wondered why myelin, the brain\u2019s essential insulation, develops at different speeds in different 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