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Aerobic glycolysis is a widespread phenomenon that underlies energetics of diverse brain activities, such as alerting, sensory processing, cognition, memory, and pathophysiological conditions, but specific cellular functions fulfilled by aerobic glycolysis are poorly understood. Evaluation of evidence derived from different disciplines reveals that aerobic glycolysis is a complex, regulated phenomenon that is prevented by propranolol, a non\u2010specific \u03b2\u2010adrenoceptor antagonist. The metabolic pathways that contribute to excess utilization of glucose compared with oxygen include glycolysis, the pentose phosphate shunt pathway, the malate\u2010aspartate shuttle, and astrocytic glycogen turnover. Increased lactate production by unidentified cells, and lactate dispersal from activated cells and lactate release from the brain, both facilitated by astrocytes, are major factors underlying aerobic glycolysis in subjects with low blood lactate levels. Astrocyte\u2010neuron lactate shuttling with local oxidation is minor. Blockade of aerobic glycolysis by propranolol implicates adrenergic regulatory processes including adrenal release of epinephrine, signaling to brain via the vagus nerve, and increased norepinephrine release from the locus coeruleus. Norepinephrine has a powerful influence on astrocytic metabolism and glycogen turnover that can stimulate carbohydrate utilization more than oxygen consumption, whereas \u03b2\u2010receptor blockade \u2018re\u2010balances\u2019 the stoichiometry of oxygen\u2010glucose or \u2010carbohydrate metabolism by suppressing glucose and glycogen utilization more than oxygen consumption. This conceptual framework may be helpful for design of future studies to elucidate functional roles of preferential non\u2010oxidative glucose utilization and glycogen turnover during brain activation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:label\/>\n                    <jats:p>\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc13630-fig-0007-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                      Aerobic glycolysis, the preferential up\u2010regulation of glucose utilization (CMR\n                      <jats:sub>glc<\/jats:sub>\n                      ) compared with oxygen consumption (CMR\n                      <jats:sub>O2<\/jats:sub>\n                      ) during brain activation, is blocked by propranolol. Epinephrine release from the adrenal gland stimulates vagus nerve signaling to the locus coeruleus, enhancing norepinephrine release in the brain, and regulation of astrocytic and neuronal metabolism to stimulate CMR\n                      <jats:sub>glc<\/jats:sub>\n                      more than CMR\n                      <jats:sub>O2<\/jats:sub>\n                      . Propranolol suppresses CMR\n                      <jats:sub>glc<\/jats:sub>\n                      more than CMR\n                      <jats:sub>O2<\/jats:sub>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jnc.13630","type":"journal-article","created":{"date-parts":[[2016,5,10]],"date-time":"2016-05-10T22:53:25Z","timestamp":1462920805000},"page":"14-52","source":"Crossref","is-referenced-by-count":152,"title":["Aerobic glycolysis during brain activation: adrenergic regulation and influence of norepinephrine on astrocytic metabolism"],"prefix":"10.1111","volume":"138","author":[{"given":"Gerald A.","family":"Dienel","sequence":"first","affiliation":[{"name":"Department of Cell Biology and Physiology University of New Mexico Albuquerque New Mexico USA"},{"name":"Department of Neurology University of Arkansas for Medical Sciences Little Rock Arkansas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nancy F.","family":"Cruz","sequence":"additional","affiliation":[{"name":"Department of Neurology University of Arkansas for Medical Sciences Little Rock Arkansas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2016,6,10]]},"reference":[{"key":"e_1_2_12_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1979.tb06467.x"},{"key":"e_1_2_12_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(79)90552-3"},{"key":"e_1_2_12_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1989.111"},{"key":"e_1_2_12_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.1995.11"},{"key":"e_1_2_12_6_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.12-03-00781.1992"},{"key":"e_1_2_12_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(92)90507-6"},{"key":"e_1_2_12_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/0361-9230(92)90055-3"},{"key":"e_1_2_12_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(87)91642-8"},{"key":"e_1_2_12_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(89)91168-2"},{"key":"e_1_2_12_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(94)91782-5"},{"key":"e_1_2_12_12_1","doi-asserted-by":"publisher","DOI":"10.1017\/S0952523800011214"},{"key":"e_1_2_12_13_1","doi-asserted-by":"publisher","DOI":"10.1093\/cercor\/8.3.269"},{"key":"e_1_2_12_14_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.01-08-00887.1981"},{"key":"e_1_2_12_15_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.2009.05943.x"},{"key":"e_1_2_12_16_1","doi-asserted-by":"publisher","DOI":"10.01042\/AN20120004"},{"key":"e_1_2_12_17_1","doi-asserted-by":"publisher","DOI":"10.1002\/jnr.21376"},{"key":"e_1_2_12_18_1","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.2009.206"},{"key":"e_1_2_12_19_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuint.2012.01.013"},{"key":"e_1_2_12_20_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.phrs.2013.09.007"},{"key":"e_1_2_12_21_1","doi-asserted-by":"publisher","DOI":"10.1038\/jcbfm.2014.233"},{"key":"e_1_2_12_22_1","doi-asserted-by":"publisher","DOI":"10.1093\/cercor\/bhn040"},{"key":"e_1_2_12_23_1","doi-asserted-by":"publisher","DOI":"10.1021\/bi00583a011"},{"key":"e_1_2_12_24_1","doi-asserted-by":"publisher","DOI":"10.1093\/cercor\/bhh138"},{"key":"e_1_2_12_25_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1978.tb06078.x"},{"key":"e_1_2_12_26_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(78)90968-X"},{"key":"e_1_2_12_27_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1748-1716.1978.tb06255.x"},{"key":"e_1_2_12_28_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1976.tb05165.x"},{"key":"e_1_2_12_29_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.2040-10.2010"},{"key":"e_1_2_12_30_1","doi-asserted-by":"crossref","first-page":"1079","DOI":"10.1016\/S0022-5347(25)00203-4","article-title":"Anatomical evidence for alpha\u20102 adrenoceptor heterogeneity: differential autoradiographic distributions of [3\u00a0H]rauwolscine and [3\u00a0H]idazoxan in rat brain","volume":"241","author":"Boyajian C. 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