title: Differential energetic response of brain vs. skeletal muscle upon glycemic variations in healthy humans.
abstract: The brain regulates all metabolic processes within the organism, and therefore, its energy supply is preserved even during fasting. However, the underlying mechanism is unknown. Here, it is shown, using (31)P-magnetic resonance spectroscopy that during short periods of hypoglycemia and hyperglycemia, the brain can rapidly increase its high-energy phosphate content, whereas there is no change in skeletal muscle. We investigated the key metabolites of high-energy phosphate metabolism as rapidly available energy stores by (31)P MRS in brain and skeletal muscle of 17 healthy men. Measurements were performed at baseline and during dextrose or insulin-induced hyperglycemia and hypoglycemia. During hyperglycemia, phosphocreatine (PCr) concentrations increased significantly in the brain (P = 0.013), while there was a similar trend in the hypopglycemic condition (P = 0.055). Skeletal muscle content remained constant in both conditions (P > 0.1). ANOVA analyses comparing changes from baseline to the respective glycemic plateau in brain (up to +15%) vs. muscle (up to -4%) revealed clear divergent effects in both conditions (P < 0.05). These effects were reflected by PCr/Pi ratio (P < 0.05). Total ATP concentrations revealed the observed divergency only during hyperglycemia (P = 0.018). These data suggest that the brain, in contrast to peripheral organs, can activate some specific mechanisms to modulate its energy status during variations in glucose supply. A disturbance of these mechanisms may have far-reaching implications for metabolic dysregulation associated with obesity or diabetes mellitus.
authors.affiliation: Department of Psychiatry and Psychotherapy, University of Luebeck, Ratzeburger Allee 160, 23538, Luebeck, Germany. Oltmanns@kfg.mu-luebeck.de
authors.forename: Kerstin M
authors.initials: KM
authors.lastname: Oltmanns
authors.forename: Uwe H
authors.initials: UH
authors.lastname: Melchert
authors.forename: Harald G
authors.initials: HG
authors.lastname: Scholand-Engler
authors.forename: Maria C
authors.initials: MC
authors.lastname: Howitz
authors.forename: Bernd
authors.initials: B
authors.lastname: Schultes
authors.forename: Ulrich
authors.initials: U
authors.lastname: Schweiger
authors.forename: Fritz
authors.initials: F
authors.lastname: Hohagen
authors.forename: Jan
authors.initials: J
authors.lastname: Born
authors.forename: Achim
authors.initials: A
authors.lastname: Peters
authors.forename: Luc
authors.initials: L
authors.lastname: Pellerin
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D001921:Brain / Q000378:metabolism*; D004734:Energy Metabolism / Q000502:physiology*; D005947:Glucose; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D006943:Hyperglycemia / Q000139:chemically induced / Q000378:metabolism*; D007003:Hypoglycemia / Q000139:chemically induced / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D007773:Lactates / Q000097:blood; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D007328:Insulin; D007773:Lactates; D000255:Adenosine Triphosphate; D005947:Glucose