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  1. Article ; Online: Human brain glycogen metabolism during and after hypoglycemia.

    Oz, Gülin / Kumar, Anjali / Rao, Jyothi P / Kodl, Christopher T / Chow, Lisa / Eberly, Lynn E / Seaquist, Elizabeth R

    Diabetes

    2009  Volume 58, Issue 9, Page(s) 1978–1985

    Abstract: Objective: We tested the hypotheses that human brain glycogen is mobilized during hypoglycemia and its content increases above normal levels ("supercompensates") after hypoglycemia.: Research design and methods: We utilized in vivo (13)C nuclear ... ...

    Abstract Objective: We tested the hypotheses that human brain glycogen is mobilized during hypoglycemia and its content increases above normal levels ("supercompensates") after hypoglycemia.
    Research design and methods: We utilized in vivo (13)C nuclear magnetic resonance spectroscopy in conjunction with intravenous infusions of [(13)C]glucose in healthy volunteers to measure brain glycogen metabolism during and after euglycemic and hypoglycemic clamps.
    Results: After an overnight intravenous infusion of 99% enriched [1-(13)C]glucose to prelabel glycogen, the rate of label wash-out from [1-(13)C]glycogen was higher (0.12 +/- 0.05 vs. 0.03 +/- 0.06 micromol x g(-1) x h(-1), means +/- SD, P < 0.02, n = 5) during a 2-h hyperinsulinemic-hypoglycemic clamp (glucose concentration 57.2 +/- 9.7 mg/dl) than during a hyperinsulinemic-euglycemic clamp (95.3 +/- 3.3 mg/dl), indicating mobilization of glucose units from glycogen during moderate hypoglycemia. Five additional healthy volunteers received intravenous 25-50% enriched [1-(13)C]glucose over 22-54 h after undergoing hyperinsulinemic-euglycemic (glucose concentration 92.4 +/- 2.3 mg/dl) and hyperinsulinemic-hypoglycemic (52.9 +/- 4.8 mg/dl) clamps separated by at least 1 month. Levels of newly synthesized glycogen measured from 4 to 80 h were higher after hypoglycemia than after euglycemia (P <or= 0.01 for each subject), indicating increased brain glycogen synthesis after moderate hypoglycemia.<br />Conclusions: These data indicate that brain glycogen supports energy metabolism when glucose supply from the blood is inadequate and that its levels rebound to levels higher than normal after a single episode of moderate hypoglycemia in humans.
    MeSH term(s) Adaptation, Physiological/physiology ; Adult ; Blood Glucose/metabolism ; Brain/metabolism ; Carbon Isotopes ; Energy Metabolism/physiology ; Female ; Glucose/administration & dosage ; Glucose Clamp Technique ; Glycogen/biosynthesis ; Glycogen/metabolism ; Humans ; Hyperinsulinism/metabolism ; Hypoglycemia/metabolism ; Infusions, Intravenous ; Magnetic Resonance Spectroscopy ; Male ; Models, Biological ; Young Adult
    Chemical Substances Blood Glucose ; Carbon Isotopes ; Glycogen (9005-79-2) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2009-06-05
    Publishing country United States
    Document type Clinical Trial ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/db09-0226
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Diffusion tensor imaging identifies deficits in white matter microstructure in subjects with type 1 diabetes that correlate with reduced neurocognitive function.

    Kodl, Christopher T / Franc, Daniel T / Rao, Jyothi P / Anderson, Fiona S / Thomas, William / Mueller, Bryon A / Lim, Kelvin O / Seaquist, Elizabeth R

    Diabetes

    2008  Volume 57, Issue 11, Page(s) 3083–3089

    Abstract: Objective: Long-standing type 1 diabetes is associated with deficits on neurocognitive testing that suggest central white matter dysfunction. This study investigated whether diffusion tensor imaging (DTI), a type of magnetic resonance imaging that ... ...

    Abstract Objective: Long-standing type 1 diabetes is associated with deficits on neurocognitive testing that suggest central white matter dysfunction. This study investigated whether diffusion tensor imaging (DTI), a type of magnetic resonance imaging that measures white matter integrity quantitatively, could identify white matter microstructural deficits in patients with long-standing type 1 diabetes and whether these differences would be associated with deficits found by neurocognitive tests.
    Research design and methods: Twenty-five subjects with type 1 diabetes for at least 15 years and 25 age- and sex-matched control subjects completed DTI on a 3.0 Tesla scanner and a battery of neurocognitive tests. Fractional anisotropy was calculated for the major white matter tracts of the brain.
    Results: Diabetic subjects had significantly lower mean fractional anisotropy than control subjects in the posterior corona radiata and the optic radiation (P < 0.002). In type 1 diabetic subjects, reduced fractional anisotropy correlated with poorer performance on the copy portion of the Rey-Osterreith Complex Figure Drawing Test and the Grooved Peg Board Test, both of which are believed to assess white matter function. Reduced fractional anisotropy also correlated with duration of diabetes and increased A1C. A history of severe hypoglycemia did not correlate with fractional anisotropy.
    Conclusions: DTI can detect white matter microstructural deficits in subjects with long-standing type 1 diabetes. These deficits correlate with poorer performance on selected neurocognitive tests of white matter function.
    MeSH term(s) Adult ; Age Factors ; Anisotropy ; Brain/pathology ; Brain/physiopathology ; Cognition/physiology ; Diabetes Mellitus, Type 1/pathology ; Diabetes Mellitus, Type 1/physiopathology ; Diabetes Mellitus, Type 1/psychology ; Diffusion Magnetic Resonance Imaging/methods ; Female ; Humans ; Male ; Middle Aged ; Neuropsychological Tests
    Language English
    Publishing date 2008-08-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/db08-0724
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.175: Show issues Location:
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  3. Article: Human brain glycogen content and metabolism: implications on its role in brain energy metabolism.

    Oz, Gülin / Seaquist, Elizabeth R / Kumar, Anjali / Criego, Amy B / Benedict, Luke E / Rao, Jyothi P / Henry, Pierre-Gilles / Van De Moortele, Pierre-Francois / Gruetter, Rolf

    American journal of physiology. Endocrinology and metabolism

    2007  Volume 292, Issue 3, Page(s) E946–51

    Abstract: The adult brain relies on glucose for its energy needs and stores it in the form of glycogen, primarily in astrocytes. Animal and culture studies indicate that brain glycogen may support neuronal function when the glucose supply from the blood is ... ...

    Abstract The adult brain relies on glucose for its energy needs and stores it in the form of glycogen, primarily in astrocytes. Animal and culture studies indicate that brain glycogen may support neuronal function when the glucose supply from the blood is inadequate and/or during neuronal activation. However, the concentration of glycogen and rates of its metabolism in the human brain are unknown. We used in vivo localized 13C-NMR spectroscopy to measure glycogen content and turnover in the human brain. Nine healthy volunteers received intravenous infusions of [1-(13)C]glucose for durations ranging from 6 to 50 h, and brain glycogen labeling and washout were measured in the occipital lobe for up to 84 h. The labeling kinetics suggest that turnover is the main mechanism of label incorporation into brain glycogen. Upon fitting a model of glycogen metabolism to the time courses of newly synthesized glycogen, human brain glycogen content was estimated at approximately 3.5 micromol/g, i.e., three- to fourfold higher than free glucose at euglycemia. Turnover of bulk brain glycogen occurred at a rate of 0.16 micromol.g-1.h-1, implying that complete turnover requires 3-5 days. Twenty minutes of visual stimulation (n=5) did not result in detectable glycogen utilization in the visual cortex, as judged from similar [13C]glycogen levels before and after stimulation. We conclude that the brain stores a substantial amount of glycogen relative to free glucose and metabolizes this store very slowly under normal physiology.
    MeSH term(s) Adult ; Brain/metabolism ; Brain Chemistry ; Energy Metabolism ; Female ; Glucose/administration & dosage ; Glucose/pharmacokinetics ; Glycogen/analysis ; Glycogen/metabolism ; Glycogen/physiology ; Humans ; Magnetic Resonance Imaging ; Male ; Middle Aged ; Models, Theoretical ; Photic Stimulation
    Chemical Substances Glycogen (9005-79-2) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2007-03
    Publishing country United States
    Document type Clinical Trial ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603841-4
    ISSN 1522-1555 ; 0193-1849
    ISSN (online) 1522-1555
    ISSN 0193-1849
    DOI 10.1152/ajpendo.00424.2006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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