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  1. Article: Brain glucose sensing, counterregulation, and energy homeostasis.

    Marty, Nell / Dallaporta, Michel / Thorens, Bernard

    Physiology (Bethesda, Md.)

    2007  Volume 22, Page(s) 241–251

    Abstract: Neuronal circuits in the central nervous system play a critical role in orchestrating the control of glucose and energy homeostasis. Glucose, beside being a nutrient, is also a signal detected by several glucose-sensing units that are located at ... ...

    Abstract Neuronal circuits in the central nervous system play a critical role in orchestrating the control of glucose and energy homeostasis. Glucose, beside being a nutrient, is also a signal detected by several glucose-sensing units that are located at different anatomical sites and converge to the hypothalamus to cooperate with leptin and insulin in controlling the melanocortin pathway.
    MeSH term(s) Animals ; Appetite Regulation/physiology ; Energy Metabolism/physiology ; Glucose/metabolism ; Homeostasis/physiology ; Humans ; Hypothalamus/physiology ; Insulin/physiology ; Leptin/physiology ; Melanocortins/physiology
    Chemical Substances Insulin ; Leptin ; Melanocortins ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2007-08
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2158667-6
    ISSN 1548-9221 ; 1548-9213
    ISSN (online) 1548-9221
    ISSN 1548-9213
    DOI 10.1152/physiol.00010.2007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2164: Show issues Location:
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  2. Article ; Online: Glut2-dependent glucose-sensing controls thermoregulation by enhancing the leptin sensitivity of NPY and POMC neurons.

    Mounien, Lourdes / Marty, Nell / Tarussio, David / Metref, Salima / Genoux, David / Preitner, Frédéric / Foretz, Marc / Thorens, Bernard

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2010  Volume 24, Issue 6, Page(s) 1747–1758

    Abstract: The physiological contribution of glucose in thermoregulation is not completely established nor whether this control may involve a regulation of the melanocortin pathway. Here, we assessed thermoregulation and leptin sensitivity of hypothalamic arcuate ... ...

    Abstract The physiological contribution of glucose in thermoregulation is not completely established nor whether this control may involve a regulation of the melanocortin pathway. Here, we assessed thermoregulation and leptin sensitivity of hypothalamic arcuate neurons in mice with inactivation of glucose transporter type 2 (Glut2)-dependent glucose sensing. Mice with inactivation of Glut2-dependent glucose sensors are cold intolerant and show increased susceptibility to food deprivation-induced torpor and abnormal hypothermic response to intracerebroventricular administration of 2-deoxy-d-glucose compared to control mice. This is associated with a defect in regulated expression of brown adipose tissue uncoupling protein I and iodothyronine deiodinase II and with a decreased leptin sensitivity of neuropeptide Y (NPY) and proopiomelanocortin (POMC) neurons, as observed during the unfed-to-refed transition or following i.p. leptin injection. Sites of central Glut-2 expression were identified by a genetic tagging approach and revealed that glucose-sensitive neurons were present in the lateral hypothalamus, the dorsal vagal complex, and the basal medulla but not in the arcuate nucleus. NPY and POMC neurons were, however, connected to nerve terminals from Glut2-expressing neurons. Thus, our data suggest that glucose controls thermoregulation and the leptin sensitivity of NPY and POMC neurons through activation of Glut2-dependent glucose-sensing neurons located outside of the arcuate nucleus.
    MeSH term(s) Adipose Tissue, Brown/metabolism ; Animals ; Blotting, Western ; Body Temperature Regulation ; Female ; Glucose/analysis ; Glucose/metabolism ; Glucose Transporter Type 2/physiology ; Humans ; Immunoenzyme Techniques ; Integrases ; Iodide Peroxidase/genetics ; Iodide Peroxidase/metabolism ; Ion Channels/genetics ; Ion Channels/metabolism ; Leptin/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Neurons/drug effects ; Neurons/metabolism ; Neuropeptide Y/genetics ; Neuropeptide Y/metabolism ; Pro-Opiomelanocortin/genetics ; Pro-Opiomelanocortin/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Uncoupling Protein 1 ; Iodothyronine Deiodinase Type II
    Chemical Substances Glucose Transporter Type 2 ; Ion Channels ; Leptin ; Mitochondrial Proteins ; Neuropeptide Y ; RNA, Messenger ; Slc2a2 protein, mouse ; Uncoupling Protein 1 ; Pro-Opiomelanocortin (66796-54-1) ; Iodide Peroxidase (EC 1.11.1.8) ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2010-01-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.09-144923
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2266: Show issues Location:
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    Zs.MO 296: Show issues

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  3. Article: Glut2-dependent glucose-sensing controls thermoregulation by enhancing the leptin sensitivity of NPY and POMC neurons

    Mounien, Lourdes / Marty, Nell / Tarussio, David / Metref, Salima / Genoux, David / Preitner, Frédéric / Foretz, Marc / Thorens, Bernard

    FASEB journal. 2010 June, v. 24, no. 6

    2010  

    Abstract: ... located outside of the arcuate nucleus.--Mounien, L., Marty, N., Tarussio, D., Metref, S., Genoux, D ...

    Abstract The physiological contribution of glucose in thermoregulation is not completely established nor whether this control may involve a regulation of the melanocortin pathway. Here, we assessed thermoregulation and leptin sensitivity of hypothalamic arcuate neurons in mice with inactivation of glucose transporter type 2 (Glut2)-dependent glucose sensing. Mice with inactivation of Glut2-dependent glucose sensors are cold intolerant and show increased susceptibility to food deprivation-induced torpor and abnormal hypothermic response to intracerebroventricular administration of 2-deoxy-D-glucose compared to control mice. This is associated with a defect in regulated expression of brown adipose tissue uncoupling protein I and iodothyronine deiodinase II and with a decreased leptin sensitivity of neuropeptide Y (NPY) and proopiomelanocortin (POMC) neurons, as observed during the unfed-to-refed transition or following i.p. leptin injection. Sites of central Glut-2 expression were identified by a genetic tagging approach and revealed that glucose-sensitive neurons were present in the lateral hypothalamus, the dorsal vagal complex, and the basal medulla but not in the arcuate nucleus. NPY and POMC neurons were, however, connected to nerve terminals from Glut2-expressing neurons. Thus, our data suggest that glucose controls thermoregulation and the leptin sensitivity of NPY and POMC neurons through activation of Glut2-dependent glucose-sensing neurons located outside of the arcuate nucleus.--Mounien, L., Marty, N., Tarussio, D., Metref, S., Genoux, D., Preitner, F., Foretz, M., Thorens, B. Glut2-dependent glucose-sensing controls thermoregulation by enhancing the leptin sensitivity of NPY and POMC neurons.
    Language English
    Dates of publication 2010-06
    Size p. 1747-1758.
    Publishing place The Federation of American Societies for Experimental Biology
    Document type Article
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    Database NAL-Catalogue (AGRICOLA)

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  4. Article: Evidence from glut2-null mice that glucose is a critical physiological regulator of feeding.

    Bady, Isabelle / Marty, Nell / Dallaporta, Michel / Emery, Martine / Gyger, Jöel / Tarussio, David / Foretz, Marc / Thorens, Bernard

    Diabetes

    2006  Volume 55, Issue 4, Page(s) 988–995

    Abstract: A role for glucose in the control of feeding has been proposed, but its precise physiological importance is unknown. Here, we evaluated feeding behavior in glut2-null mice, which express a transgenic glucose transporter in their beta-cells to rescue ... ...

    Abstract A role for glucose in the control of feeding has been proposed, but its precise physiological importance is unknown. Here, we evaluated feeding behavior in glut2-null mice, which express a transgenic glucose transporter in their beta-cells to rescue insulin secretion (ripglut1;glut2-/- mice). We showed that in the absence of GLUT2, daily food intake was increased and feeding initiation and termination following a fasting period were abnormal. This was accompanied by suppressed regulation of hypothalamic orexigenic and anorexigenic neuropeptides expression during the fast-to-refed transition. In these conditions, however, there was normal regulation of the circulating levels of insulin, leptin, or glucose but a loss of regulation of plasma ghrelin concentrations. To evaluate whether the abnormal feeding behavior was due to suppressed glucose sensing, we evaluated feeding in response to intraperitoneal or intracerebroventricular glucose or 2-deoxy-D-glucose injections. We showed that in GLUT2-null mice, feeding was no longer inhibited by glucose or activated by 2-deoxy-D-glucose injections and the regulation of hypothalamic neuropeptide expression by intracerebroventricular glucose administration was lost. Together, these data demonstrate that absence of GLUT2 suppressed the function of central glucose sensors, which control feeding probably by regulating the hypothalamic melanocortin pathway. Furthermore, inactivation of these glucose sensors causes overeating.
    MeSH term(s) Animals ; Base Sequence ; DNA Primers ; Feeding Behavior/physiology ; Ghrelin ; Glucose Transporter Type 2/deficiency ; Glucose Transporter Type 2/genetics ; Glucose Transporter Type 2/physiology ; Hypothalamus/physiology ; Insulin/blood ; Leptin/blood ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neuropeptides/genetics ; Peptide Hormones/blood ; Pro-Opiomelanocortin/genetics ; RNA, Messenger/genetics ; RNA, Messenger/isolation & purification ; Reverse Transcriptase Polymerase Chain Reaction ; alpha-MSH/physiology
    Chemical Substances DNA Primers ; Ghrelin ; Glucose Transporter Type 2 ; Insulin ; Leptin ; Neuropeptides ; Peptide Hormones ; RNA, Messenger ; alpha-MSH (581-05-5) ; Pro-Opiomelanocortin (66796-54-1)
    Language English
    Publishing date 2006-02-20
    Publishing country United States
    Document type Journal Article ; 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/diabetes.55.04.06.db05-1386
    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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  5. Article: Regulation of glucagon secretion by glucose transporter type 2 (glut2) and astrocyte-dependent glucose sensors.

    Marty, Nell / Dallaporta, Michel / Foretz, Marc / Emery, Martine / Tarussio, David / Bady, Isabelle / Binnert, Christophe / Beermann, Friedrich / Thorens, Bernard

    The Journal of clinical investigation

    2005  Volume 115, Issue 12, Page(s) 3545–3553

    Abstract: Ripglut1;glut2-/- mice have no endogenous glucose transporter type 2 (glut2) gene expression but rescue glucose-regulated insulin secretion. Control of glucagon plasma levels is, however, abnormal, with fed hyperglucagonemia and insensitivity to ... ...

    Abstract Ripglut1;glut2-/- mice have no endogenous glucose transporter type 2 (glut2) gene expression but rescue glucose-regulated insulin secretion. Control of glucagon plasma levels is, however, abnormal, with fed hyperglucagonemia and insensitivity to physiological hypo- or hyperglycemia, indicating that GLUT2-dependent sensors control glucagon secretion. Here, we evaluated whether these sensors were located centrally and whether GLUT2 was expressed in glial cells or in neurons. We showed that ripglut1;glut2-/- mice failed to increase plasma glucagon levels following glucoprivation induced either by i.p. or intracerebroventricular 2-deoxy-D-glucose injections. This was accompanied by failure of 2-deoxy-D-glucose injections to activate c-Fos-like immunoreactivity in the nucleus of the tractus solitarius and the dorsal motor nucleus of the vagus. When glut2 was expressed by transgenesis in glial cells but not in neurons of ripglut1;glut2-/- mice, stimulated glucagon secretion was restored as was c-Fos-like immunoreactive labeling in the brainstem. When ripglut1;glut2-/- mice were backcrossed into the C57BL/6 genetic background, fed plasma glucagon levels were also elevated due to abnormal autonomic input to the alpha cells; glucagon secretion was, however, stimulated by hypoglycemic stimuli to levels similar to those in control mice. These studies identify the existence of central glucose sensors requiring glut2 expression in glial cells and therefore functional coupling between glial cells and neurons. These sensors may be activated at different glycemic levels depending on the genetic background.
    MeSH term(s) Animals ; Astrocytes/metabolism ; Blood Glucose/metabolism ; Blotting, Northern ; Blotting, Southern ; Blotting, Western ; DNA, Complementary/metabolism ; Deoxyglucose/chemistry ; Gene Expression Regulation ; Glucagon/blood ; Glucagon/chemistry ; Glucagon/metabolism ; Glucagon/secretion ; Glucagon-Secreting Cells/metabolism ; Glucose/metabolism ; Glucose Transporter Type 2/genetics ; Glucose Transporter Type 2/metabolism ; Glucose Transporter Type 2/physiology ; Hypoglycemia/pathology ; Immunohistochemistry ; Insulin/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Biological ; Models, Genetic ; Neuroglia/metabolism ; Neuroglia/pathology ; Neurons/metabolism ; Proto-Oncogene Proteins c-fos/metabolism ; Time Factors ; Transgenes
    Chemical Substances Blood Glucose ; DNA, Complementary ; Glucose Transporter Type 2 ; Insulin ; Proto-Oncogene Proteins c-fos ; Slc2a2 protein, mouse ; Glucagon (9007-92-5) ; Deoxyglucose (9G2MP84A8W) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2005-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI26309
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.184: Show issues Location:
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  6. Article: Pandemic-driven Community Collaboration in Western North Carolina: The Silver Lining Around the COVID-19 Cloud.

    Hathaway, William R / Mims, Susan R / Ellis, David / Herbert, Teresa M / Saunders, Stacie Turpin / Gregory, Nelle / Stargell, Lucretia / Ammerman, Adrienne / Stamey, Marty L / Bunio, Richard / Smith, Steven

    North Carolina medical journal

    2021  Volume 82, Issue 4, Page(s) 259–265

    Language English
    Publishing date 2021-07-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 422795-5
    ISSN 0029-2559
    ISSN 0029-2559
    DOI 10.18043/ncm.82.4.259
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 169: Show issues Location:
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