Anaesthesia generates neuronal insulin resistance by inducing hypothermia.

Christian Holscher, Lidy van Aalten, Calum Sutherland

    Research output: Contribution to journalArticle

    13 Citations (Scopus)

    Abstract

    BACKGROUND: Anaesthesia is commonly employed prior to surgical investigations and to permit icv injections in rodents. Indeed it is standard practise in many studies examining the subsequent actions of hormones and growth factors on the brain. Recent evidence that the basal activity of specific intracellular signalling proteins can be affected by anaesthesia prompted us to examine the effect of anaesthesia not only on the basal activity but also the insulin sensitivity of the major insulin signalling pathways. RESULTS: We find that urethane- and ketamine-induced anaesthesia results in rapid activation of the phosphatidylinositol (PI) 3-kinase-protein kinase B (PKB) signalling pathway in the brain, increases tau phosphorylation while at the same time reducing basal activity of the Ras-ERK pathway. Subsequent injection of insulin does not alter the activity of either the PI 3-kinase or ERK signalling pathways, indicating a degree of neuronal molecular insulin resistance. However, if body temperature is maintained during anaesthesia then there is no alteration in the basal activity of these signalling molecules. Subsequent response of both pathways to insulin injection is restored. CONCLUSION: The data is consistent with a hypothermia related alteration in neuronal signalling following anaesthesia, and emphasises the importance of maintaining the body temperature of rodents when monitoring insulin (or growth factor/neurotrophic agent) action in the brain of anesthetised rodents.
    LanguageEnglish
    Pages100
    JournalBMC Neuroscience
    Volume9
    Publication statusPublished - 2008

    Fingerprint

    Hypothermia
    Insulin Resistance
    Anesthesia
    Phosphatidylinositol 3-Kinase
    Insulin
    Rodentia
    MAP Kinase Signaling System
    Body Temperature
    Injections
    Intercellular Signaling Peptides and Proteins
    Brain
    Intracellular Signaling Peptides and Proteins
    Proto-Oncogene Proteins c-akt
    Urethane
    Ketamine
    Phosphorylation
    Hormones

    Cite this

    Holscher, C., van Aalten, L., & Sutherland, C. (2008). Anaesthesia generates neuronal insulin resistance by inducing hypothermia. BMC Neuroscience, 9, 100.
    Holscher, Christian ; van Aalten, Lidy ; Sutherland, Calum. / Anaesthesia generates neuronal insulin resistance by inducing hypothermia. In: BMC Neuroscience. 2008 ; Vol. 9. pp. 100.
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    abstract = "BACKGROUND: Anaesthesia is commonly employed prior to surgical investigations and to permit icv injections in rodents. Indeed it is standard practise in many studies examining the subsequent actions of hormones and growth factors on the brain. Recent evidence that the basal activity of specific intracellular signalling proteins can be affected by anaesthesia prompted us to examine the effect of anaesthesia not only on the basal activity but also the insulin sensitivity of the major insulin signalling pathways. RESULTS: We find that urethane- and ketamine-induced anaesthesia results in rapid activation of the phosphatidylinositol (PI) 3-kinase-protein kinase B (PKB) signalling pathway in the brain, increases tau phosphorylation while at the same time reducing basal activity of the Ras-ERK pathway. Subsequent injection of insulin does not alter the activity of either the PI 3-kinase or ERK signalling pathways, indicating a degree of neuronal molecular insulin resistance. However, if body temperature is maintained during anaesthesia then there is no alteration in the basal activity of these signalling molecules. Subsequent response of both pathways to insulin injection is restored. CONCLUSION: The data is consistent with a hypothermia related alteration in neuronal signalling following anaesthesia, and emphasises the importance of maintaining the body temperature of rodents when monitoring insulin (or growth factor/neurotrophic agent) action in the brain of anesthetised rodents.",
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    Holscher, C, van Aalten, L & Sutherland, C 2008, 'Anaesthesia generates neuronal insulin resistance by inducing hypothermia.', BMC Neuroscience, vol. 9, pp. 100.

    Anaesthesia generates neuronal insulin resistance by inducing hypothermia. / Holscher, Christian; van Aalten, Lidy; Sutherland, Calum.

    In: BMC Neuroscience, Vol. 9, 2008, p. 100.

    Research output: Contribution to journalArticle

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    T1 - Anaesthesia generates neuronal insulin resistance by inducing hypothermia.

    AU - Holscher, Christian

    AU - van Aalten, Lidy

    AU - Sutherland, Calum

    PY - 2008

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    N2 - BACKGROUND: Anaesthesia is commonly employed prior to surgical investigations and to permit icv injections in rodents. Indeed it is standard practise in many studies examining the subsequent actions of hormones and growth factors on the brain. Recent evidence that the basal activity of specific intracellular signalling proteins can be affected by anaesthesia prompted us to examine the effect of anaesthesia not only on the basal activity but also the insulin sensitivity of the major insulin signalling pathways. RESULTS: We find that urethane- and ketamine-induced anaesthesia results in rapid activation of the phosphatidylinositol (PI) 3-kinase-protein kinase B (PKB) signalling pathway in the brain, increases tau phosphorylation while at the same time reducing basal activity of the Ras-ERK pathway. Subsequent injection of insulin does not alter the activity of either the PI 3-kinase or ERK signalling pathways, indicating a degree of neuronal molecular insulin resistance. However, if body temperature is maintained during anaesthesia then there is no alteration in the basal activity of these signalling molecules. Subsequent response of both pathways to insulin injection is restored. CONCLUSION: The data is consistent with a hypothermia related alteration in neuronal signalling following anaesthesia, and emphasises the importance of maintaining the body temperature of rodents when monitoring insulin (or growth factor/neurotrophic agent) action in the brain of anesthetised rodents.

    AB - BACKGROUND: Anaesthesia is commonly employed prior to surgical investigations and to permit icv injections in rodents. Indeed it is standard practise in many studies examining the subsequent actions of hormones and growth factors on the brain. Recent evidence that the basal activity of specific intracellular signalling proteins can be affected by anaesthesia prompted us to examine the effect of anaesthesia not only on the basal activity but also the insulin sensitivity of the major insulin signalling pathways. RESULTS: We find that urethane- and ketamine-induced anaesthesia results in rapid activation of the phosphatidylinositol (PI) 3-kinase-protein kinase B (PKB) signalling pathway in the brain, increases tau phosphorylation while at the same time reducing basal activity of the Ras-ERK pathway. Subsequent injection of insulin does not alter the activity of either the PI 3-kinase or ERK signalling pathways, indicating a degree of neuronal molecular insulin resistance. However, if body temperature is maintained during anaesthesia then there is no alteration in the basal activity of these signalling molecules. Subsequent response of both pathways to insulin injection is restored. CONCLUSION: The data is consistent with a hypothermia related alteration in neuronal signalling following anaesthesia, and emphasises the importance of maintaining the body temperature of rodents when monitoring insulin (or growth factor/neurotrophic agent) action in the brain of anesthetised rodents.

    M3 - Article

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