Fasting mediated increase in p-BADser155 and p-AKTser473 in the prefrontal cortex of mice

Vigneshwaran Pitchaimani, Somasundaram Arumugam, Rajarajan Amirthalingam Thandavarayan, Vengadeshprabhu Karuppagounder, Remya Sreedhar, Rejina Afrin, Meilei Harima, Hiroshi Suzuki, Shizuka Miyashita, Mayumi Nomoto, Hirohito Sone, Kenji Suzuki, Kenichi Watanabe

    Research output: Contribution to journalArticlepeer-review

    2 Scopus citations


    BAD-deficient mice and fasting have several common functional roles in seizures, beta-hydroxybutyrate (BHB) uptake in brain and alteration in counterregulatory hormonal regulation during hypoglycemia. Neuronal specific insulin receptor knockout (NIRKO) mice display impaired counterregulatory hormonal responses during hypoglycemia. In this study we investigated the fasting mediated expression of p-BADser155 and p-AKTser473 in different regions of brain (prefrontal cortex, hippocampus, midbrain and hypothalamus). Fasting specifically increases p-BADser155 and p-AKTser473 in prefrontal cortex and decreases in other regions of brain. Our results suggest that fasting may increase the uptake BHB by decreasing p-BADser155 in the brain during hypoglycemia except prefrontal cortex and it uncovers specific functional area of p-BADser155 and p-AKTser473 that may regulates counter regulatory hormonal response. Overall in support with previous findings, fasting mediated hypoglycemia activates prefrontal cortex insulin signaling which influences the hypothalamic paraventricular nucleus mediated activation of sympathoadrenal hormonal responses.

    Original languageEnglish (US)
    Pages (from-to)134-139
    Number of pages6
    JournalNeuroscience Letters
    StatePublished - Sep 5 2014


    • AKT
    • BAD
    • Betahydroxybutyrate
    • Fasting
    • Hypoglycemia
    • Prefrontal cortex

    ASJC Scopus subject areas

    • Neuroscience(all)


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