Exercise in rats does not alter hypothalamic AMP-activated protein kinase activity

Ulrika Andersson, Jonas Thue Treebak, Jakob Nis Nielsen, Kirsty L. Smith, Caroline R. Abbott, Caroline J. Small, David Carling, Erik Richter

    31 Citationer (Scopus)

    Abstract

    Recent studies have demonstrated that AMP-activated protein kinase (AMPK) in the hypothalamus is involved in the regulation of food intake. Because exercise is known to influence appetite and cause substrate depletion, it may also influence AMPK in the hypothalamus. Male rats that either rested or ran for 30 or 60 min on a treadmill (22 m/min, 10% slope) were sacrificed immediately after exercise or after 60 min recovery either in the fasted state or after oral gavage with glucose (3 g/kg body weight). Exercise decreased muscle and liver glycogen substantially. Hypothalamic total or a2-associated AMPK activity and phosphorylation state of the AMPK substrate acetyl-CoA carboxylase were not changed significantly immediately following treadmill running or during fed or fasted recovery. Plasma ghrelin increased (P < 0.05) by 40% during exercise whereas the concentration of PYY was unchanged. In recovery, glucose feeding increased plasma glucose and insulin concentrations whereas ghrelin and PYY decreased to (ghrelin) or below (PPY) resting levels. It is concluded that 1 h of strenuous exercise in rats does not elicit significant changes in hypothalamic AMPK activity despite an increase in plasma ghrelin. Thus, changes in energy metabolism during or after exercise are likely not coordinated by changes in hypothalamic AMPK activity.
    OriginalsprogEngelsk
    TidsskriftBiochemical and Biophysical Research Communications
    Vol/bind329
    Udgave nummer2
    Sider (fra-til)719-725
    Antal sider7
    ISSN0006-291X
    DOI
    StatusUdgivet - 2005

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