AMP-activated protein kinase α (AMPKα) is a key regulator of energy balance in many model species during
hypoxia. In a marine bivalve, the Pacific oyster Crassostrea gigas, we analyzed the
protein content of adductor muscle in response to
hypoxia during 6 h. In both smooth and striated muscles, the amount of full-length
AMP-activated protein kinase α (AMPKα) remained unchanged during
hypoxia. However,
hypoxia induced a rapid and muscle-specific response concerning truncated
isoforms of AMPKα. In the smooth muscle, a truncated
isoform of AMPKα was increased from 1 to 6 h of
hypoxia, and was linked with accumulation of AKT
kinase, a key
enzyme of the
insulin signaling pathway which controls intracellular
glucose metabolism. In this muscle, aerobic metabolism was maintained over the 6 h of
hypoxia, as mitochondrial
citrate synthase activity remained constant. In contrast, in striated muscle,
hypoxia did not induce any significant modification of neither truncated AMPKα nor AKT
protein content, and
citrate synthase activity was altered after 6 h of
hypoxia. Together, our results demonstrate that
hypoxia response is specific to muscle type in Pacific oyster, and that truncated AMPKα and AKT
proteins might be involved in maintaining aerobic metabolism in smooth muscle. Such regulation might occur in vivo during tidal intervals that cause up to 6 h of
hypoxia.