Sleep loss alters metabolism across the organism.
Sleep loss–induced metabolic alterations in purinergic signaling (purple), glucose metabolism (green), lipid oxidation (blue), and cell phenotypes (orange) are apparent throughout the central nervous system, peripheral tissues, and blood plasma in humans and other model systems. These changes reduce the amount of energy available to support anabolic processes—an effect that is most pronounced in highly metabolically active cells such as myocytes, hepatocytes, adipocytes, and brain cells.CREDIT: A. MASTIN/SCIENCE SIGNALING
Molecular changes at the tripartite synapse after sleep loss.
Increased neuronal oxidative stress promotes lipid droplet accumulation in neighboring glia, which then catabolize these droplets using β-oxidation. In addition, neuronal ATP generation efficiency decreases, marked by increased expression of mitochondrial electron transport chain genes simultaneously with uncoupling proteins and increased phosphorylation of AMPK (blue). Increased cellular activity during sleep loss leads to increased glutamate release, which up-regulates activity and gene expression related to the ANLS (green). The effects of sleep loss on glycogen storage are unclear. Sleep loss leads to an increase in extracellular adenosine, released from astrocytes, which binds to A1Rs to decrease expression of synaptic plasticity genes through Gαi-cAMP-PKA signaling (purple).CREDIT: A. MASTIN/SCIENCE SIGNALING
#medsky🧪 #immunosky #neurosky #publichealth An emerging body of research implicating #SleepLoss as a #metabolicdisorder and discuss its impact on the metabolism of neurons and parallels to #neurodegenerativedisorders.
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