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The mechanism involves direct action on GLP-1 receptors in the liver

In some physiological conditions, endogenous production does not fully cover the muscle requirement for this component

Pre-publication history The pre-publication history for this paper can be accessed here: Acknowledgements This study was funded by intramural funds from the New Jersey Neuroscience Institute and the Neurogenetics Foundation

These keywords were previously identified through the MeSH (Medical Subject Heading) database as descriptors for the realization of this work

Mitochondrial damage due to SOD1 deficiency in SH-SY5Y neuroblastoma cells: a rationale for the redundancy of SOD1