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Results We report that pre-stroke weight loss by GLP-1R activation, and more potently by dual co-activation of GLP-1 and NPY2 receptors, is a pharmacologically targetable mechanism, upstream of glycaemic regulation, through which post-stroke recovery is achieved

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This hypoxia, coupled with increased erythropoietin production, can lead to a rise in red cell mass and subsequent iron accumulation in hepatocytes [13]

Researchers in an international collaboration across the University of Ottawa Eye Institute, University of Toronto, McMaster University, and Doheny Eye Institute UCLA conducted one of the largest global studies on the topic to date