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In spontaneously hypertensive rats with HF, for instance, continued administration of GLP-1 (736) for three months decreased both the apoptotic index and the activation of caspase-3, preserved left ventricular function, and prolonged animal survival.64 Similarly, in rats with post-MI HF, treatment with GLP-1 (736) or exenatide significantly improved cardiac remodeling, cardiac function, and the survival of the model.65 In agreement with these results, infusion of GLP-1 (736) in dogs with dilated cardiomyopathy for 48hours increased myocardial glucose uptake, improving left ventricular function and decreasing systemic vascular resistance.66 These findings were confirmed one year later in the same experimental model, where GLP-1 (936) was also shown to have actions similar to GLP-1 (736) in terms of the stimulation of glucose uptake and the improvement of left ventricular function,67 thus supporting the cardioprotective role of GLP-1 (936) in experimental HF

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5.1.3.3 Traumatic brain injury TBI is characterized by structural or functional brain damage caused by external forces, and ferroptosis, a form of programmed cell death, is closely associated with TBI

doi:10.3945/jn.110.122697 Institute of Medicine