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1810): glucagon receptors also couple to Gi protein in human atrial myocytes, and Gi upregulation in the cardiomyocyte inhibits cAMP formation and Gs-coupled signal transduction, so glucagon action in the chronically failing heart "may theoretically be impaired." Two limits on how far that carries: the condition Petersen describes is heart failure , not obesity or sedentary metabolic dysfunction, and the impairment is offered as a hypothesis, not an observation
Evidence : Animal studies suggest that BPC 157-treated subjects had better recovery outcomes, including functional improvements
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