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Glucose-induced translational control of proinsulin biosynthesis is proportional to preproinsulin mRNA levels in islet cells but not regulated via a positive feedback of secreted insulin
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As there is no meaningful expression of GLP-1 receptors on hepatocytes, the major effect of GLP-1 agonists on MASH is likely to be indirect and may be related to a reduction in calorie intake, body weight and insulin resistance, all of which would lead to reduced liver lipid accumulation and hepatic inflammation 7,8
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