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For example, other antidiabetic agents (such as insulin, metformin, glyburide, sitagliptin, and canagliflozin) taken along with GLP-1 RAs potentiate hypoglycemic risk and may necessitate dose adjustments

Uraemic cardiomyopathy is characterized by myriad cardiac metabolic maladaptations, including altered mitochondrial function, changes in myocardial substrate utilization, altered metabolic transporter function and expression, and impaired insulin response and phosphoinositide-3 kinaseAKT signalling, which collectively lead to impaired cardiac energetics

[1] [2] These mechanistic interpretations remain under active investigation in human trials