Malak Almutairi

TL;DR: The described actions of GLP-1/GLp-1R agonists on the vascular endothelium, which include antiproliferative actions on VSMCs and endothelial cells, reductions in oxidative stress, and increases in nitric oxide generation, are reviewed.

TL;DR: It is demonstrated that pyruvate dehydrogenase kinase 4 is a direct transcriptional target of FoxO1 (but not FoxO3/FoxO4) in the heart, thereby controlling PDH activity and subsequent glucose oxidation rates.

TL;DR: Liraglutide treatment attenuated declining diastolic function in mice with T2D, which was associated with enhanced pyruvate dehydrogenase activity, the rate-limiting enzyme of glucose oxidation, and associated with increased circulating insulin levels.

TL;DR: It does appear that forced restriction of glucose oxidation in the hearts of Pdha1Cardiac−/− mice is sufficient to produce a cardiomyopathy-like phenotype, independent of the perturbed metabolic milieu observed in obesity and/or T2D.

TL;DR: A fundamental contribution of enhanced ketone body oxidation to the pathology of obesity-induced T2D is defined, while suggesting pharmacological SCOT inhibition as a new class of anti-diabetes therapy is suggested.