Jiten D. Patel

This study identifies that SGLT2 inhibitors activate pantothenate kinase 1 (PANK1) in the human heart, enhancing coenzyme-A synthesis and fuel use, which may explain their clinical benefits in heart failure.

This paper shows that deleting MondoA globally protects against diet-induced obesity by increasing energy expenditure through enhanced glucose uptake and glycolytic flux, leading to elevated glycerol synthesis and lipolysis.

This study shows that BT2, an inhibitor of BCKDK, reduces plasma tryptophan by displacing it from albumin, revealing an off-target effect on tryptophan metabolism.

This paper develops a two-hit mouse model of HFpEF combining diet-induced obesity and renin-mediated hypertension, showing key features of the disease and response to therapy.

This study shows that SGLT2 inhibitors improve heart failure in mice independently of their metabolic effects, even when SGLT2 is absent.