Yuejuan Qin, MD, PhD

My main interest is in the pathophysiology, and treatment of type 2 diabetes and its associated cardiovascular disturbances, especially HFpEF and HFrEF. I am a clinical endocrinologist, having spent over 10-years of practice in mainland China before joining UT Health San Antonio faculty in 2006. From 2006 to 2016, I worked in a genetics lab here, I discovered a novel pheochromocytoma susceptibility gene TMEM127 using integrative genomics and identified the location of TMEM127 and its association with the endomembrane system by florescent microscopy. I expressed genetic TMEM127 constructs and knocked down endogenous TMEM127 gene expression in different cells lines to identify its cellular function. I investigated the signaling pathway via which this new protein TMEM127 is involved in regulation of cell growth, proliferation and apoptosis. I generated a TMEM127 null mouse model to facilitate studies to elucidate the function of TMEM127 in vivo.

In 2016 I joined the Diabetes Division where my current research focuses on elucidating the mechanisms via which SGLT2 inhibition influences ketone metabolism and cardiovascular function. My hypothesis was that the SGLT2 inhibition-induced hyperketonemia contributes to its heart failure benefits. I used varying ketone infusion rates and cardiac magnetic resonance imaging (MRI) to quantitate parameters of left ventricular (LV) systolic and diastolic function. Using positron emission tomography (PET) with 18F-fluoro-2-deoxy-D-glucose and [150]-water I also examined the effect of SGLT2i on myocardial blood flow and myocardial and skeletal muscle glucose uptake in type 2 diabetic patients with NYHA class II, NYHA class III {New York Heart Association (NYHA)} heart failure and reduced ejection fraction. The results have been oral, and poster presented during American Diabetes Association. Two manuscripts are in the press. I have completed another study-Combination Therapy in T2DM. Using a double tracer glucose turnover technique, I demonstrated that the addition of saxagliptin to the SGLT2i inhibitor resulted in superior glycemic control compared with dapagliflozin monotherapy because increased glucose utilization/oxidation and enhanced suppression of endogens (hepatic) glucose production.