Sudha Biddinger, MD, PhD

Cardiovascular disease is the most important cause of death in diabetic patients.  Despite the fact that over 23 million Americans have been diagnosed with diabetes, the mechanisms by which diabetes promotes CVD remain unclear.  Hyperglycemia and hypertriglyceridemia are both closely associated with diabetes, and much effort has been put forth to understand how they might promote CVD.  However, tight control of either serum glucose or serum triglyceride levels fails to consistently prevent CVD in diabetic patients. 

The overall mission of the Biddinger lab is to determine how diabetes increases cardiovascular disease.  The primary goal of our research is to determine the specific signaling pathways and molecules by which insulin resistance, a central feature of Type 2 diabetes, alters lipid metabolism to produce dyslipidemia.  To accomplish this goal, we will integrate biochemical, molecular, cellular, proteomic and mouse genetic approaches with clinical studies in humans.  We expect that this work will ultimately change our understanding of the pathophysiology of atherosclerosis in the diabetic state, leading to more effective therapeutic interventions. 

Sudha Biddinger completed her undergraduate studies at Princeton University, where she majored in Molecular Biology.  She obtained her MD/PhD from the Johns Hopkins School of Medicine.  Her PhD was performed with Dr. Richard Huganir, studying the signaling events underlying synapse formation.  She completed her internship, pediatrics residency, and fellowship in pediatric endocrinology at the Children’s Hospital Boston.  During her fellowship, she worked with Dr. C. Ronald Kahn, studying the pathogenesis of the metabolic syndrome, particularly the mechanisms by which hepatic insulin resistance promotes dyslipidemia, atherosclerosis and cholesterol gallstones.  In 2009, she joined the faculty of the Children’s Hospital Boston, where she continues to study the mechanisms by which insulin regulates lipid and lipoprotein metabolism. 

Biddinger SB, Hernandez-Ono A, Rask-Madsen C, Haas JT, Alemán JO, Suzuki R, Scapa EF, Agarwal C, Carey MC, Stephanopoulos G, Cohen DE, King GL, Ginsberg HN, Kahn CR. Hepatic insulin resistance is sufficient to produce dyslipidemia and susceptibility to atherosclerosis. Cell Metab. 2008;7(2):125-34. 

Biddinger SB, Haas JT, Yu BB, Bezy O, Jing E, Zhang W, Unterman TG, Carey MC, Kahn CR. Hepatic insulin resistance directly promotes formation of cholesterol gallstones. Nat Med. 2008;14(7):778-82. 

Haas JT, Biddinger SB. Dissecting the role of insulin resistance in the metabolic syndrome.  Curr Opin Lipidol. 2009;20(3):206-10. 

Haas JT, Miao J, Chanda D, Wang Y, Zhao E, Haas ME, Hirschey M, Vaitheesvaran B, Farese RV, Kurland I, Graham M, Crooke R, Foufelle F, Biddinger SB.  Hepatic Insulin Signaling Is Required for Obesity-Dependent Expression of SREBP-1c mRNA but Not for Feeding-Dependent Expression.  Cell Metab. 2012; 15(6):  873-884.