David Stepp

Scholarship

Selected Recent Publications

• Obesity Induces Disruption of Microvascular Endothelial Circadian Rhythm, 2022
  Journal Article, Academic Journal
• Protective role of Cav-1 in pneumolysin-induced endothelial barrier dysfunction, 2022
  Journal Article, Academic Journal
• The biological clock enhancer nobiletin ameliorates steatosis in genetically obese mice by restoring aberrant hepatic circadian rhythm, 2022
  Journal Article, Academic Journal
• Nf1 heterozygous mice recapitulate the anthropometric and metabolic features of human neurofibromatosis type 1, 2021
  Journal Article, Academic Journal
• Obesity and the Bidirectional Risk of Cancer and Cardiovascular Diseases in African Americans: Disparity vs. Ancestry, 2021
  Other

Research Interests

Work in our lab is devoted to unraveling links between obesity and cardiometabolic dysfunction. While weight loss is ideal, the overwhelming majority of the obese population – either due to chronic entrainment of metabolism or behavior, increased age or accumulation of injuries – retain or regain excess weight. A critical need therefore is to break the links between obesity and its cardiovascular outcomes. The CORE HYPOTHESIS of our laboratory is that resolution of endocrine and metabolic abnormalities in obesity is the path to preventing cardiovascular disease in overweight patients. Currently, the central theme of these studies is that the balance of nitric oxide (NO) derived from eNOS and the loss of its bioavailability from NADPH Oxidase (NOX)-generated super-oxide is a key determinant of cardiometabolic health. Changes in glycemic status, either absolute levels or pattern of hyperglycemia, appear to be a primary determinant of states in which super-oxide excess reduces NO below a threshold needed for full cardiovascular function. Thus, the glucose-NOS/NOX axis in the primary focus of studies in our lab.