Disruption of STIM1-mediated Ca²⁺ sensing and energy metabolism in adult skeletal muscle compromises exercise tolerance, proteostasis, and lean mass.

My research is focused on 1) understanding metabolic perturbations that occur in subpopulations of skeletal muscle mitochondria in response to a chronic high lipid environment, 2) identifying specific metabolites of lipid-induced mitochondrial stress that contribute to skeletal muscle insulin resistance and type II diabetes, and 3) understanding how mitochondrial adaptations in response to exercise confer protection against lipid-induced mitochondrial dysfunction.

Paul Grimsrud is an Assistant professor of Medicine—in the Division of Endocrinology, Metabolism, and Nutrition—and Proteomics Section Leader at the Duke Molecular Physiology Institute. He completed a PhD in Biochemistry at the University of Minnesota-Twin Cities and a postdoctoral fellowship at the University of Wisconsin-Madison. His research combines mass spectrometry-based proteomics with complementary biochemical approaches to characterize the regulation of metabolism and signaling by protein post-translational modifications (PTMs). He is particularly interested in mechanisms that link altered mitochondrial function to metabolic diseases, such as heart failure, type 2 diabetes, and cancer. He works with colleagues to apply quantitative PTM measurements to relevant model systems, leverage bioinformatics tools to develop testable hypotheses from large-scale data, and characterize mechanisms of PTM-mediated metabolic control.