Commitment to glycolysis sustains survival of NO-producing inflammatory dendritic cells. Differentiation of murine macrophages to express nonspecific cytotoxicity for tumor cells results in L-arginine-dependent inhibition of mitochondrial iron-sulfur enzymes in the macrophage effector cells. Macrophage-restricted interleukin-10 receptor deficiency, but not IL-10 deficiency, causes severe spontaneous colitis. Anti-inflammatory effect of IL-10 mediated by metabolic reprogramming of macrophages. Cell-intrinsic glycogen metabolism supports early glycolytic reprogramming required for dendritic cell immune responses. Dimethyl fumarate targets GAPDH and aerobic glycolysis to modulate immunity. Pyruvate kinase M2 regulates Hif-1α activity and IL-1β induction and is a critical determinant of the Warburg effect in LPS-activated macrophages. mTOR- and HIF-1α-mediated aerobic glycolysis as metabolic basis for trained immunity. Substrate fate in activated macrophages: a comparison between innate, classic, and alternative activation. HIF-1α is essential for myeloid cell-mediated inflammation. mTORC1-dependent metabolic reprogramming is a prerequisite for NK cell effector function. Antigen receptor-mediated changes in glucose metabolism in B lymphocytes: role of phosphatidylinositol 3-kinase signaling in the glycolytic control of growth. The CD28 signaling pathway regulates glucose metabolism. Endotoxin-induced enhancement of glucose influx into murine peritoneal macrophages via GLUT1. Immunometabolism governs dendritic cell and macrophage function. New insights into the multidimensional concept of macrophage ontogeny, activation and function. Protective and pathogenic functions of macrophage subsets. Unraveling the complex interplay between T cell metabolism and function.

Channeling controls both lipid signals that regulate cell metabolism and the partitioning of fatty acids within cells towards either synthetic or degradative pathways.Geltink, R. Current studies have led to the concept that lipids do not move freely within cells compartments, but instead, are channeled within cells. Her own work is designed to understand how excess synthesis of triacylglycerol links obesity with defective insulin signaling and how the inability of heart and muscle to switch between lipid and glucose fuels can impair function. In co-founding the FASEB summer conference on lipid droplets in 2007, she united diverse groups of investigators who focus on commonalities that span lipid biochemistry, lipid metabolism, the cellular biology of lipids, whole body metabolism, and the pathophysiology of obesity and the metabolic syndrome. Coleman’s impact on the field of lipid metabolism has been far-reaching. She is most proud of the fact that six of her graduate students have won the Young Investigator Award from the American Society for Nutrition.ĭr. Wu Lecture at the Columbia University Institute of Nutrition and the Laurens Van Deenen Lecture at the International Conference on the Bioscience of Lipids in Helsinki. She was awarded the 2003 Osbourne and Mendel Award, the 2014 Journal of Lipid Research Lectureship Award, and the 2017 Biochimica et Biophysica Acta – Molecular and Cell Biology of Lipids Lectureship Award, and she has given numerous keynote lectures on enzymes that control the synthesis and metabolism of triacylglycerol. Coleman is an internationally recognized leader in the field of lipid metabolism. In 1991, she moved to the University of North Carolina as Professor of Nutrition and Pediatrics.ĭr. Bell before joining the Pediatric Department at Duke as an Assistant Professor. She conducted postdoctoral studies in lipid biochemistry with Robert M.

After an internship and residency in Pediatrics at Cornell and then Duke University, she completed a fellowship in Metabolism and Endocrinology at Duke where she focused on genetic disorders of carbohydrate and lipid metabolism. Coleman received her B.A cum laude from Harvard University and her M.D.

Cellular metabolism