Jacob E. Friedman
University of Oklahoma Health Sciences Center
218 Papers
995 Citations
Jacob E. Friedman is an academic researcher from University of Oklahoma Health Sciences Center. The author has contributed to research in topics: Insulin & Insulin resistance. The author has an hindex of 65, co-authored 191 publications. Previous affiliations of Jacob E. Friedman include University of Colorado Boulder & University of Pennsylvania.
Chat about Author
Papers
Cellular Mechanisms for Insulin Resistance in Normal Pregnancy and Gestational Diabetes
Linda A. Barbour,Carrie E. McCurdy,Teri L. Hernandez,John P. Kirwan,Patrick M. Catalano,Jacob E. Friedman +5 more
TL;DR: In this article, the authors investigated the critical molecular mechanisms involved in increasing maternal lipid flux in obese women throughout pregnancy that may underlie skeletal muscle insulin resistance and increased fetal fuels are just beginning to be investigated.
718
TNF-α Is a Predictor of Insulin Resistance in Human Pregnancy
John P. Kirwan,Sylvie Hauguel-de Mouzon,Jacques Lepercq,Jean-Claude Challier,Larraine Huston-Presley,Jacob E. Friedman,Satish C. Kalhan,Patrick M. Catalano +7 more
TL;DR: In this article, the longitudinal changes in insulin sensitivity during pregnancy were correlated with changes in placental hormones, cortisol, leptin, and tumor necrosis factor (TNF)-alpha.
699
Maternal high-fat diet triggers lipotoxicity in the fetal livers of nonhuman primates
Carrie E. McCurdy,Jacalyn M. Bishop,Sarah M. Williams,Bernadette E. Grayson,M. Susan Smith,Jacob E. Friedman,Kevin L. Grove +6 more
TL;DR: It is found that fetal offspring from both lean and obese mothers chronically consuming a HFD had a 3-fold increase in liver triglycerides (TGs), and exposure to this may increase the risk of pediatric NAFLD.
Maternal obesity and fetal metabolic programming: a fertile epigenetic soil
TL;DR: Current literature on maternal-fetal lipid metabolism and maternal obesity outcomes are reviewed and some potential mechanisms for fetal metabolic programming in key organ systems that regulate postnatal energy balance are suggested, with an emphasis on epigenetics and the intrauterine environment.
528
Fatty liver is associated with reduced SIRT3 activity and mitochondrial protein hyperacetylation.
Agnieszka A. Kendrick,Mahua Choudhury,Shaikh M. Rahman,Carrie E. McCurdy,Marisa W. Friederich,Johan L.K. Van Hove,Peter A. Watson,Nicholas Birdsey,Jianjun Bao,David Gius,Michael N. Sack,Enxuan Jing,C. Ronald Kahn,Jacob E. Friedman,Karen R. Jonscher +14 more
TL;DR: The results suggest that SIRT3 is an integral regulator of mitochondrial function and its depletion results in hyperacetylation of critical mitochondrial proteins that protect against hepatic lipotoxicity under conditions of nutrient excess.