Dr. De Jesus is an Assistant Professor of Medicine in the Department of Medicine, Section of Genetic Medicine, at the University of Chicago. With over a decade of experience in molecular biology and metabolism research, his work focuses on uncovering how molecular mechanisms govern health and metabolic disease, particularly in the context of RNA modifications, diabetes, and aging.
His scientific journey began during his Master’s studies as a Fulbright Research Scholar in the laboratory of Professor Rohit N. Kulkarni at the Joslin Diabetes Center. This work continued through his PhD in the Graduate Program of Basic and Applied Biology (GABBA) at the University of Porto, where he investigated the epigenetic reprogramming of hepatic metabolism.
Before joining the University of Chicago, he served as an Instructor in Medicine at Harvard Medical School and as a Research Associate at the Joslin Diabetes Center in Boston. His independent research has been supported by the European Association for the Study of Diabetes (EASD), the American Diabetes Association (ADA), and more recently by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) through a K99/R00 award. His current projects focus on understanding how RNA modifications, particularly m⁶A, shape metabolic regulation and aging — with the ultimate goal of paving the way for new therapeutic strategies against metabolic disease.
Beyond research, he is deeply passionate about academia, teaching, and mentoring. Having once worked as a high school biology teacher in Portugal, he remains committed to advancing the careers of trainees at all levels, creating an environment where young scientists can thrive and achieve their professional goals.
Divergent roles of m6A in orchestrating brown and white adipocyte transcriptomes and systemic metabolism.
Divergent roles of m6A in orchestrating brown and white adipocyte transcriptomes and systemic metabolism. Nat Commun. 2025 Jan 09; 16(1):533.
PMID: 39788955
m6A mRNA methylation by METTL14 regulates early pancreatic cell differentiation.
m6A mRNA methylation by METTL14 regulates early pancreatic cell differentiation. EMBO J. 2024 Nov; 43(22):5445-5468.
PMID: 39322760
m6A mRNA methylation in brown fat regulates systemic insulin sensitivity via an inter-organ prostaglandin signaling axis independent of UCP1.
m6A mRNA methylation in brown fat regulates systemic insulin sensitivity via an inter-organ prostaglandin signaling axis independent of UCP1. Cell Metab. 2024 Oct 01; 36(10):2207-2227.e9.
PMID: 39255799
SUCNR1 regulates insulin secretion and glucose elevates the succinate response in people with prediabetes.
SUCNR1 regulates insulin secretion and glucose elevates the succinate response in people with prediabetes. J Clin Invest. 2024 May 07; 134(12).
PMID: 38713514
Redox regulation of m6A methyltransferase METTL3 in ß-cells controls the innate immune response in type 1 diabetes.
Redox regulation of m6A methyltransferase METTL3 in ß-cells controls the innate immune response in type 1 diabetes. Nat Cell Biol. 2024 Mar; 26(3):421-437.
PMID: 38409327
Fluorescein-based sensors to purify human a-cells for functional and transcriptomic analyses.
Fluorescein-based sensors to purify human a-cells for functional and transcriptomic analyses. Elife. 2023 Sep 21; 12.
PMID: 37732504
m 6 A mRNA Methylation Regulates Early Pancreatic ß-Cell Differentiation.
m 6 A mRNA Methylation Regulates Early Pancreatic ß-Cell Differentiation. bioRxiv. 2023 Aug 03.
PMID: 37577492
Deficiency of the metabolic enzyme SCHAD in pancreatic ß-cells promotes amino acid-sensitive hypoglycemia.
Deficiency of the metabolic enzyme SCHAD in pancreatic ß-cells promotes amino acid-sensitive hypoglycemia. J Biol Chem. 2023 08; 299(8):104986.
PMID: 37392854
NREP contributes to development of NAFLD by regulating one-carbon metabolism in primary human hepatocytes.
NREP contributes to development of NAFLD by regulating one-carbon metabolism in primary human hepatocytes. Cell Chem Biol. 2023 09 21; 30(9):1144-1155.e4.
PMID: 37354909
Excess pancreatic elastase alters acinar-ß cell communication by impairing the mechano-signaling and the PAR2 pathways.
Excess pancreatic elastase alters acinar-ß cell communication by impairing the mechano-signaling and the PAR2 pathways. Cell Metab. 2023 07 11; 35(7):1242-1260.e9.
PMID: 37339634