Jed Friedman, PhD

  • Position: Chickasaw Nation Endowed Chair, HHDC Director, Diabetes Research Member, Professor

Biography

Dr. Jacob E. (Jed) Friedman is the director of the Harold Hamm Diabetes Center and vice provost for diabetes programs at the University of Oklahoma Health Sciences Center and Chickasaw Professor of Physiology at the University of Oklahoma College of Medicine. Dr. Friedman’s precious experience spans 18 years as the director of the Colorado NIH-Nutrition and Obesity Research Center (NORC) Molecular and Cellular Analytical core lab, with appointments in Pediatrics, Medicine, Biochemistry and Molecular Genetics. He has an established record of collaborative research in humans, primates, and mouse models of diabetes and obesity focused on pathways for developmental programming of metabolism from mothers to infants during the first 1000 days of life.

Dr. Friedman’s research spans the gamut from cells to humans and back again. His recent data demonstrate that mechanisms underlying development of obesity, diabetes, and neuro-cognitive behaviors across the lifespan may begin operating in fetal life and may permanently change the body’s structure, physiology, and metabolism that drive health risks in the next generation. Dr. Friedman uses a team science approach ranging from human epidemiology to metabolic studies in human tissues and cells and pre-clinical models of disease, to identify new targets and tools for diagnosis and treatment of mothers with obesity (1 in 3), diabetes (1 in 5), including nutritional countermeasures to halt obesity and diabetes in the next generation.

Dr. Friedman has authored more than 150 studies with multiple clinical investigators in the area of body composition, insulin action, metabolomics, liver disease, and more recently the human microbiome. Over the last 10 years, he has been part of seven NIH-based, omics-driven team science grants (as principle investigator or co-investigator) in partnership with biostatistics, bioinformatics, and informatics experts at Colorado Anschutz Medical Center, and Baylor College of Medicine, ranging from RNA transcriptomics, metabolomics, epigenetics, to metagenomics of the microbiome. Dr. Friedman has mentored more than seven M.D. and Ph.D. post-doctoral fellows (9 Ks, 4 F32s, 5 RO1s), the majority of whom hold faculty positions (instructor, or above) at biomedical research institutes across the US.

Email

Jed-Friedman@ouhsc.edu

Additional Websites

Health Education
  • Graduate School
  • Post-doctoral Training, Endocrinology & Diabetes East Caroline University
    Greenville, NC
  • Post-doctoral Training, Biochemistry & Molecular Biology Case Western Reserve University
    Cleveland, OH
  • PhD, Applied Physiology Kent State University
    Kent, OH
Research Interests:
  • Maternal Obesity/GDM and Developmental programming in Infant Stem Cells and Innate Immunity.
  • The Microbiome role in development of Innate Immunity and Non-alcoholic Fatty Liver Disease (NAFLD).
  • Metabolic/genomic determinants of Umbilical-cord derived Mesenchymal Stem Cell fate in Infants of Obese Mothers.
  • Nutritional intervention and Pediatric Non-Alcoholic Fatty Liver Disease (NAFLD) in mouse, monkey, and man.

Grant Funding

NIH R24-DK102766-06
MPI-Friedman, Aagaard, Powers, Grove
07/1/15-06/30/20

Interrupting the Vicious Cycle of Obesity and Metabolic Syndrome. Total annual direct costs: $1,479,219

This grant examines the effects of high fat diet exposure during pregnancy in obese and non-obese Non-Human Primates on liver, muscle, and pancreas in juvenile animals. Diet reversal in obese mothers will explore mechanisms underlying b cell function, hepatic NAFLD, response to diet challenge, and mitochondrial dysfunction in the offspring. Role: contact PI (MPI)

NIH-R56DK114711
Friedman, PI
9/1/18-8/31/20

Discerning the influence of maternal obesity, weight gain, and diet on the infant microbiota and programming of NAFLD. $300,000 dc. This project focuses on understanding how maternal OB, excess GWG, and maternal diet in mothers with GDM alters the pioneering infant microbiome over the first year of life to trigger inflammation, macrophage programming to accelerate weight gain and pediatric NAFLD using stool transfer in germ-free mice. Role: PI

NIH-P30 DK048520-20
Hill, PI
07/01/15-06/30/20

Nutrition and Obesity Research Center (NORC) - Molecular and Cellular Analytic Core. JF: $114,000

A major goal of the NORC is to promote clinical and basic nutrition research at the University of Colorado. The Molecular and Cellular Analytical Core performs assays of hormones, metabolites, cell signaling, qRT-PCR, and Seahorse technology for interrogating mitochondrial function. Role: Core-PI

NIH-NIDDK R01-DK140443
Hernandez, PI
01/14-09/30/19

Randomized Trial of Diet in GDM: Metabolic Consequences for Mother and Offspring. $385,134 dc.

This is an RCT to examine the effect of a strict low fat-complex carbohydrate diet on maternal-infant microbiome, placental function, infant adiposity and infant liver steatosis. The major goal is to study the effects of fixed diets in human GDM on maternal metabolism, placenta transporters, infant liver fat, breast milk composition and infant growth through the first year of life. Role: Co-I

NIH-1UG3OD023248-01
Dabelea, PI
9/1/16 – 8/31/23

Environmental Influences on Child Health Outcomes (ECHO) –The Healthy Start Study $30,000 dc.

This study focuses on a longitudinal cohort of maternal/child outcomes in multiple domains prospectively focused on biomarkers and measurements of exposures/outcomes relative to obesity. New research questions relevant to diet, placental nutrient transporters, and infant stem cell metabolism will be pursued. Role: Co-I.

NIH-R01 HL109517
Janssen, PI
7/1/17 - 6/30/19

Hif-1 alpha metabolically reprograms recruited alveolar macrophages to promote lung repair. $754,250 annual dc. The aim of this grant is to dissect out the role of resident vs. recruited lung macrophages and remodeling to repair epithelial and endothelial cell proliferation following acute lung injury. Role: Co-I.

Publications
  • Maternal western-style diet impairs offspring glucose homeostasis and skeletal muscle oxidative metabolism in lean adolescent Japanese macaques 2022

    Molecular Metabolism, 2022 (In review).

  • Placental insulin/IGF-1 signaling and inflammation are associated with metabolic outcomes at 4-6 years of age 2021

    The ECHO Healthy Start Cohort. Diabetes, 70(3):745-751 2021.

  • Nutrition in Pregnancy: Lifelong Consequences Conference Consensus Statement 2021

    American Journal of Obstetrics & Gynecology, 2021 (In Press).

  • Maternal Western diet exposure increases periportal fibrosis beginning in utero in non-human primate offspring 2021

    Journal of Clinical Investigation Insights 2021. (In Press) *Corresponding Author.

  • Pharmacological inhibition of cullin neddylation improves hepatic insulin sensitivity 2021

    Proceedings of the National Academy of Sciences 2021 (In revision).

  • Gestational diabetes is uniquely associated with altered early seeding of the infant gut microbiota 2020

    Frontiers in Endocrinology, 2020

  • Maternal diet alters trained immunity in the pathogenesis of pediatric NAFLD 2020

    Journal of Cellular Immunology. 2020; 2(6): 315-325.

  • The development and ecology of the Japanese macaque gut microbiome from weaning to early adolescence 2019

    In association with diet American Journal of Primatology, October 81(10-11), 2019.

  • Developmental Programming of Obesity and Diabetes in Mouse, Monkey, and Man 2018

    Where Are We Headed? Diabetes, 67(11):2137-2151, 2018

  • The gut microbiota in infants of obese mothers increases inflammation and susceptibility to obesity and NAFLD 2018

    Nature Communications, 26;9(1):4462, 2018.