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Dr. Lia Rae Edmunds, Ph. D.

About Lia Rae Edmunds, Ph. D.

Admission Female Placeholder Image by LECOM

Background and Interests

My long-term research interests center on understanding how cellular and mitochondrial bioenergetics integrate with gut-derived signals to regulate metabolic health, particularly in the context of nutritional stress, obesity, and insulin resistance. As I transition into my new faculty role as Assistant Professor of Molecular Genetics and Developmental Biology at the Lake Erie College of Osteopathic Medicine (LECOM), my goal is to establish an independent research program investigating how enteroendocrine cell function, microbial metabolites, and gut–brain signaling pathways converge to influence systemic glucose homeostasis and metabolic disease progression.

My training has provided a strong foundation in biochemistry, cellular and molecular biology, mitochondrial physiology, and multi-OMICs approaches, positioning me to address mechanistic questions at the interface of metabolism and gut-brain communication. During my doctoral studies with Dr. Edward Prochownik, I examined mechanisms of cancer metabolism and mitochondrial dysfunction using cellular and mouse models of c-Myc deletion, leading to three first-author publications and several collaborative co-authored works. This early work established my expertise in dissecting mitochondrial signaling and metabolic flux at the molecular level.

As a postdoctoral fellow in the Division of Endocrinology and Metabolism at the University of Pittsburgh, I expanded my research into in vivo metabolic physiology under the combined mentorship of Dr. Robert O’Doherty and Dr. Michael Jurczak. I investigated bioenergetic disturbances in whole-body PARKIN knockout mice, contributing to one publication and preparing an additional first-author manuscript. Through this work, I gained direct experience performing stable and radioactive isotope metabolic flux studies, live metabolic infusions, and hyperinsulinemic–euglycemic clamps. Intensive NIH/MMPC training at Vanderbilt University further strengthened my expertise in tracer methodology and metabolic turnover analysis.

These prior experiences directly inform my evolving research program at LECOM. My proposed work focuses on how nutritional stress alters enteroendocrine cell mitochondrial function, microbial metabolite production, and neurohormonal communication with the enteric and central nervous systems. By integrating mitochondrial physiology and gut microbiota analysis, my goal is to uncover bioenergetic mechanisms that drive metabolic dysfunction and identify potential therapeutic targets along the gut–brain axis.
 

Current research projects:

Regulation of Gut-Derived Metabolites and Mitochondrial Dysfunction under Nutrient Excess
The gut-brain axis plays a critical role in regulating metabolic and neuropsychiatric health as the largest endocrine organ. Gut enteroendocrine cells synthesize neurotransmitters such as serotonin and dopamine, and satiety hormones such as cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and Peptide YY (PYY), which influence satiety, mood, and energy balance. Emerging evidence suggests that mitochondrial function within neuroendocrine cells is central to this regulation, and that nutrient overload—a hallmark of obesity and type 2 diabetes—disrupts mitochondrial bioenergetics, potentially impairing gut-brain signaling. Meanwhile, gut microbial metabolites such as short-chain fatty acids (SCFAs) may modulate mitochondrial function, either protecting against or exacerbating nutrient-induced dysfunction. The mechanisms allowing SCFAs to modulate cellular signaling, metabolism, and gene regulation are understood to be receptor-dependent (FFAR 2 and 3) and receptor-independent mechanisms (epigenetic modifications by SCFA acting directly as a HDAC inhibitor). Understanding these interactions is essential for developing novel metabolic and neuropsychiatric interventions. We hypothesize that nutrient excess impairs mitochondrial function in gut enteroendocrine cells, reducing serotonin/dopamine biosynthesis, and microbial metabolites (e.g., SCFAs) modulate these effects through bioenergetic and epigenetic mechanisms.

Outcomes of Physician Assistants-to-Medical Students Compared to their Traditional Medical School Classmates: The Accelerated Physician Assistant Pathway (APAP) Study
This study aims to address a major gap in medical education research: whether prior clinical experience can substitute for time in training. Demonstrating equivalent or superior outcomes among APAP graduates would justify broader adoption of accelerated PA-to-physician pathways, potentially reducing training time, cost, and physician workforce shortages—particularly in primary care. Our hypothesis is that prior clinical training as a PA may function as a surrogate for clinical rotations in third and fourth year students, enabling safe and effective acceleration of physician training without compromising outcomes.

 

Complete List of Publications:

  1. Undamatla R, Fagunloye OG, Chen J, Edmunds LR, Murali A, Mills A, Xie B, Pangburn MM, Sipula I, Gibson G, St Croix C, Jurczak MJ. Reduced mitophagy is an early feature of NAFLD and liver-specific PARKIN knockout hastens the onset of steatosis, inflammation and fibrosis. Sci Rep. 2023 May 10;13(1):7575. doi: 10.1038/s41598-023-34710-x.
  2. Thapa D, Bugga P, Mushala BAS, Manning JR, Stoner MW, McMahon B, Zeng X, Cantrell PS, Yates N, Xie B, Edmunds LR, Jurczak MJ, Scott I. GCN5L1 impairs diastolic function in mice exposed to a high fat diet by restricting cardiac pyruvate oxidation. Physiol Rep. 2022 Aug;10(15):e15415. doi: 10.14814/phy2.15415.
  3. Edmunds LR, Xie B, Mills AM, Huckestein BR, Undamatla R, Murali A, Pangburn MM, Martin J, Sipula I, Kaufman BA, Scott I, Jurczak MJ. Liver-specific Prkn knockout mice are more susceptible to diet-induced hepatic steatosis and insulin resistance. Mol Metab. 2020 Jul 10;41:101051. doi: 10.1016/j.molmet.2020.101051.
  4. Mooli RGR, Mukhi D, Watt M, Edmunds LR, Xie B, Capooci J, Reslink M, Eze C, Mills A, Stolz DB, Jurczak M, Ramakrishnan SK. Metabolism. Sustained mitochondrial biogenesis is essential to maintain caloric restriction-induced beige adipocytes. 2020 Jun;107:154225. doi: 10.1016/j.metabol.2020.154225.
  5. Edmunds LR, Huckestein BR, Kahn M, Zhang D, Chu Y, Zhang Y, Wendell SG, Shulman GI, Jurczak MJ. Hepatic insulin sensitivity is improved in high-fat diet-fed Park2 knockout mice in association with increased hepatic AMPK activation and reduced steatosis. Physiol Rep. 2019 Nov;7(21):e14281. doi: 10.14814/phy2.14281.
  6. Argemi J, Latasa MU, Atkinson SR, Blokhin IO, Massey V, Gue JP, Cabezas J, Lozano JJ, Van Booven D, Bell A, Cao S, Vernetti LA, Arab JP, Ventura-Cots M, Edmunds LR, Fondevilla C, Stärkel P, Dubuquoy L, Louvet A, Odena G, Gomez JL, Aragon T, Altamirano J, Caballeria J, Jurczak MJ, Taylor DL, Berasain C, Wahlestedt C, Monga SP, Morgan MY, Sancho-Bru P, Mathurin P, Furuya S, Lackner C, Rusyn I, Shah VH, Thursz MR, Mann J, Avila MA, Bataller R. Defective HNF4alpha-dependent gene expression as a driver of hepatocellular failure in alcoholic hepatitis. Nat Commun. 2019 Jul 16;10(1):3126. doi: 10.1038/s41467-019-11004-3.
  7. Ren Q, Gliozzi ML, Rittenhouse NL, Edmunds LR, Rbaibi Y, Locker JD, Poholek AC, Jurczak MJ, Baty CJ, Weisz OA. Shear stress and oxygen availability drive differential changes in opossum kidney proximal tubule cell metabolism and endocytosis. Traffic. 2019 Jun;20(6):448-459. doi: 10.1111/tra.12648. Epub 2019 May 9.
  8. Thapa D, Xie B, Manning JR, Zhang M, Stoner MW, Huckestein BR, Edmunds LR, Zhang X, Dedousis NL, O’Doherty RM, Jurczak MJ, Scott I. Adropin reduces blood glucose levels in mice by limiting hepatic glucose production. Physiol Rep. 2019 Apr;7(8):e14043. doi: 10.14814/phy2.14043.
  9. Thapa D, Xie B, Zhang M, Stoner MW, Manning JR, Huckestein BR, Edmunds LR, Mullett SJ, McTiernan CF, Wendell SG, Jurczak MJ, Scott I. Adropin treatment restores cardiac glucose oxidation in pre-diabetic obese mice. J Mol Cell Cardiol. 2019 Apr;129:174-178. doi: 10.1016/j.yjmcc.2019.02.012. Epub 2019 Feb 26.
  10. Xiong J, Kawagishi H, Yan Y, Liu J, Wells QS, Edmunds LR, Fergusson MM, Yu ZX, Rovira II, Brittain EL, Wolfgang MJ, Jurczak MJ, Fessel JP, Finkel T. A Metabolic Basis for Endothelial-to-Mesenchymal Transition. Mol Cell. 2018 Feb 15;69(4):689-698.e7. doi: 10.1016/j.molcel.2018.01.010. Epub 2018 Feb 8.
  11. Corbit KC, Camporez JPG, Edmunds LR, Tran JL, Vera NB, Erion DM, Deo RC, Perry RJ, Shulman GI, Jurczak MJ, Weiss EJ. Adipocyte JAK2 Regulates Hepatic Insulin Sensitivity Independently of Body Composition, Liver Lipid Content, and Hepatic Insulin Signaling. Diabetes. 2018 Feb;67(2):208-221. doi: 10.2337/db17-0524. Epub 2017 Dec 4.
  12. Wang H, Lu J, Edmunds LR, Kulkarni S, Dolezal J, Tao J, Ranganathan S, Jackson L, Fromherz M, Beer-Stolz D, Uppala R, Bharathi S, Monga SP, Goetzman ES, Prochownik EV. Coordinated Activities of Multiple Myc-dependent and Myc-independent Biosynthetic Pathways in Hepatoblastoma. J Biol Chem. 2016 Dec 16;291(51):26241-26251. doi: 10.1074/jbc.M116.754218. Epub 2016 Oct 13.
  13. Casinelli G, LaRosa J, Sharma M, Cherok E, Banerjee S, Branca M, Edmunds L, Wang Y, Sims-Lucas S, Churley L, Kelly S, Sun M, Stolz D, Graves JA. N-Myc overexpression increases cisplatin resistance in neuroblastoma via deregulation of mitochondrial dynamics. Cell Death Discov. 2016;2:16082. doi: 10.1038/cddiscovery.2016.82. eCollection 2016.
  14. Costa DK, Huckestein BR, Edmunds LR, Petersen MC, Nasiri A, Butrico GM, Abulizi A, Harmon DB, Lu C, Mantell BS, Hartman DJ, Camporez JP, O’Doherty RM, Cline GW, Shulman GI, Jurczak MJ. Reduced intestinal lipid absorption and body weight-independent improvements in insulin sensitivity in high-fat diet-fed Park2 knockout mice. Am J Physiol Endocrinol Metab. 2016 Jul 1;311(1):E105-16. doi: 10.1152/ajpendo.00042.2016. Epub 2016 May 10.
  15. Edmunds LR, Otero PA, Sharma L, D’Souza S, Dolezal JM, David S, Lu J, Lamm L, Basantani M, Zhang P, Sipula IJ, Li L, Zeng X, Ding Y, Ding F, Beck ME, Vockley J, Monga SP, Kershaw EE, O’Doherty RM, Kratz LE, Yates NA, Goetzman EP, Scott D, Duncan AW, Prochownik EV. Abnormal lipid processing but normal long-term repopulation potential of myc-/- hepatocytes. Oncotarget. 2016 May 24;7(21):30379-95. doi: 10.18632/oncotarget.8856.
  16. Edmunds LR, Sharma L, Wang H, Kang A, d’Souza S, Lu J, McLaughlin M, Dolezal JM, Gao X, Weintraub ST, Ding Y, Zeng X, Yates N, Prochownik EV. c-Myc and AMPK Control Cellular Energy Levels by Cooperatively Regulating Mitochondrial Structure and Function. PLoS One. 2015;10(7):e0134049. doi: 10.1371/journal.pone.0134049. eCollection 2015.
  17. Prabhu D, Goldstein AC, El-Khoury R, Rak M, Edmunds L, Rustin P, Vockley J, Schiff M. ANT2-defective fibroblasts exhibit normal mitochondrial bioenergetics. Mol Genet Metab Rep. 2015 Jun 1;3:43-46. doi: 10.1016/j.ymgmr.2015.03.005.
  18. Edmunds LR, Sharma L, Kang A, Lu J, Vockley J, Basu S, Uppala R, Goetzman ES, Beck ME, Scott D, Prochownik EV. c-Myc programs fatty acid metabolism and dictates acetyl-CoA abundance and fate. J Biol Chem. 2014 Sep 5;289(36):25382-92. doi: 10.1074/jbc.M114.580662. Epub 2014 Jul 22. PubMed PMID: 25053415; PubMed Central PMCID: PMC4155699.
  19. Weissgerber TL, Rajakumar A, Myerski AC, Edmunds LR, Powers RW, Roberts JM, Gandley RE, Hubel CA. Vascular pool of releasable soluble VEGF receptor-1 (sFLT1) in women with previous preeclampsia and uncomplicated pregnancy. J Clin Endocrinol Metab. 2014 Mar;99(3):978-87. doi: 10.1210/jc.2013-3277. Epub 2013 Dec 11.
  20. Rajakumar A, Cerdeira AS, Rana S, Zsengeller Z, Edmunds L, Jeyabalan A, Hubel CA, Stillman IE, Parikh SM, Karumanchi SA. Transcriptionally active syncytial aggregates in the maternal circulation may contribute to circulating soluble fms-like tyrosine kinase 1 in preeclampsia. Hypertension. 2012 Feb;59(2):256-64. doi: 10.1161/HYPERTENSIONAHA.111.182170. Epub 2012 Jan 3.
  21. Luppi P, Powers RW, Verma V, Edmunds L, Plymire D, Hubel CA. Maternal circulating CD34+VEGFR-2+ and CD133+VEGFR-2+ progenitor cells increase during normal pregnancy but are reduced in women with preeclampsia. Reprod Sci. 2010 Jul;17(7):643-52. doi: 10.1177/1933719110366164. Epub 2010 Apr 1.
  22. Bainbridge SA, Roberts JM, von Versen-Höynck F, Koch J, Edmunds L, Hubel CA. Uric acid attenuates trophoblast invasion and integration into endothelial cell monolayers. Am J Physiol Cell Physiol. 2009 Aug;297(2):C440-50. doi: 10.1152/ajpcell.00593.2008. Epub 2009 Jun 17.