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Philip Gordts

Associate Professor and Microbiology & Immunology

Inflammation, Insulin resistance, Metabolic disease, Atherosclerosis, Human milk oligosaccharides, Heparan sulfate, Glycosaminoglycans, Adipose tissue, Iron metabolism, Extracellular matrix, Cell signaling

Gordts

Molecular Biology Program

Biological Chemistry Program

Education

B.S. Katholieke Universiteit Leuven

Ph.D. Katholieke Universiteit Leuven

Links

Lab Page

PubMed Literature Search

philip.gordts@path.utah.edu

Research

Our lab investigates how glycans—specifically the complex sugar chains known as heparan sulfate and human milk oligosaccharides—regulate immune function and metabolic health. These extracellular matrix molecules are chemically intricate and biologically potent, influencing signaling pathways that govern inflammation, insulin sensitivity, iron metabolism, and vascular function. Our research sits at the intersection of biochemistry and molecular biology. We use a multidisciplinary approach that combines glycomics, metabolic phenotyping, genetic mouse models, and translational tools to tackle key questions in chronic diseases like obesity, type 2 diabetes, and atherosclerosis.

Current projects in the lab include:

  • Mapping how structural diversity in heparan sulfate controls adipose tissue inflammation and systemic metabolism
  • Investigating the role of endothelial glycans in iron homeostasis and BMP/SMAD signaling
  • Exploring the therapeutic use of human milk oligosaccharides to resolve low-grade inflammatory disease

If you're driven by curiosity and want to push boundaries at the intersection of molecular biology, biochemistry, and disease-focused research, this is a place where your ideas can take shape—and make an impact.

References

Selected Publications

  1. The human milk oligosaccharide 3'sialyllactose reduces low-grade inflammation and atherosclerosis development in mice. Pessentheiner AR, Spann NJ, Autran CA, Oh TG, Grunddal KV, Coker JK, Painter CD, Ramms B, Chiang AW, Wang CY, Hsiao J, Wang Y, Quach A, Booshehri LM, Hammond A, Tognaccini C, Latasiewicz J, Willemsen L, Zengler K, de Winther MP, Hoffman HM, Philpott M, Cribbs AP, Oppermann U, Lewis NE, Witztum JL, Yu R, Atkins AR, Downes M, Evans RM, Glass CK, Bode L, Gordts PL.JCI Insight. 2024 Nov 8;9(21):e181329. doi: 10.1172/jci.insight.181329.PMID: 39325548
  2. Glycocalyx engineering with heparan sulfate mimetics attenuates Wnt activity during adipogenesis to promote glucose uptake and metabolism. Trieger GW, Pessentheiner AR, Purcell SC, Green CR, DeForest N, Willert K, Majithia AR, Metallo CM, Godula K, Gordts PLSM.J Biol Chem. 2023 May;299(5):104611. doi: 10.1016/j.jbc.2023.104611. Epub 2023 Mar 15.PMID: 36931394
  3. Impaired mitophagy in Sanfilippo a mice causes hypertriglyceridemia and brown adipose tissue activation. Tillo M, Lamanna WC, Dwyer CA, Sandoval DR, Pessentheiner AR, Al-Azzam N, Sarrazin S, Gonzales JC, Kan SH, Andreyev AY, Schultheis N, Thacker BE, Glass CA, Dickson PI, Wang RY, Selleck SB, Esko JD, Gordts PLSM.J Biol Chem. 2022 Aug;298(8):102159. doi: 10.1016/j.jbc.2022.102159. Epub 2022 Jun 22.PMID: 35750212
  4. Interventional hepatic apoC-III knockdown improves atherosclerotic plaque stability and remodeling by triglyceride lowering. Ramms B, Patel S, Sun X, Pessentheiner AR, Ducasa GM, Mullick AE, Lee RG, Crooke RM, Tsimikas S, Witztum JL, Gordts PL.JCI Insight. 2022 Jul 8;7(13):e158414. doi: 10.1172/jci.insight.158414.PMID: 35653195
  5. Dietary Neu5Ac Intervention Protects Against Atherosclerosis Associated With Human-Like Neu5Gc Loss-Brief Report. Kawanishi K, Coker JK, Grunddal KV, Dhar C, Hsiao J, Zengler K, Varki N, Varki A, Gordts PLSM.Arterioscler Thromb Vasc Biol. 2021 Nov;41(11):2730-2739. doi: 10.1161/ATVBAHA.120.315280. Epub 2021 Sep 30.PMID: 34587757
  6. ApoC-III Glycoforms Are Differentially Cleared by Hepatic TRL (Triglyceride-Rich Lipoprotein) Receptors. Kegulian NC, Ramms B, Horton S, Trenchevska O, Nedelkov D, Graham MJ, Lee RG, Esko JD, Yassine HN, Gordts PLSM.Arterioscler Thromb Vasc Biol. 2019 Oct;39(10):2145-2156. doi: 10.1161/ATVBAHA.119.312723. Epub 2019 Aug 8.PMID: 31390883
  7. ApoC-III ASO promotes tissue LPL activity in the absence of apoE-mediated TRL clearance. Ramms B, Patel S, Nora C, Pessentheiner AR, Chang MW, Green CR, Golden GJ, Secrest P, Krauss RM, Metallo CM, Benner C, Alexander VJ, Witztum JL, Tsimikas S, Esko JD, Gordts PLSM.J Lipid Res. 2019 Aug;60(8):1379-1395. doi: 10.1194/jlr.M093740. Epub 2019 May 14.PMID: 31092690
  8. ApoC-III inhibits clearance of triglyceride-rich lipoproteins through LDL family receptors.Gordts PL, Nock R, Son NH, Ramms B, Lew I, Gonzales JC, Thacker BE, Basu D, Lee RG, Mullick AE, Graham MJ, Goldberg IJ, Crooke RM, Witztum JL, Esko JD.J Clin Invest. 2016 Aug 1;126(8):2855-66. doi: 10.1172/JCI86610. Epub 2016 Jul 11.PMID: 27400128
  9. Reducing macrophage proteoglycan sulfation increases atherosclerosis and obesity through enhanced type I interferon signaling.Gordts PLSM, Foley EM, Lawrence R, Sinha R, Lameda-Diaz C, Deng L, Nock R, Glass CK, Erbilgin A, Lusis AJ, Witztum JL, Esko JD.Cell Metab. 2014 Nov 4;20(5):813-826. doi: 10.1016/j.cmet.2014.09.016. Epub 2014 Nov 4.PMID: 25440058
Last Updated: 8/8/25