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BMC veterinary research2025; 22(1); 36; doi: 10.1186/s12917-025-05173-1

Sodium-glucose transporters SGLT1 and SGLT2 in equine renal, hepatic and pancreatic tissue.

Abstract: Insulin dysregulation is a hallmark of equine metabolic syndrome (EMS), and in recent years, pharmacological treatment with sodium-dependent glucose transporter 2 inhibitors (SGLT2i) have shown promise in reducing the risk of hyperinsulinemia-associated laminitis in horses diagnosed with EMS. In humans and laboratory animals, this transporter protein is responsible for the majority of renal tubular glucose reabsorption, however, the presence of this and the related sodium-dependent glucose transporter 1 (SGLT1) have not yet been studied in equine kidneys. Additionally, studies in humans and laboratory animals have documented the presence of SGLT1 and SGLT2 also in hepatic and pancreatic tissue, which may explain extra-renal treatment effects of SGLT2i. Since the specificity towards SGLT2 and SGLT1 differ between the various SGLT2i drugs currently in use in horses, investigating SGLT2 and SGLT1 protein expression in equine tissues may help understanding potential differences in treatment effect and/or side effect profile between substances. The objective of this study was therefore to evaluate the presence of SGLT2 and SGLT1 in equine kidneys, liver and pancreas. Results: Tissue samples from ten healthy Norwegian/Swedish Coldblood Trotters were collected. Using immunohistochemistry with antibodies raised against human SGLT1 and SGLT2, a strong SGLT2 antibody signal was present in the apical membranes of epithelial cells in the cortical labyrinth of the kidney, while SGLT1 positive cells were predominantly found in medullary rays. Both of these results concur with those in humans and rats. Using electron microscopy, ultrastructural localisation of positive SGLT2 antibody signal was confirmed to the microvilli of tubular epithelial cells. Positive SGLT2 signal was also detected in periportal hepatocytes and in cells within islet of Langerhans in the endocrine pancreas. Positive SGLT1 signal was seen in cholangiocytes in the portal areas of the liver, and in Kuppfer cells. Conclusions: The present study confirms presence of SGLT2 and SGLT1 in the equine kidney, localized to the proximal tubule. Also, presence of SGLT2 in the liver and pancreas, suggest that SGLT2i may have both renal and extrarenal effects.
Publication Date: 2025-12-17 PubMed ID: 41408266PubMed Central: PMC12822031DOI: 10.1186/s12917-025-05173-1Google Scholar: Lookup
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  • Journal Article

Summary

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SGLT2 and SGLT1 proteins, responsible for glucose transport, are present in horse kidneys, liver, and pancreas. This discovery helps explain how drugs targeting these transporters might work to treat insulin-related conditions in horses.

Background and Rationale

  • Equine Metabolic Syndrome (EMS) is characterized by insulin dysregulation, leading to health issues like laminitis in horses.
  • SGLT2 inhibitors (SGLT2i) are drugs that reduce blood sugar by blocking glucose reabsorption in kidneys, showing promise for EMS treatment.
  • In humans and laboratory animals, SGLT2 is primarily responsible for kidney glucose reabsorption; SGLT1 is a related glucose transporter with different tissue distribution.
  • The presence and location of SGLT1 and SGLT2 in horse (equine) organs, especially kidney, liver, and pancreas, were previously unknown.
  • Studying the presence of these transporters in horses can clarify the mechanisms of SGLT2i drugs and explain varied drug effects or side effects based on their selectivity for SGLT2 vs. SGLT1.

Objective

  • To evaluate the presence and localization of SGLT2 and SGLT1 proteins in equine kidney, liver, and pancreas tissues.

Methods

  • Tissue samples were collected from ten healthy Norwegian/Swedish Coldblood Trotter horses.
  • Immunohistochemistry was performed using antibodies designed against human SGLT1 and SGLT2 proteins to detect these transporters in horse tissues.
  • Electron microscopy was used to explore the ultrastructural details of SGLT protein localization, especially in renal tissue.

Results

  • Kidney:
    • SGLT2 showed a strong presence in the apical membranes of epithelial cells in the cortical labyrinth (part of the proximal tubule).
    • SGLT1-positive cells were predominantly localized in medullary rays of the kidney.
    • Electron microscopy confirmed SGLT2 localization on microvilli of proximal tubular epithelial cells.
    • Findings parallel those previously observed in humans and rats, indicating conserved transporter localization across species.
  • Liver:
    • SGLT2 was detected in hepatocytes located in the periportal areas (regions near portal triads).
    • SGLT1 was found in cholangiocytes (cells lining bile ducts) and Kupffer cells (liver macrophages) in portal areas.
  • Pancreas:
    • SGLT2 protein was present in cells within the islet of Langerhans, which are responsible for endocrine functions including insulin secretion.
    • The distribution of SGLT1 in pancreas was not specifically highlighted beyond liver-related findings.

Conclusions and Implications

  • The study confirms that SGLT2 and SGLT1 are present in specific compartments of equine kidneys, mainly localized to the proximal tubule, consistent with their known function in glucose handling.
  • SGLT2 expression in equine liver and pancreas provides evidence that SGLT2 inhibitors may exert effects beyond the kidney, potentially influencing hepatic and pancreatic functions.
  • This broader tissue distribution suggests that pharmacological treatments targeting SGLT2 in horses could have both renal and extrarenal therapeutic or side effects.
  • Understanding the localization and function of these transporters in horses informs better use and development of SGLT2i drugs for managing insulin dysregulation associated with EMS.

Cite This Article

APA
Anger-Håål C, Fjordbakk CT, Ekstrand C, Skedsmo FS, Rørtveit R. (2025). Sodium-glucose transporters SGLT1 and SGLT2 in equine renal, hepatic and pancreatic tissue. BMC Vet Res, 22(1), 36. https://doi.org/10.1186/s12917-025-05173-1

Publication

ISSN: 1746-6148
NlmUniqueID: 101249759
Country: England
Language: English
Volume: 22
Issue: 1
Pages: 36
PII: 36

Researcher Affiliations

Anger-Håål, Camilla
  • Department of Preclinical Sciences and Pathology, Faculty of Veterinary Medicine, Norwegian University of Life Sciences, Ås, Norway.
Fjordbakk, Cathrine T
  • Department of Companion Animal Clinical Sciences, Faculty of Veterinary Medicine, Norwegian University of Life Sciences, Ås, Norway.
Ekstrand, Carl
  • Department of Animal Biosciences, Faculty of Veterinary Medicine and Animal Science, Swedish University of Agricultural Sciences, Uppsala, Sweden. carl.ekstrand@slu.se.
Skedsmo, Fredrik S
  • Department of Preclinical Sciences and Pathology, Faculty of Veterinary Medicine, Norwegian University of Life Sciences, Ås, Norway.
Rørtveit, Runa
  • Department of Preclinical Sciences and Pathology, Faculty of Veterinary Medicine, Norwegian University of Life Sciences, Ås, Norway.

MeSH Terms

  • Animals
  • Horses / metabolism
  • Pancreas / metabolism
  • Sodium-Glucose Transporter 2 / metabolism
  • Kidney / metabolism
  • Liver / metabolism
  • Sodium-Glucose Transporter 1 / metabolism
  • Male
  • Female

Conflict of Interest Statement

Declarations. Ethics approval and consent to participate: In accordance to journal policies ( https://eur03.safelinks.protection.outlook.com/?url=https%3A%2F%2Fwww.biomedcentral.com%2Fgetpublished%2Feditorial-policies%23research%2Binvolving%2Banimals&data=05%7C02%7Ccarl.ekstrand%40slu.se%7C1940d598096c453d2cd608de220a6d35%7Ca3b5f0710e4947a0a40e9b7c9c4d647e%7C1%7C0%7C638985625347286187%7CUnknown%7CTWFpbGZsb3d8eyJFbXB0eU1hcGkiOnRydWUsIlYiOiIwLjAuMDAwMCIsIlAiOiJXaW4zMiIsIkFOIjoiTWFpbCIsIldUIjoyfQ%3D%3D%7C0%7C%7C%7C&sdata=5Hs2pK5MgfO%2FWMt%2FVK6J8wvaiSA8vBNnGhrlgcbFayQ%3D&reserved=0 ) the study was reviewed by the Ethical committee for approval of studies with animal patients, an ethical committee affiliated to the Norwegian University of Life Sciences. The ethical committee concluded that the study did not meet the criteria for studies that require application to or approval from any ethical committee. Signed informed consent was obtained from owners of all horses included in the study. Consent for publication:: Not applicable. Competing interests: CE is pharmacological advisor to Svensk Travsport (Swedish Trotting Association).

References

This article includes 64 references
  1. Durham AE, Frank N, McGowan CM, Menzies-Gow NJ, Roelfsema E, Vervuert I. ECEIM consensus statement on equine metabolic syndrome. J Vet Intern Med 2019;33(2):335–49.
    pmc: PMC6430910pubmed: 30724412
  2. Frank N, Tadros EM. Insulin dysregulation. Equine Vet J 2014;46(1):103-12.
    pubmed: 24033478
  3. Carslake HB, Pinchbeck GL, McGowan CM. Equine metabolic syndrome in UK native ponies and cobs is highly prevalent with modifiable risk factors. Equine Vet J 2021;53(5):923–34.
    pmc: PMC8451835pubmed: 33128277
  4. Group EE. Recommendations for the diagnosis and management of equine metabolic syndrome (EMS). Equine Endocrinology Group; 2024.
  5. Karikoski NP, Horn I, McGowan TW, McGowan CM. The prevalence of endocrinopathic laminitis among horses presented for laminitis at a first-opinion/referral equine hospital. Domest Anim Endocr 2011;41(3):111–7.
    pubmed: 21696910
  6. de Laat MA, McGowan CM, Sillence MN, Pollitt CC. Equine laminitis: induced by 48 h hyperinsulinaemia in Standardbred horses. Equine Vet J 2010;42(2):129–35.
    pubmed: 20156248
  7. Asplin KE, Sillence MN, Pollitt CC, McGowan CM. Induction of laminitis by prolonged hyperinsulinaemia in clinically normal ponies. Vet J 2007;174(3):530–5.
    pubmed: 17719811
  8. Tinworth KD, Boston RC, Harris PA, Sillence MN, Raidal SL, Noble GK. The effect of oral metformin on insulin sensitivity in insulin-resistant ponies. Vet J 2012;191(1):79–84.
    pubmed: 21349749
  9. Durham AE, Rendle DI, Newton JR. Effect of metformin on measurements of insulin sensitivity and β cell response in 18 horses and ponies with insulin resistance. Equine Vet J 2008;40(5):493–500.
    pubmed: 18482898
  10. Colmer SF, Adams AA, Adam E, Miller R, Stefanovski D, Kulp JC. The effect of pre‐dosing with metformin on the insulin response to oral sugar in insulin‐dysregulated horses. Equine Vet J 2024;56(2):318–25.
    pubmed: 37545128
  11. Rendle DI, Rutledge F, Hughes KJ, Heller J, Durham AE. Effects of metformin hydrochloride on blood glucose and insulin responses to oral dextrose in horses. Equine Vet J 2013;45(6):751–4.
    pubmed: 23600690
  12. Frank N, Elliott SB, Boston RC. Effects of long-term oral administration of levothyroxine sodium on glucose dynamics in healthy adult horses. Am J Vet Res 2008;69(1):76–81.
    pubmed: 18167090
  13. Frank N, Buchanan BR, Elliott SB. Effects of long-term oral administration of levothyroxine sodium on serum thyroid hormone concentrations, clinicopathologic variables, and echocardiographic measurements in healthy adult horses. Am J Vet Res 2008;69(1):68–75.
    pubmed: 18167089
  14. Frank N, Sommardahl CS, Eiler H, Webb LL, Denhart JW, Boston RC. Effects of oral administration of levothyroxine sodium on concentrations of plasma lipids, concentration and composition of very-low-density lipoproteins, and glucose dynamics in healthy adult mares. American J Vet Res 2005;66(6):1032–8.
    pubmed: 16008228
  15. Sommardahl CS, Frank N, Elliott SB, Webb LL, Refsal KR, Denhart JW. Effects of oral administration of levothyroxine sodium on serum concentrations of thyroid gland hormones and responses to injections of thyrotropin-releasing hormone in healthy adult mares. Am J Vet Res 2005;66(6):1025–31.
    pubmed: 16008227
  16. Kellon E, Gustafson K. Use of the SGLT2 inhibitor canagliflozin for control of refractory equine hyperinsulinemia and laminitis. Open Vet J 2022;12(4):511–8.
    pmc: PMC9473365pubmed: 36118716
  17. Lindåse S, Nostell K, Forslund A, Bergsten P, Bröjer J. Short-term effects of canagliflozin on glucose and insulin responses in insulin dysregulated horses: A randomized, placebo-controlled, double-blind, study. J Vet Intern Med 2023;37(6):2520–8.
    pmc: PMC10658518pubmed: 37864426
  18. Meier A, de Laat M, Reiche D, Fitzgerald D, Sillence M. The efficacy and safety of velagliflozin over 16 weeks as a treatment for insulin dysregulation in ponies. BMC Vet Res 2019;15(1):65–10.
    pmc: PMC6390376pubmed: 30808423
  19. Meier A, Reiche D, de Laat M, Pollitt C, Walsh D, Sillence M. The sodium-glucose co-transporter 2 inhibitor velagliflozin reduces hyperinsulinemia and prevents laminitis in insulin-dysregulated ponies. PLoS One 2018;13(9):e0203655-e.
    pmc: PMC6136744pubmed: 30212530
  20. Sundra T, Kelty E, Rendle D. Preliminary observations on the use of ertugliflozin in the management of hyperinsulinaemia and laminitis in 51 horses: a case series. Equine Vet Educ 2023;35(6):311–20.
  21. Sundra T, Rossi G, Kelty E, Lester G, Rendle D. Oral sugar test responses to ertugliflozin in ten horses with insulin dysregulation. Equine Vet Educ 2024;36(6):317–24.
  22. Rieg T, Masuda T, Gerasimova M, Mayoux E, Platt K, Powell DR. Increase in SGLT1-mediated transport explains renal glucose reabsorption during genetic and pharmacological SGLT2 inhibition in euglycemia. American J Physiol-Ren Physiol 2014;306(2):F188–F93.
    pmc: PMC3920019pubmed: 24226519
  23. Nakano D, Akiba J, Tsutsumi T, Kawaguchi M, Yoshida T, Koga H. Hepatic expression of sodium–glucose cotransporter 2 (SGLT2) in patients with chronic liver disease. Med Mol Morphol 2022;55(4):304–15.
    pmc: PMC9606064pubmed: 36131166
  24. Bonner C, Kerr-Conte J, Gmyr V, Queniat G, Moerman E, Thévenet J. Inhibition of the glucose transporter SGLT2 with dapagliflozin in pancreatic alpha cells triggers glucagon secretion. Nat Med 2015;21(5):512–7.
    pubmed: 25894829
  25. Saponaro C, Mühlemann M, Acosta-Montalvo A, Piron A, Gmyr V, Delalleau N. Interindividual Heterogeneity of SGLT2 Expression and Function in Human Pancreatic Islets. Diabetes 2020;69(5):902–14.
    pubmed: 31896553
  26. Hu Z, Liao Y, Wang J, Wen X, Shu L. Potential impacts of diabetes mellitus and anti-diabetes agents on expressions of sodium-glucose transporters (SGLTs) in mice. Endocrine 2021;74(3):571–81.
    pubmed: 34255273
  27. Schwertheim S, Alhardan M, Manka PP, Sowa J-P, Canbay A, Schmidt HH-J. Higher pNRF2, SOCS3, IRF3, and RIG1 Tissue Protein Expression in NASH Patients versus NAFL Patients: pNRF2 Expression Is Concomitantly Associated with Elevated Fasting Glucose Levels. J Personalized Med 2023;13(7):1152.
    pmc: PMC10381647pubmed: 37511764
  28. Madunić IV, Breljak D, Karaica D, Koepsell H, Sabolić I. Expression profiling and immunolocalization of Na+-d-glucose-cotransporter 1 in mice employing knockout mice as specificity control indicate novel locations and differences between mice and rats. Pflügers Archiv - European Journal of Physiology 2017;469(12):1545-65.
    pmc: PMC5691098pubmed: 28842746
  29. Vrhovac I, Balen Eror D, Klessen D, Burger C, Breljak D, Kraus O. Localizations of Na(+)-D-glucose cotransporters SGLT1 and SGLT2 in human kidney and of SGLT1 in human small intestine, liver, lung, and heart. Pflugers Archiv: Eur J Physiol 2015;467(9):1881–98.
    pubmed: 25304002
  30. Vallon V, Platt KA, Cunard R, Schroth J, Whaley J, Thomson SC. SGLT2 mediates glucose reabsorption in the early proximal tubule. J Am Soc Nephrol: JASN 2011;22(1):104–12.
    pmc: PMC3014039pubmed: 20616166
  31. Sabolic I, Vrhovac I, Eror DB, Gerasimova M, Rose M, Breljak D. Expression of Na+-D-glucose cotransporter SGLT2 in rodents is kidney-specific and exhibits sex and species differences. Am J Physiol Cell Physiol 2012;302(8):C1174–C88.
    pmc: PMC3774553pubmed: 22262063
  32. Balen D, Ljubojević M, Breljak D, Brzica H, Z̆lender V, Koepsell H. Revised immunolocalization of the Na+-d-glucose cotransporter SGLT1 in rat organs with an improved antibody. Am J Physiol-Cell Physiol 2008;295(2):C475–C89.
    pubmed: 18524944
  33. Gorboulev V, Schürmann A, Vallon V, Kipp H, Jaschke A, Klessen D. Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption and glucose dependent incretin secretion. Diabetes 2012(1).
    pmc: PMC3237647pubmed: 22124465
  34. Du F, Hinke SA, Cavanaugh C, Polidori D, Wallace N, Kirchner T. Potent Sodium/Glucose Cotransporter SGLT1/2 dual inhibition improves glycemic control without marked gastrointestinal adaptation or colonic microbiota changes in Rodents. J Pharmacol Exp Ther 2018;365(3):676–87.
    pubmed: 29674332
  35. Kurosaki E, Ogasawara H. Ipragliflozin and other sodium–glucose cotransporter-2 (SGLT2) inhibitors in the treatment of type 2 diabetes: Preclinical and clinical data. Pharmacol Ther 2013;139(1):51–9.
    pubmed: 23563279
  36. Dyer J, Fernandez-Castano Merediz E, Salmon KS, Proudman CJ, Edwards GB, Shirazi-Beechey SP. Molecular characterisation of carbohydrate digestion and absorption in equine small intestine. Equine Vet J 2002;34(4):349–58.
    pubmed: 12117106
  37. Dyer J, Al-Rammahi M, Waterfall L, Salmon KSH, Geor RJ, Bouré L. Adaptive response of equine intestinal Na+/glucose co-transporter (SGLT1) to an increase in dietary soluble carbohydrate. Pflügers Archiv - Eur J Physiol 2009;458(2):419–30.
    pubmed: 19048283
  38. Weil M-T, Ruhwedel T, Meschkat M, Sadowski B, Möbius W. Transmission electron microscopy of Oligodendrocytes and Myelin. In: Lyons DA, Kegel L, editors. Oligodendrocytes: methods and protocols. New York: Springer New York; 2019. pp. 343–75.
    pubmed: 30820909
  39. Abdul-Ghani MA, DeFronzo RA, Norton L. Novel Hypothesis to Explain Why SGLT2 Inhibitors Inhibit Only 30–50% of Filtered Glucose Load in Humans. Diabetes 2013;62(10):3324–8.
    doi: 10.2337/db13-0604pmc: PMC3781482pubmed: 24065789google scholar: lookup
  40. Norton L, Shannon CE, Fourcaudot M, Hu C, Wang N, Ren W. Sodium-glucose co-transporter (SGLT) and glucose transporter (GLUT) expression in the kidney of type 2 diabetic subjects. Diabetes Obes Metab 2017;19(9):1322–6.
    pubmed: 28477418
  41. Guzelian P, Boyer JL. Glucose reabsorption from bile. Evidence for a biliohepatic circulation. J Clin Invest 1974;53(2):526–35.
    pmc: PMC301495pubmed: 11344566
  42. Olson JR, Fujimoto JM. Demonstration of a d-glucose transport system in the biliary tree of the rat by use of the segmented retrograde intrabiliary injection technique. Biochem Pharmacol 1980;29(2):213–9.
    pubmed: 6767480
  43. Tsutsumi Y. Pitfalls and caveats in applying chromogenic immunostaining to histopathological diagnosis. Cells 2021;10(6).
    pmc: PMC8232789pubmed: 34203756
  44. Ogawa A, Kurita K, Ikezawa Y, Igarashi M, Kuzumaki T, Daimon M. Functional localization of glucose transporter 2 in rat liver. J Histochem Cytochem 1996;44(11):1231–6.
    pubmed: 8918897
  45. Berndt N, Holzhütter H-G. Dynamic metabolic zonation of the hepatic glucose metabolism is accomplished by sinusoidal plasma gradients of nutrients and hormones. Front Physiol 2018;9:2018.
    pmc: PMC6315134pubmed: 30631280
  46. Nishimura M, Naito S. Tissue-specific mRNA expression profiles of human atp-binding cassette and solute carrier transporter superfamilies. Drug Metab Pharmacokinet 2005;20(6):452–77.
    pubmed: 16415531
  47. Zhao FQ, McFadden TB, Wall EH, Dong B, Zheng YC. Cloning and expression of bovine sodium/glucose cotransporter SGLT2*. J Dairy Sci 2005;88(8):2738–48.
    pubmed: 16027187
  48. Zhao FQ, Zheng YC, Wall EH, McFadden TB. Cloning and expression of bovine sodium/glucose cotransporters. J Dairy Sci 2005;88(1):182–94.
    pubmed: 15591382
  49. Wang D, Jinxian M, Lihua Z, Zhang L. Research advances in the diagnosis and treatment of MASLD/MASH. Ann Med 2025;57(1):2445780.
    pmc: PMC11703476pubmed: 41421798
  50. Berger C, Zdzieblo D. Glucose transporters in pancreatic islets. Pflügers Archiv - Eur J Physiol 2020;472(9):1249–72.
    pmc: PMC7462922pubmed: 32394191
  51. Steiner DJ, Abraham K, Kevin M, Hara M. Pancreatic islet plasticity: Interspecies comparison of islet architecture and composition. Islets 2010;2(3):135–45.
    pmc: PMC2908252pubmed: 20657742
  52. Helmstaedter V, Feurle GE, Forssmann WG. Insulin-, glucagon-, and somatostatin immunoreactive endocrine cells in the equine pancreas. Cell Tissue Res 1976;172(4):447–54.
    pubmed: 791497
  53. Forssmann A. The ultrastructure of the cell types in the endocrine pancreas of the horse. Cell Tissue Res 1976;167(2):179–95.
    pubmed: 769989
  54. Newkirk KM, Ehrensing G, Odoi A, Boston RC, Frank N. Immunohistochemical expression of insulin, glucagon, and somatostatin in pancreatic islets of horses with and without insulin resistance. American Vet Res 2018;79(2):191–8.
    pubmed: 29359971
  55. Kellon EM, Gustafson KM. Hypertriglyceridemia in equines with refractory hyperinsulinemia treated with SGLT2 inhibitors. Open Vet J 2023;13(3):365–75.
    pmc: PMC10072834pubmed: 37026076
  56. Pedersen MG, Ahlstedt I, El Hachmane MF, Göpel SO. Dapagliflozin stimulates glucagon secretion at high glucose: experiments and mathematical simulations of human A-cells. Sci Rep 2016;6(1):31214.
    pmc: PMC4989223pubmed: 27535321
  57. Chae H, Augustin R, Gatineau E, Mayoux E, Bensellam M, Antoine N. SGLT2 is not expressed in pancreatic α-and β-cells, and its inhibition does not directly affect glucagon and insulin secretion in rodents and humans. Mol Metab 2020;42:101071.
    pmc: PMC7554656pubmed: 32896668
  58. Kuhre RE, Ghiasi SM, Adriaenssens AE, Wewer Albrechtsen NJ, Andersen DB, Aivazidis A. No direct effect of SGLT2 activity on glucagon secretion. Diabetologia 2019;62(6):1011–23.
    pmc: PMC7212061pubmed: 30903205
  59. Brown PJ, Whitbread TJ, Bell NJ, Burden FA. Haemosiderin deposition in Donkey (Equus asinus) liver: comparison of liver histopathology with liver iron content. Res Vet Sci 2011;90(2):275–9.
    pubmed: 20656308
  60. Durham AE, Smith KC, Newton JR, Hillyer MH, Hillyer LL, Smith MRW. Development and application of a scoring system for prognostic evaluation of equine liver biopsies. Equine Vet J 2003;35(6):534–40.
    pubmed: 14515951
  61. Theelen MJP, Beukers M, Grinwis GCM, Sloet van Oldruitenborgh‐Oosterbaan MM. Chronic iron overload causing haemochromatosis and hepatopathy in 21 horses and one donkey. Equine Vet J 2019;51(3):304–9.
    pubmed: 30269378
  62. Consortium TU. UniProt: the Universal Protein Knowledgebase in 2025. Nucleic Acids Res 2025;53:D609–D17.
    pmc: PMC11701636pubmed: 39552041
  63. Takata K, Kasahara T, Kasahara M, Ezaki O, Hirano H. Immunohistochemical localization of Na+-dependent glucose transporter in rat jejunum. Cell Tissue Res 1992;267(1):3–9.
    pubmed: 1735116
  64. Chichger H, Cleasby ME, Srai SK, Unwin RJ, Debnam ES, Marks J. Experimental type II diabetes and related models of impaired glucose metabolism differentially regulate glucose transporters at the proximal tubule brush border membrane. Exp Physiol 2016;101(6):731–42.
    pubmed: 27164183

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