---
title: "Oral L‑Serine and D‑Serine Reduce Postprandial Hyperglycemia by Inhibiting Intestinal Glucose Abso"
id: "pubmed-42361737"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42361737"
content_type: "clinical_feed_article"
specialty: "Pharmacology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42361737/"
doi: "10.1016/j.bbrc.2026.154174"
published_at: "2026-09-03T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Oral L‑Serine and D‑Serine Reduce Postprandial Hyperglycemia by Inhibiting Intestinal Glucose Abso
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42361737
- **Specialty:** [Pharmacology](https://medichelpline.com/clinical-feed/pharmacology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42361737/)
- **DOI:** [10.1016/j.bbrc.2026.154174](https://doi.org/10.1016%2Fj.bbrc.2026.154174)
- **Published At:** 2026-09-03T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- This study compared acute oral effects of **L‑Serine** and **D‑Serine** on postprandial blood glucose regulation in healthy C57BL/6J mice. - Single oral doses of L‑Ser or D‑Ser (2.0 g/kg body weight) given with glucose loading significantly suppressed postprandial hyperglycemia versus control. - Neither enantiomer altered serum insulin levels after glucose loading, and insulin tolerance tests showed no change in insulin sensitivity, indicating an insulin‑independent mechanism. - Intraperitoneal glucose tolerance tests showed no significant changes after L‑Ser or D‑Ser, supporting an effect localized to the gut rather than systemic glucose handling. - Ex vivo everted intestine assays demonstrated that both L‑Ser and D‑Ser significantly suppressed intestinal glucose absorption. - Western blot analysis of brush border membranes revealed differential effects on transporters: **L‑Serine** reduced **GLUT2** expression, while **D‑Serine** reduced both **SGLT1** and **GLUT2** expression. - Authors conclude that single oral administration of L‑/D‑Ser acutely suppresses postprandial hyperglycemia by inhibiting **intestinal glucose absorption**, with stereospecific differences in transporter regulation. - The study was performed in healthy mice; details on dose‑response, longer‑term effects, or translation to humans were not reported in the abstract.
## Clinical Analysis & Structured Key Points
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Epub 2026 Jun 19. # Oral L-Serine and D-Serine acutely suppress postprandial hyperglycemia through inhibition of intestinal glucose absorption in healthy mice [Akira Toda](https://pubmed.ncbi.nlm.nih.gov/?term=Toda+A&cauthor_id=42361737)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361737/#full-view-affiliation-1 "Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan."), [Shinsuke Mohri](https://pubmed.ncbi.nlm.nih.gov/?term=Mohri+S&cauthor_id=42361737)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361737/#full-view-affiliation-1 "Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan."), [Kisara Ueda](https://pubmed.ncbi.nlm.nih.gov/?term=Ueda+K&cauthor_id=42361737)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361737/#full-view-affiliation-1 "Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan."), [Koki Daido](https://pubmed.ncbi.nlm.nih.gov/?term=Daido+K&cauthor_id=42361737)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361737/#full-view-affiliation-1 "Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan."), [Daichi Fuchisawa](https://pubmed.ncbi.nlm.nih.gov/?term=Fuchisawa+D&cauthor_id=42361737)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361737/#full-view-affiliation-1 "Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan."), [Futoshi Furuya](https://pubmed.ncbi.nlm.nih.gov/?term=Furuya+F&cauthor_id=42361737)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361737/#full-view-affiliation-1 "Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan."), [Eri Mukai](https://pubmed.ncbi.nlm.nih.gov/?term=Mukai+E&cauthor_id=42361737)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42361737/#full-view-affiliation-2 "Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan. Electronic address: emukai@fc.ritsumei.ac.jp.") Affiliations Expand ### Affiliations * 1 Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan. * 2 Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan. Electronic address: emukai@fc.ritsumei.ac.jp. * PMID: **42361737** * DOI: [ 10.1016/j.bbrc.2026.154174 ](https://doi.org/10.1016/j.bbrc.2026.154174) Item in Clipboard # Oral L-Serine and D-Serine acutely suppress postprandial hyperglycemia through inhibition of intestinal glucose absorption in healthy mice Akira Toda et al. Biochem Biophys Res Commun. 2026. Show details Display options Display options Format Abstract PubMed PMID Biochem Biophys Res Commun Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Biochem+Biophys+Res+Commun%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Biochem+Biophys+Res+Commun%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42361737/) . 2026 Sep 3:829:154174. doi: 10.1016/j.bbrc.2026.154174. Epub 2026 Jun 19. ### Authors [Akira Toda](https://pubmed.ncbi.nlm.nih.gov/?term=Toda+A&cauthor_id=42361737)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361737/#short-view-affiliation-1 "Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan."), [Shinsuke Mohri](https://pubmed.ncbi.nlm.nih.gov/?term=Mohri+S&cauthor_id=42361737)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361737/#short-view-affiliation-1 "Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan."), [Kisara Ueda](https://pubmed.ncbi.nlm.nih.gov/?term=Ueda+K&cauthor_id=42361737)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361737/#short-view-affiliation-1 "Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan."), [Koki Daido](https://pubmed.ncbi.nlm.nih.gov/?term=Daido+K&cauthor_id=42361737)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361737/#short-view-affiliation-1 "Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan."), [Daichi Fuchisawa](https://pubmed.ncbi.nlm.nih.gov/?term=Fuchisawa+D&cauthor_id=42361737)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361737/#short-view-affiliation-1 "Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan."), [Futoshi Furuya](https://pubmed.ncbi.nlm.nih.gov/?term=Furuya+F&cauthor_id=42361737)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42361737/#short-view-affiliation-1 "Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan."), [Eri Mukai](https://pubmed.ncbi.nlm.nih.gov/?term=Mukai+E&cauthor_id=42361737)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42361737/#short-view-affiliation-2 "Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan. Electronic address: emukai@fc.ritsumei.ac.jp.") ### Affiliations * 1 Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan. * 2 Medical Physiology and Metabolism Laboratory, Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga, 525-8577, Japan. Electronic address: emukai@fc.ritsumei.ac.jp. * PMID: **42361737** * DOI: [ 10.1016/j.bbrc.2026.154174 ](https://doi.org/10.1016/j.bbrc.2026.154174) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract D-Serine (D-Ser), an enantiomer of L-Serine (L-Ser), has been reported to exert unique physiological effects distinct from those of L-Ser. Chronic oral administration of L-Ser has been reported to improve glucose tolerance in diabetic model mice. In this study, we compared the acute effects of oral administration of L-Ser and D-Ser on postprandial blood glucose regulation and the underlying mechanisms in healthy mice. Oral glucose tolerance tests were performed in C57BL/6J mice administered L-Ser or D-Ser (2.0 g/kg BW) simultaneously with glucose loading. Both L-Ser and D-Ser significantly suppressed postprandial hyperglycemia compared with the control group. However, neither L-Ser nor D-Ser significantly affected serum insulin levels after glucose loading or insulin sensitivity during insulin tolerance tests, suggesting that their glucose-lowering effects were independent of insulin secretion and insulin sensitivity. In addition, intraperitoneal glucose tolerance tests showed no significant changes in postprandial hyperglycemia after administration of either L-Ser or D-Ser. In intestinal glucose absorption assays using everted intestine, both L-Ser and D-Ser significantly suppressed glucose absorption. Furthermore, Western blotting analysis demonstrated that L-Ser reduced GLUT2 expression in the brush border membrane, whereas D-Ser reduced both SGLT1 and GLUT2 expression. These findings demonstrate that single oral administration of l-/D-Ser acutely suppresses postprandial hyperglycemia independently of insulin secretion and insulin sensitivity by inhibiting intestinal glucose absorption. In addition, the underlying mechanisms may differ between L-Ser and D-Ser, as reflected by their distinct effects on intestinal glucose transporters, suggesting stereospecific regulation of intestinal glucose metabolism. **Keywords:** Glucose transporters; Intestinal glucose absorption; Postprandial hyperglycemia; l-/D-Serine. Copyright © 2026 Elsevier Inc. All rights reserved. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. ## Similar articles * [ Intestinal absorption of glucose in mice as determined by positron emission tomography. ](https://pubmed.ncbi.nlm.nih.gov/29707805/) Sala-Rabanal M, Ghezzi C, Hirayama BA, Kepe V, Liu J, Barrio JR, Wright EM.Sala-Rabanal M, et al.J Physiol. 2018 Jul;596(13):2473-2489. doi: 10.1113/JP275934. Epub 2018 Jun 5.J Physiol. 2018.PMID: 29707805Free PMC article. * [ Fibroblast growth factor 21 improves glucose homeostasis partially via down-regulation of Na+-d-glucose cotransporter SGLT1 in the small intestine. ](https://pubmed.ncbi.nlm.nih.gov/30551357/) Wang N, Li S, Guo XC, Li JY, Ren GP, Li DS.Wang N, et al.Biomed Pharmacother. 2019 Jan;109:1070-1077. doi: 10.1016/j.biopha.2018.10.198. Epub 2018 Nov 6.Biomed Pharmacother. 2019.PMID: 30551357 * [ The role of SGLT1 and GLUT2 in intestinal glucose transport and sensing. ](https://pubmed.ncbi.nlm.nih.gov/24587162/) Röder PV, Geillinger KE, Zietek TS, Thorens B, Koepsell H, Daniel H.Röder PV, et al.PLoS One. 2014 Feb 26;9(2):e89977. doi: 10.1371/journal.pone.0089977. eCollection 2014.PLoS One. 2014.PMID: 24587162Free PMC article. * [ Glucose transporters in the small intestine in health and disease. ](https://pubmed.ncbi.nlm.nih.gov/32829466/) Koepsell H.Koepsell H.Pflugers Arch. 2020 Sep;472(9):1207-1248. doi: 10.1007/s00424-020-02439-5. Epub 2020 Aug 23.Pflugers Arch. 2020.PMID: 32829466Free PMC article.Review. * [ Effects of hyperglycemia on glucose transporters of the muscle: use of the renal glucose reabsorption inhibitor phlorizin to control glycemia. ](https://pubmed.ncbi.nlm.nih.gov/1482748/) Dimitrakoudis D, Vranic M, Klip A.Dimitrakoudis D, et al.J Am Soc Nephrol. 1992 Nov;3(5):1078-91. doi: 10.1681/ASN.V351078.J Am Soc Nephrol. 1992.PMID: 1482748Review. 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