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phlorizin inhibits SGLT1

Leans support(preclinical) Supplements 🐭 Non-human evidence
RefutedContestedStrong support
consensus score 1.00
🔬 Capped to leans support — preclinical evidence only. The raw signal looked like strong support, but a claim about human health can't be graded that high on animal or lab evidence alone. It stays capped until human trials weigh in.

📅 Last reviewed: 2026-08-11

Evidence ladder

How far up the ladder this claim has climbed. A high consensus on a low rung means "consistent so far," not "proven in people."

Top evidence so far: Animal studies (Animal)

MechanismIn-vitroAnimalObservationalRCTMeta-analysis

How the studies fall

12 support 0 contradict 0 tested null 0 mixed · 12 sources, 10 independent groups

What the evidence shows

Textbook pharmacology and the anchor of H2's chain: phlorizin is the natural glucoside from which the gliflozin drug class was derived, and it inhibits both SGLT1 and SGLT2. Not controversial.

The evidence (12)

SourceGradeStanceQualityFinding
Palmer RK
2024 · PLoS One
in-vitro supports high CHO cells transiently expressing human SGLT1 gave a glucose EC50 of 452 uM; phlorizin inhibited the membrane-potential response to 10 mM glucose with an IC50 of 3.5 uM. Direct, quantitative inhibition of the HUMAN transporter, and incidental to the paper's own question (taste), so not selected to prove this claim.
Yamaguchi K, et al.
2011 · Drug metabolism and disposition: the biological fate of chemicals
animal supports moderate PK/PD model of phlorizin's inhibition of renal glucose reabsorption in rats, built on SGLT1- and SGLT2-mediated transport parameters from in-vitro vesicle experiments. Characterises phlorizin as an SGLT inhibitor quantitatively.
Karaki SI
2025 · Biomedical Research (Tokyo)
animal supports moderate Ussing chamber, mouse small intestinal mucosa: phlorizin inhibited glucose-induced short-circuit current (electrogenic Na+ transport via SGLTs) with apparent Ki 1.88 ug/mL, and accounted for 86% of a whole apple-polyphenol extract's effect. Mechanistic wrinkle worth recording: inhibition read NONCOMPETITIVE here, against phlorizin's classical competitive mode.
?
2023 · study_type: animal
animal supports moderate Describes phlorizin explicitly as a dual SGLT1/SGLT2 inhibitor and uses it to reduce glucose transport in an experimental peritoneal dialysis model, confirming transporter blockade in vivo.
Rieg T
2018 · Diabetologia
mechanism supports moderate Diabetologia review of SGLT inhibitor development: phlorizin is 'a naturally occurring competitive inhibitor of SGLT1 and SGLT2' and provided the first insights into efficacy, limited in clinical use by intestinal side effects and a short half-life. Secondary source, graded as mechanism rather than as an experiment: it summarises the primary work rather than adding an independent measurement, and its weight is set accordingly.
Baech-Laursen C
2025 · Acta Physiologica
animal supports high Isolated vascularly perfused rat small intestine with 14C-D-glucose tracing: blocking SGLT1 with phlorizin reduced glucose absorption by 60%. Functional confirmation of transporter blockade in intact tissue. Same paper shows ~30% of absorption survives combined SGLT1/GLUT2 blockade (paracellular), which bounds what inhibiting SGLT1 can achieve without contradicting that it inhibits it.
Sato K
2026 · Nuclear Medicine and Biology
in-vitro supports moderate Radioiodinated phlorizin bound SGLT1 in HEK293 cells singly transfected with GLUT1, GLUT3, SGLT1 or SGLT2 - a clean selectivity panel. Two caveats recorded rather than smoothed: the authors label phlorizin an SGLT2 inhibitor, and [125I]phlorizin also showed GLUT3 affinity, so it is not an SGLT1-selective probe.
Sala-Rabanal M
2018 · J Physiol
animal supports high PET imaging of intestinal glucose absorption in wild-type, Sglt1-/- and Glut2-/- mice using transporter-specific non-metabolizable probes: oral phlorizin reduced absorption by SGLT1 in the intact animal, with the knockouts providing the specificity control. In-vivo counterpart to the same lab's electrophysiology, and the closest thing in this ledger to the bakery-relevant question of blocking intestinal SGLT1 with an ingested glucoside. Third paper from the UCLA group (shared group_id with s21940664 and s22159082), so it adds evidence but NOT an independent group.
Sala-Rabanal M
2012 · Am J Physiol Cell Physiol
in-vitro supports high Human SGLT1 mutagenesis in Xenopus oocytes: changes in phlorizin Ki tracked changes in sugar K0.5 across binding-site mutants, and F101C raised phlorizin Ki by orders of magnitude with no change in glucose affinity. Authors conclude glucose and phlorizin occupy the SAME binding site, with F101 binding the phloretin moiety - competitive inhibition localised to a residue. Same lab as s21940664 (shared group_id), so the two are weighted as one group.
Wang Y
2014 · J Agric Food Chem
in-vitro supports high Two-electrode voltage clamp of SGLT1-expressing Xenopus oocytes screening 26 medicinal herbs: phlorizin was measured as the high-affinity reference inhibitor at IC50 0.21 uM, against which the best gymnemic acid (0.17 uM) was judged comparable. Independent group, and the phlorizin figure is incidental to the paper's own question, so it is not a number selected to support this claim.
David-Silva A
2020 · Diabetes Metab Syndr Obes
animal supports moderate One week of phlorizin in obese type-2 diabetic mice improved glycaemia, hepatic glucose production and NAFLD features, with the authors using it as a dual SGLT1/SGLT2 inhibitor. Weaker than the electrophysiology for this claim and marked so deliberately: the study PRESUPPOSES the inhibition rather than measuring it, and contributes a functional in-vivo consequence consistent with transporter blockade.
Hummel CS
2012 · Am J Physiol Cell Physiol
in-vitro supports high Electrophysiology of human SGLT1 and SGLT2 expressed in HEK-293T cells, with phlorizin as the reference inhibitor against which dapagliflozin and analogues were benchmarked (dapagliflozin Ki 400 nM at hSGLT1, ~100-fold SGLT2-selective). Phlorizin's inhibition of the human transporter is the assay's baseline, not its hypothesis.

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