Nutrient chapter

Phlorizin

Phloretin 2'-O-glucoside, also spelled phloridzin or phlorhizin. Parent glycoside, phloretin aglycone and conjugated metabolites are distinct actors.

12 recorded mechanisms · 1 availability situations · 1 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

  1. Human SGLT2 expressed in Xenopus oocytes transported glucose with a 1:1 sodium-to-glucose ratio and was phlorizin-sensitive.

    Phlorizin → Human SGLT2 sodium/glucose cotransport source_derived_draftungraded
    Experimental context and source evidence
    dose
    Glucose or alpha-methylglucose with sodium and phlorizin
    duration
    Acute transport assay
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Human SGLT2 expressed in Xenopus oocytes
    limitations
    Oocyte transport identifies function but does not define human oral phlorizin exposure or renal selectivity in vivo.
    nutrient_topic
    Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
    organism
    Human SGLT2 expressed in Xenopus oocytes
    plain_language
    Human SGLT2 expressed in Xenopus oocytes transported glucose with a 1:1 sodium-to-glucose ratio and was phlorizin-sensitive.
    primary_references
    The human kidney low affinity Na+/glucose cotransporter SGLT2. Delineation of the major renal reabsorptive mechanism for D-glucose. (1994). https://pubmed.ncbi.nlm.nih.gov/8282810/ DOI: 10.1172/JCI116972
    route
    In vitro
    tissue
    Radiotracer uptake and voltage-clamp current

    Phlorizin: mechanism of action and interactions (2026-09-20) · lines 11–20

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Human SGLT2 expressed in Xenopus oocytes · source_derived_draft · unverified_draft

    ## phlorizin-human-sglt2-identification Human SGLT2 expressed in Xenopus oocytes transported glucose with a 1:1 sodium-to-glucose ratio and was phlorizin-sensitive. Model/species: Human SGLT2 expressed in Xenopus oocytes Tissue/system: Radiotracer uptake and voltage-clamp current Exposure: Glucose or alpha-methylglucose with sodium and phlorizin Route: In vitro Duration: Acute transport assay Limits: Oocyte transport identifies function but does not define human oral phlorizin exposure or renal selectivity in vivo. Primary reference: The human kidney low affinity Na+/glucose cotransporter SGLT2. Delineation of the major renal reabsorptive mechanism for D-glucose. (1994). https://pubmed.ncbi.nlm.nih.gov/8282810/ DOI: 10.1172/JCI116972 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  2. Phlorizin inhibited human SGLT2 more strongly than SGLT1 in HEK293T electrophysiology, with reported Ki values of 11 and 140 nM, respectively.

    Phlorizin → Human SGLT1 and SGLT2 transport activity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    dose
    Phlorizin concentration-response
    duration
    Acute
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    HEK293T cells expressing human SGLT2 or SGLT1
    limitations
    The indexed article has an erratum notice; the exact correction was not recovered in this curation and the numerical values require rechecking before quantitative reuse.
    nutrient_topic
    Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
    organism
    HEK293T cells expressing human SGLT2 or SGLT1
    plain_language
    Phlorizin inhibited human SGLT2 more strongly than SGLT1 in HEK293T electrophysiology, with reported Ki values of 11 and 140 nM, respectively.
    primary_references
    Glucose transport by human renal Na+/D-glucose cotransporters SGLT1 and SGLT2. (2011). https://pubmed.ncbi.nlm.nih.gov/20980548/ DOI: 10.1152/ajpcell.00388.2010
    route
    In vitro
    tissue
    Whole-cell sodium/glucose cotransport current
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Phlorizin: mechanism of action and interactions (2026-09-20) · lines 22–31

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · HEK293T cells expressing human SGLT2 or SGLT1 · source_derived_draft · unverified_draft

    ## phlorizin-sglt1-sglt2-affinity Phlorizin inhibited human SGLT2 more strongly than SGLT1 in HEK293T electrophysiology, with reported Ki values of 11 and 140 nM, respectively. Model/species: HEK293T cells expressing human SGLT2 or SGLT1 Tissue/system: Whole-cell sodium/glucose cotransport current Exposure: Phlorizin concentration-response Route: In vitro Duration: Acute Limits: The indexed article has an erratum notice; the exact correction was not recovered in this curation and the numerical values require rechecking before quantitative reuse. Primary reference: Glucose transport by human renal Na+/D-glucose cotransporters SGLT1 and SGLT2. (2011). https://pubmed.ncbi.nlm.nih.gov/20980548/ DOI: 10.1152/ajpcell.00388.2010 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  3. Cryo-EM placed phlorizin in an inward-facing human SGLT2-MAP17 complex, and biphasic kinetics suggested access from extracellular and intracellular sides.

    Phlorizin → Human SGLT2-MAP17 transporter complex source_derived_draftungraded
    Experimental context and source evidence
    dose
    Phlorizin and comparator synthetic inhibitors
    duration
    Acute
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Purified human SGLT2-MAP17 complex
    limitations
    A bound structure explains inhibition but does not establish human pharmacokinetics; synthetic inhibitors used different outward-facing poses.
    nutrient_topic
    Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
    organism
    Purified human SGLT2-MAP17 complex
    plain_language
    Cryo-EM placed phlorizin in an inward-facing human SGLT2-MAP17 complex, and biphasic kinetics suggested access from extracellular and intracellular sides.
    primary_references
    Transport and inhibition mechanism of the human SGLT2-MAP17 glucose transporter. (2024). https://pubmed.ncbi.nlm.nih.gov/38057552/ DOI: 10.1038/s41594-023-01134-0
    route
    Cell-free structural and transport analysis
    tissue
    Cryo-EM structures and inhibitor kinetics

    Phlorizin: mechanism of action and interactions (2026-09-20) · lines 33–42

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Purified human SGLT2-MAP17 complex · source_derived_draft · unverified_draft

    ## phlorizin-sglt2-structure Cryo-EM placed phlorizin in an inward-facing human SGLT2-MAP17 complex, and biphasic kinetics suggested access from extracellular and intracellular sides. Model/species: Purified human SGLT2-MAP17 complex Tissue/system: Cryo-EM structures and inhibitor kinetics Exposure: Phlorizin and comparator synthetic inhibitors Route: Cell-free structural and transport analysis Duration: Acute Limits: A bound structure explains inhibition but does not establish human pharmacokinetics; synthetic inhibitors used different outward-facing poses. Primary reference: Transport and inhibition mechanism of the human SGLT2-MAP17 glucose transporter. (2024). https://pubmed.ncbi.nlm.nih.gov/38057552/ DOI: 10.1038/s41594-023-01134-0 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  4. In rat jejunum/ileum perfusion, phlorizin hydrolysis to aglycone preceded intestinal conjugation and transport, and only conjugated forms entered mesenteric blood.

    Phlorizin → Phloretin source_derived_draftungraded
    Experimental context and source evidence
    dose
    Phlorizin or phloretin 15 nmol/min for 30 minutes
    duration
    30 minutes
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    In-situ rat jejunum plus ileum perfusion
    limitations
    Rat intestinal handling may not quantify human exposure; conjugate identities and free fractions determine downstream action.
    nutrient_topic
    Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
    organism
    In-situ rat jejunum plus ileum perfusion
    plain_language
    In rat jejunum/ileum perfusion, phlorizin hydrolysis to aglycone preceded intestinal conjugation and transport, and only conjugated forms entered mesenteric blood.
    primary_references
    Comparison of the intestinal absorption of quercetin, phloretin and their glucosides in rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11481403/ DOI: 10.1093/jn/131.8.2109
    route
    Intestinal perfusion
    tissue
    Luminal, mucosal and mesenteric-blood metabolites

    Phlorizin: mechanism of action and interactions (2026-09-20) · lines 44–53

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · In-situ rat jejunum plus ileum perfusion · source_derived_draft · unverified_draft

    ## phlorizin-intestinal-hydrolysis In rat jejunum/ileum perfusion, phlorizin hydrolysis to aglycone preceded intestinal conjugation and transport, and only conjugated forms entered mesenteric blood. Model/species: In-situ rat jejunum plus ileum perfusion Tissue/system: Luminal, mucosal and mesenteric-blood metabolites Exposure: Phlorizin or phloretin 15 nmol/min for 30 minutes Route: Intestinal perfusion Duration: 30 minutes Limits: Rat intestinal handling may not quantify human exposure; conjugate identities and free fractions determine downstream action. Primary reference: Comparison of the intestinal absorption of quercetin, phloretin and their glucosides in rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11481403/ DOI: 10.1093/jn/131.8.2109 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  5. Phloretin absorption was lower when perfused as its 2'-O-glucoside phlorizin than when the aglycone was perfused directly.

    Phlorizin → Phloretin source_derived_draftungraded
    Experimental context and source evidence
    dose
    Phlorizin versus phloretin
    duration
    30 minutes
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    In-situ rat intestinal perfusion
    limitations
    This substrate comparison is not a human food-bioavailability estimate and does not transfer phloretin effects to intact phlorizin.
    nutrient_topic
    Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
    organism
    In-situ rat intestinal perfusion
    plain_language
    Phloretin absorption was lower when perfused as its 2'-O-glucoside phlorizin than when the aglycone was perfused directly.
    primary_references
    Comparison of the intestinal absorption of quercetin, phloretin and their glucosides in rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11481403/ DOI: 10.1093/jn/131.8.2109
    route
    Intestinal perfusion
    tissue
    Net aglycone absorption

    Phlorizin: mechanism of action and interactions (2026-09-20) · lines 55–64

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · In-situ rat intestinal perfusion · source_derived_draft · unverified_draft

    ## phlorizin-glucoside-lowers-phloretin-absorption Phloretin absorption was lower when perfused as its 2'-O-glucoside phlorizin than when the aglycone was perfused directly. Model/species: In-situ rat intestinal perfusion Tissue/system: Net aglycone absorption Exposure: Phlorizin versus phloretin Route: Intestinal perfusion Duration: 30 minutes Limits: This substrate comparison is not a human food-bioavailability estimate and does not transfer phloretin effects to intact phlorizin. Primary reference: Comparison of the intestinal absorption of quercetin, phloretin and their glucosides in rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11481403/ DOI: 10.1093/jn/131.8.2109 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  6. Glucosylation improved net quercetin absorption as isoquercitrin but reduced phloretin absorption as phlorizin, demonstrating substrate-specific effects of glycosylation.

    Isoquercitrin / quercetin 3-O-glucoside → Phlorizin source_derived_draftungraded
    Experimental context and source evidence
    dose
    Quercetin/isoquercitrin and phloretin/phlorizin pairs
    duration
    30 minutes
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    In-situ rat intestinal perfusion
    limitations
    This is a mechanistic nutrient-to-nutrient comparison in rats, not evidence that the flavonoids compete in humans.
    nutrient_topic
    Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
    organism
    In-situ rat intestinal perfusion
    plain_language
    Glucosylation improved net quercetin absorption as isoquercitrin but reduced phloretin absorption as phlorizin, demonstrating substrate-specific effects of glycosylation.
    primary_references
    Comparison of the intestinal absorption of quercetin, phloretin and their glucosides in rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11481403/ DOI: 10.1093/jn/131.8.2109
    route
    Intestinal perfusion
    tissue
    Comparative flavonoid absorption

    Phlorizin: mechanism of action and interactions (2026-09-20) · lines 66–75

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · In-situ rat intestinal perfusion · source_derived_draft · unverified_draft

    ## phlorizin-quercetin-comparison Glucosylation improved net quercetin absorption as isoquercitrin but reduced phloretin absorption as phlorizin, demonstrating substrate-specific effects of glycosylation. Model/species: In-situ rat intestinal perfusion Tissue/system: Comparative flavonoid absorption Exposure: Quercetin/isoquercitrin and phloretin/phlorizin pairs Route: Intestinal perfusion Duration: 30 minutes Limits: This is a mechanistic nutrient-to-nutrient comparison in rats, not evidence that the flavonoids compete in humans. Primary reference: Comparison of the intestinal absorption of quercetin, phloretin and their glucosides in rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11481403/ DOI: 10.1093/jn/131.8.2109 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  7. Recombinant Eubacterium ramulus phloretin hydrolase cleaved phloretin but did not transform phlorizin.

    Eubacterium ramulus phloretin hydrolase → Phlorizin source_derived_draftungraded
    Experimental context and source evidence
    dose
    Phloretin or phlorizin
    duration
    Acute enzyme assay
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Purified recombinant bacterial enzyme
    limitations
    The null for phlorizin separates glycoside hydrolysis from downstream aglycone cleavage; it does not exclude other microbial enzymes.
    nutrient_topic
    Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
    organism
    Purified recombinant bacterial enzyme
    plain_language
    Recombinant Eubacterium ramulus phloretin hydrolase cleaved phloretin but did not transform phlorizin.
    primary_references
    Cloning and expression of a phloretin hydrolase gene from Eubacterium ramulus and characterization of the recombinant enzyme. (2004). https://pubmed.ncbi.nlm.nih.gov/15466559/ DOI: 10.1128/AEM.70.10.6131-6137.2004
    route
    In vitro
    tissue
    Substrate-specific carbon-carbon hydrolysis

    Phlorizin: mechanism of action and interactions (2026-09-20) · lines 77–86

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Purified recombinant bacterial enzyme · source_derived_draft · unverified_draft

    ## phlorizin-bacterial-hydrolase-specificity Recombinant Eubacterium ramulus phloretin hydrolase cleaved phloretin but did not transform phlorizin. Model/species: Purified recombinant bacterial enzyme Tissue/system: Substrate-specific carbon-carbon hydrolysis Exposure: Phloretin or phlorizin Route: In vitro Duration: Acute enzyme assay Limits: The null for phlorizin separates glycoside hydrolysis from downstream aglycone cleavage; it does not exclude other microbial enzymes. Primary reference: Cloning and expression of a phloretin hydrolase gene from Eubacterium ramulus and characterization of the recombinant enzyme. (2004). https://pubmed.ncbi.nlm.nih.gov/15466559/ DOI: 10.1128/AEM.70.10.6131-6137.2004 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  8. High-dose rat studies identified hydroxylated, reduced, methylated, acetylated, sulfated and glucuronidated phlorizin metabolites in plasma, urine or feces.

    Phlorizin → Rat phlorizin phase-I and phase-II metabolite pool source_derived_draftungraded
    Experimental context and source evidence
    dose
    Phlorizin; reported pharmacokinetic arm included 400 mg/kg intraperitoneally
    duration
    1-6 hour parent/aglycone peaks and excretion sampling
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Sprague-Dawley rats
    limitations
    The dose is very high; proposed stronger metabolite inhibition of SGLTs came from docking, not functional transport experiments.
    nutrient_topic
    Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
    organism
    Sprague-Dawley rats
    plain_language
    High-dose rat studies identified hydroxylated, reduced, methylated, acetylated, sulfated and glucuronidated phlorizin metabolites in plasma, urine or feces.
    primary_references
    A pharmacokinetic study to correlate the hypoglycemic effect of phlorizin in rats: Identification of metabolites as inhibitors of sodium/glucose cotransporters. (2023). https://pubmed.ncbi.nlm.nih.gov/37464563/ DOI: 10.1002/jms.4964
    route
    Intraperitoneal and sampled excreta; oral samples also described
    tissue
    LC-MS/MS pharmacokinetics and metabolite identification

    Phlorizin: mechanism of action and interactions (2026-09-20) · lines 88–97

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Sprague-Dawley rats · source_derived_draft · unverified_draft

    ## phlorizin-rat-metabolites High-dose rat studies identified hydroxylated, reduced, methylated, acetylated, sulfated and glucuronidated phlorizin metabolites in plasma, urine or feces. Model/species: Sprague-Dawley rats Tissue/system: LC-MS/MS pharmacokinetics and metabolite identification Exposure: Phlorizin; reported pharmacokinetic arm included 400 mg/kg intraperitoneally Route: Intraperitoneal and sampled excreta; oral samples also described Duration: 1-6 hour parent/aglycone peaks and excretion sampling Limits: The dose is very high; proposed stronger metabolite inhibition of SGLTs came from docking, not functional transport experiments. Primary reference: A pharmacokinetic study to correlate the hypoglycemic effect of phlorizin in rats: Identification of metabolites as inhibitors of sodium/glucose cotransporters. (2023). https://pubmed.ncbi.nlm.nih.gov/37464563/ DOI: 10.1002/jms.4964 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  9. Four weeks of phlorizin lowered hyperglycemia and normalized clamp-measured hepatic and peripheral insulin action in neonatal-streptozotocin diabetic rats without changing insulin secretion or pancreatic insulin content.

    Phlorizin → Hepatic and peripheral insulin sensitivity in diabetic rats source_derived_draftungraded
    Experimental context and source evidence
    dose
    Chronic phlorizin by osmotic minipump
    duration
    4 weeks
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Adult rats with neonatal-streptozotocin-induced diabetes
    limitations
    The study supports reversal of glucose toxicity in this rat model, not direct insulin-receptor agonism or human use.
    nutrient_topic
    Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
    organism
    Adult rats with neonatal-streptozotocin-induced diabetes
    plain_language
    Four weeks of phlorizin lowered hyperglycemia and normalized clamp-measured hepatic and peripheral insulin action in neonatal-streptozotocin diabetic rats without changing insulin secretion or pancreatic insulin content.
    primary_references
    Insulin resistance in rats with non-insulin-dependent diabetes induced by neonatal (5 days) streptozotocin: evidence for reversal following phlorizin treatment. (1990). https://pubmed.ncbi.nlm.nih.gov/2198430/ DOI: 10.1016/0026-0495(90)90120-2
    route
    Parenteral infusion
    tissue
    Euglycemic-hyperinsulinemic clamp and insulin secretion

    Phlorizin: mechanism of action and interactions (2026-09-20) · lines 99–108

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Adult rats with neonatal-streptozotocin-induced diabetes · source_derived_draft · unverified_draft

    ## phlorizin-diabetic-rat-insulin-sensitivity Four weeks of phlorizin lowered hyperglycemia and normalized clamp-measured hepatic and peripheral insulin action in neonatal-streptozotocin diabetic rats without changing insulin secretion or pancreatic insulin content. Model/species: Adult rats with neonatal-streptozotocin-induced diabetes Tissue/system: Euglycemic-hyperinsulinemic clamp and insulin secretion Exposure: Chronic phlorizin by osmotic minipump Route: Parenteral infusion Duration: 4 weeks Limits: The study supports reversal of glucose toxicity in this rat model, not direct insulin-receptor agonism or human use. Primary reference: Insulin resistance in rats with non-insulin-dependent diabetes induced by neonatal (5 days) streptozotocin: evidence for reversal following phlorizin treatment. (1990). https://pubmed.ncbi.nlm.nih.gov/2198430/ DOI: 10.1016/0026-0495(90)90120-2 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  10. Phlorizin normalization of glycemia restored adipocyte insulin-stimulated glucose transport and whole-body disposal despite persistently reduced transporter protein and mRNA.

    Phlorizin → Insulin-stimulated glucose transport in diabetic-rat adipocytes source_derived_draftungraded
    Experimental context and source evidence
    dose
    Phlorizin sufficient to normalize blood glucose
    duration
    Chronic normalization interval
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Ninety-percent-pancreatectomized diabetic rats and isolated adipocytes
    limitations
    Restored function without restored expression points to ambient-glucose effects; it does not identify a direct phlorizin target in adipocytes.
    nutrient_topic
    Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
    organism
    Ninety-percent-pancreatectomized diabetic rats and isolated adipocytes
    plain_language
    Phlorizin normalization of glycemia restored adipocyte insulin-stimulated glucose transport and whole-body disposal despite persistently reduced transporter protein and mRNA.
    primary_references
    Normalization of blood glucose in diabetic rats with phlorizin treatment reverses insulin-resistant glucose transport in adipose cells without restoring glucose transporter gene expression. (1991). https://pubmed.ncbi.nlm.nih.gov/1991839/ DOI: 10.1172/JCI115031
    route
    In vivo treatment followed by ex-vivo cells
    tissue
    Glucose clamps, 3-O-methylglucose transport and transporter expression

    Phlorizin: mechanism of action and interactions (2026-09-20) · lines 110–119

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Ninety-percent-pancreatectomized diabetic rats and isolated adipocytes · source_derived_draft · unverified_draft

    ## phlorizin-adipocyte-transport-restoration Phlorizin normalization of glycemia restored adipocyte insulin-stimulated glucose transport and whole-body disposal despite persistently reduced transporter protein and mRNA. Model/species: Ninety-percent-pancreatectomized diabetic rats and isolated adipocytes Tissue/system: Glucose clamps, 3-O-methylglucose transport and transporter expression Exposure: Phlorizin sufficient to normalize blood glucose Route: In vivo treatment followed by ex-vivo cells Duration: Chronic normalization interval Limits: Restored function without restored expression points to ambient-glucose effects; it does not identify a direct phlorizin target in adipocytes. Primary reference: Normalization of blood glucose in diabetic rats with phlorizin treatment reverses insulin-resistant glucose transport in adipose cells without restoring glucose transporter gene expression. (1991). https://pubmed.ncbi.nlm.nih.gov/1991839/ DOI: 10.1172/JCI115031 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  11. Millimolar phlorizin inhibited glucose transport in isolated rat diaphragm with and without insulin and added a smaller inhibition of glycogen synthesis.

    Phlorizin → Glucose transport in isolated rat diaphragm source_derived_draftungraded
    Experimental context and source evidence
    dose
    Millimolar phlorizin with or without insulin
    duration
    Acute
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Isolated surviving rat diaphragm
    limitations
    This high-concentration extra-renal effect does not represent selective SGLT2 inhibition or typical human exposure.
    nutrient_topic
    Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
    organism
    Isolated surviving rat diaphragm
    plain_language
    Millimolar phlorizin inhibited glucose transport in isolated rat diaphragm with and without insulin and added a smaller inhibition of glycogen synthesis.
    primary_references
    The combined action of insulin and phlorizin on transport and metabolism of sugars and nucleotide turnover in the isolated rat diaphragm. (1977). https://pubmed.ncbi.nlm.nih.gov/889936/ DOI: 10.1016/s0300-9084(77)80058-8
    route
    Ex vivo
    tissue
    Sugar transport, glycogen synthesis and nucleotide turnover

    Phlorizin: mechanism of action and interactions (2026-09-20) · lines 121–130

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Isolated surviving rat diaphragm · source_derived_draft · unverified_draft

    ## phlorizin-insulin-diaphragm Millimolar phlorizin inhibited glucose transport in isolated rat diaphragm with and without insulin and added a smaller inhibition of glycogen synthesis. Model/species: Isolated surviving rat diaphragm Tissue/system: Sugar transport, glycogen synthesis and nucleotide turnover Exposure: Millimolar phlorizin with or without insulin Route: Ex vivo Duration: Acute Limits: This high-concentration extra-renal effect does not represent selective SGLT2 inhibition or typical human exposure. Primary reference: The combined action of insulin and phlorizin on transport and metabolism of sugars and nucleotide turnover in the isolated rat diaphragm. (1977). https://pubmed.ncbi.nlm.nih.gov/889936/ DOI: 10.1016/s0300-9084(77)80058-8 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

  12. Phlorizin and vanadate both prevented diabetes-associated hepatic insulin-receptor overexpression in vivo, but only vanadate directly lowered transcripts in hepatoma cells.

    Phlorizin → Liver insulin-receptor expression in streptozotocin-diabetic rats source_derived_draftungraded
    Experimental context and source evidence
    dose
    Daily phlorizin or vanadate from days 5-23; direct cell exposures
    duration
    18 days in rats; 4 hours in cells
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Streptozotocin-diabetic rats and Fao hepatoma cells
    limitations
    The contrast supports an indirect glycemia route for phlorizin and a distinct direct action for vanadate.
    nutrient_topic
    Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
    organism
    Streptozotocin-diabetic rats and Fao hepatoma cells
    plain_language
    Phlorizin and vanadate both prevented diabetes-associated hepatic insulin-receptor overexpression in vivo, but only vanadate directly lowered transcripts in hepatoma cells.
    primary_references
    Treatment of streptozotocin-induced diabetic rats with vanadate and phlorizin prevents the over-expression of the liver insulin receptor gene. (1999). https://pubmed.ncbi.nlm.nih.gov/10037256/ DOI: 10.1530/eje.0.1400079
    route
    In vivo and in vitro
    tissue
    Insulin-receptor number and mRNA

    Phlorizin: mechanism of action and interactions (2026-09-20) · lines 132–141

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Streptozotocin-diabetic rats and Fao hepatoma cells · source_derived_draft · unverified_draft

    ## phlorizin-vanadate-comparator Phlorizin and vanadate both prevented diabetes-associated hepatic insulin-receptor overexpression in vivo, but only vanadate directly lowered transcripts in hepatoma cells. Model/species: Streptozotocin-diabetic rats and Fao hepatoma cells Tissue/system: Insulin-receptor number and mRNA Exposure: Daily phlorizin or vanadate from days 5-23; direct cell exposures Route: In vivo and in vitro Duration: 18 days in rats; 4 hours in cells Limits: The contrast supports an indirect glycemia route for phlorizin and a distinct direct action for vanadate. Primary reference: Treatment of streptozotocin-induced diabetic rats with vanadate and phlorizin prevents the over-expression of the liver insulin receptor gene. (1999). https://pubmed.ncbi.nlm.nih.gov/10037256/ DOI: 10.1530/eje.0.1400079 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

Phlorizin blocks sodium-coupled glucose transport through SGLT1 and SGLT2

Condition: machinery_impairment · Phlorizin occupies and inhibits the transporters.

Normal role: SGLT1 and SGLT2 use sodium gradients to transport glucose.

Recorded consequence: Sodium/glucose cotransport current falls.

Scope: In-vitro electrophysiology.

The sources

Every document behind this chapter is preserved word for word. Open one to read it in full with its recorded conflicts marked in place.

  • Phlorizin: mechanism of action and interactions (2026-09-20)Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · unverified_draftRead preserved source

Recorded disagreements

Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.

    Open questions in this collection

    Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.

      Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.

      Your LLM prompt is ready

      This browser would not copy it automatically. Select the text below, copy it, and paste it into your LLM.
      Evidence, AI assistance and curation standards