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MyDeficiencies

Ertugliflozin

SGLT2 Inhibitor

Also sold as Steglatro.

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Findings for this medication

Research about this medication, graded for how strongly each finding can be attributed to it. Nothing here describes your own levels.

Ertugliflozin has no classical depletion mechanism. Its regulatory label (DailyMed, setid e6f3e718-bb99-48f1-ab94-b9f0af05fed6) shows it is cleared almost entirely as inactive glucuronide conjugates (UGT1A9/UGT2B7), does not induce or meaningfully inhibit any CYP450 enzyme, is not primarily excreted unchanged in urine (only 1.5% of dose), and has no documented chelation, gastric-acid-suppression, or bile-acid-sequestrant action. There is no absorption-interference or enzyme-induction machinery here to drive a classical vitamin or mineral depletion, and none was found in the literature search for this drug specifically.

SGLT2 inhibitor · ATC A10BK04 · also sold as Steglatro and Segluromet and Steglujan · reviewed 2026-09-20. This describes research about the medication. It does not say anything about your own levels or health.

How to read the evidence grades

These colours describe how strongly a finding can be attributed to the medication in the research. They are not a severity score and they say nothing about your own health.

Grades describe how strongly a finding can be attributed to Ertugliflozin in the research — not how common it is, how serious it would be, and not anything about you personally.

Red — Severe
severe: ≥2 independent Tier A sources, this drug in the cohort, nutrient directly measured, consistent direction, clinically meaningful magnitude, named mechanism, no substantial contradicting Tier A evidence.
Orange — Moderate
moderate: ≥1 Tier A source with this drug in the cohort showing a real effect, but bounded by exposure window, subgroup, frequency, or functional (not full clinical) deficit/excess.
Yellow — Low
low/theoretical: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also context flags and reverse-direction/protective findings.
Not graded — disclosed evidence gap
Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result.Source definition: evidence gap: no Tier B/C evidence to support even yellow, and no circulating claim to rebut as white. A disclosed absence of evidence (sometimes a tooling limitation at time of writing), never reworded as reassurance.

What the research found

Phosphate

Orange — Moderate

See study details

Ertugliflozin raises serum phosphate in a dose-dependent, drug-specific pattern seen in its own pivotal trial program; this is a retention/excess signal, not a phosphate deficiency.

Full detail and limits

What the grade means here: moderate: ≥1 Tier A source with this drug in the cohort showing a real effect, but bounded by exposure window, subgroup, frequency, or functional (not full clinical) deficit/excess. Orange

Limits on what this shows

  • At-risk subgroups: Patients with pre-existing moderate renal impairment, where the proportion affected roughly doubled versus the unselected trial population.

Regulatory status

Labeled laboratory finding under Adverse Reactions.

Population evidence

Pooled phase 3 trial program (label laboratory-abnormalities table): serum phosphate increase from baseline in 1.9% of placebo patients versus 6.8% (5 mg) and 8.5% (15 mg) of ertugliflozin patients. In the moderate renal impairment subgroup this rose to 9.7% (5 mg) and 7.8% (15 mg) versus 0.8% placebo.

Mechanism

Not fully characterized in the label itself; plausible route is SGLT2-inhibition-driven osmotic diuresis and volume contraction altering renal phosphate handling, consistent with the mineral/electrolyte-axis mechanism described for the SGLT2 inhibitor class generally (Cianciolo et al., see Magnesium entry).

Counter-evidence held on record

The label reports this as a laboratory-threshold finding across a defined trial-exposure window; it does not report clinical hyperphosphatemia, symptomatic events, or PTH/FGF23 data for ertugliflozin specifically, so the functional significance beyond the lab value is not established for this drug. Framing caution: this is a retention/excess finding, not a deficiency. Phosphate or phosphate-containing supplementation is not indicated by this signal and would be the wrong direction of intervention, particularly in patients with renal impairment.

Magnesium

Yellow — Low

See study details

SGLT2 inhibitors are mechanistically proposed to raise (not lower) serum magnesium via enhanced tubular reabsorption; ertugliflozin is named within this class discussion but has no drug-specific primary data.

Full detail, limits and 1 references

What the grade means here: low/theoretical: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also context flags and reverse-direction/protective findings. Yellow

Limits on what this shows

  • At-risk subgroups: Not established for ertugliflozin; class literature discusses patients with baseline hypomagnesemia on other therapy.

Regulatory status

Not mentioned in the ertugliflozin label; confirmed absent on a targeted re-search of the STEGLATRO prescribing information text for "magnesium."

Population evidence

Cianciolo et al., "Mineral and Electrolyte Disorders With SGLT2i Therapy," JBMR Plus 2019 (PMID 31768494), a narrative review naming empagliflozin, dapagliflozin, ertugliflozin, canagliflozin, and ipragliflozin as a class, without ertugliflozin-specific stratified data in the accessible abstract. A single case report (JCEM Case Reports 2022) documents serum magnesium rising from 1.2 to 2.2 mg/dL after starting empagliflozin in one patient with refractory hypomagnesemia; ertugliflozin was not the drug used in that case.

Mechanism

Proposed (class-level, not ertugliflozin-confirmed): reduced proximal sodium-glucose cotransport increases distal intraluminal electrical potential favoring magnesium reabsorption; RAAS activation and improved insulin sensitivity are also proposed contributors.

Counter-evidence held on record

The case report is single-patient, single-drug (empagliflozin), and this is an active-comparator-style clinical observation, not a controlled trial; it does not test ertugliflozin. No ertugliflozin-specific magnesium study was located despite a targeted search. Framing caution: if this class effect applies to ertugliflozin, the direction would be a magnesium rise, not depletion. This is not a basis for magnesium supplementation.

Zinc

Not graded — disclosed evidence gap

See study details

No evidence at any tier, and no circulating consumer claim identified, connecting ertugliflozin or the SGLT2 inhibitor class to zinc status.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: A combined PubMed search across SGLT2 inhibitors and zinc/trace elements returned zero results. No circulating consumer claim about ertugliflozin and zinc was identified. Both conditions for UNGRADED are met.

Potassium

Not graded — disclosed evidence gap

See study details

Potassium was carried forward from the mechanism screen (osmotic diuresis plausibly affects tubular electrolyte handling generally) but no ertugliflozin-specific or class-level potassium evidence could be confirmed in this session.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: The STEGLATRO label text was searched directly and contains no mention of potassium or hyperkalemia/hypokalemia. Two separate PubMed search attempts ("ertugliflozin potassium hyperkalemia" and a follow-up retry) returned empty or unrenderable results under sustained rate-limiting rather than a confirmed zero-result page, so this could not be resolved to either a clean negative or a positive finding. Tooling limitation disclosed; flagged for re-check in a future revision.

The five body-system areas

Each finding is counted once, in a single area. Where a study is mentioned in a second area it is context only.

Mitochondrial Burden

Each finding below is counted once, in this area only.

Mitochondrial burden

Yellow — Low

See study details

Two ertugliflozin-specific mouse studies found improved, not impaired, cardiac mitochondrial function and energetics; this is a reverse-direction (protective) mechanistic finding, graded yellow because it is animal-only.

Full detail, limits and 2 references

What the grade means here: low/theoretical: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also context flags and reverse-direction/protective findings. Yellow

Limits on what this shows

  • At-risk subgroups: Not applicable; animal model only, cardiac tissue, diabetic phenotype specifically.

Regulatory status

Not addressed in the label.

Population evidence

Croteau D et al., "Effects of Sodium-Glucose Linked Transporter 2 Inhibition With Ertugliflozin on Mitochondrial Function, Energetics, and Metabolic Gene Expression in the Presence and Absence of Diabetes Mellitus in Mice," J Am Heart Assoc 2021 (PMID 34169737): ertugliflozin named specifically in the title and drug-specific abstract content confirming cardiac energetics/mitochondrial function effects in diabetic and non-diabetic mouse models. Croteau D et al., "SGLT2 inhibitor ertugliflozin decreases elevated intracellular sodium, and improves energetics and contractile function in diabetic cardiomyopathy," Biomed Pharmacother 2023 (PMID 36731341): ertugliflozin "improved energetic deficit and contractile dysfunction" in a high-fat-diet diabetic cardiomyopathy model.

Mechanism

Proposed reduction of pathologically elevated intracellular sodium in diabetic cardiomyocytes, improving mitochondrial calcium handling and energetics, from the same research group's own hypothesis in the 2023 paper title.

Counter-evidence held on record

Both sources are rodent studies; this review could not open the full text (PMC access blocked by rate-limiting/bot-check during this session) so effect sizes and statistical significance could not be independently confirmed beyond the search-listing abstract snippets. No human mitochondrial-function data for ertugliflozin were located. Framing caution: this is a protective/beneficial mechanistic signal, not a burden. It should not be marketed as a depletion risk in either direction for consumers; it is preclinical and cardiac-tissue-specific.

Oxidative Stress

Each finding below is counted once, in this area only.

Oxidative stress

Not graded — disclosed evidence gap

See study details

No source on ertugliflozin and oxidative stress could be opened and cohort-verified during this review; class-level titles exist for other SGLT2 inhibitors but were not opened.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: Search listings surfaced class-level titles (an empagliflozin endothelial-function/mitochondrial-oxidative-stress study in frail hypertensive/diabetic patients, and a general SGLT2-inhibitor/GLP-1 cardiovascular-mitochondrial-oxidative-stress review), none naming ertugliflozin and none opened for content or cohort verification. Two separate WebFetch attempts to open an ertugliflozin-specific PubMed search listing for oxidative stress were blocked by sustained 429 rate-limiting across the session. This is recorded as a genuine access gap rather than a class-extrapolated yellow grade, because no candidate source was actually opened per this protocol's citation rule. Flagged for re-check in a future revision.

Copper and Iron Balance

Copper and iron are assessed separately. Nothing here is counted twice.

Copper

Not graded — disclosed evidence gap

See study details

No evidence at any tier, and no circulating consumer claim identified, connecting ertugliflozin or the SGLT2 inhibitor class to copper status.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: A dedicated PubMed search for "SGLT2 inhibitor copper" returned only unrelated chemistry/synthesis papers and one dapagliflozin cuproptosis-pathway mechanistic paper (a copper-dependent cell-death pathway study, not a copper nutrient-status study, and not ertugliflozin). No circulating consumer claim about ertugliflozin and copper was identified. Both conditions for UNGRADED are met.

Iron

Not graded — disclosed evidence gap

See study details

No source on ertugliflozin and iron status could be opened and cohort-verified during this review.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: Search listings surfaced titles on empagliflozin and iron mobilization/erythropoiesis in heart failure (the EMPEROR program, the Empire HF trial), which are not ertugliflozin and were not opened for content verification in this session. Tooling limitation: repeated 429 rate-limiting on Europe PMC and PMC-hosted full text, and a reCAPTCHA block on a PMC review of SGLT2-inhibitor erythropoietin mechanisms, prevented opening any candidate source for this category within this review. This is recorded as a genuine access gap, not a finding of no effect, and should be re-checked in a future revision when access is restored.

Gut Microbiome Risk

Each finding below is counted once, in this area only.

Gut microbiome risk

Not graded — disclosed evidence gap

See study details

No source on ertugliflozin and the gut microbiome could be opened and cohort-verified during this review.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: Search listings surfaced class-level titles (a 2025 review on "pharmacological modulation of the diabetic gut microbiome with gliflozin drugs" and a dapagliflozin gut-kidney-axis study in diabetic nephropathy), neither naming or confirmed to include ertugliflozin, and neither opened for content or cohort verification within this session's access constraints. This is a disclosed access gap, not a finding of no microbiome effect for this drug.

Oxygen and ATP Output

Oxygen delivery and ATP production are assessed separately. Nothing here is counted twice.

Oxygen delivery/utilization

Orange — Moderate

See study details

Ertugliflozin raises hemoglobin and hematocrit in its own pivotal trial program, consistent with osmotic-diuresis-driven hemoconcentration and a class-recognized secondary erythropoietic effect; this is not anemia protection and not evidence of deficiency in the treated population.

Full detail and limits

What the grade means here: moderate: ≥1 Tier A source with this drug in the cohort showing a real effect, but bounded by exposure window, subgroup, frequency, or functional (not full clinical) deficit/excess. Orange

Limits on what this shows

  • At-risk subgroups: Not stratified by subgroup in the extracted label data; volume-depleted or elderly patients are separately flagged in the label for hypotension risk from the same underlying diuretic mechanism.

Regulatory status

Labeled laboratory finding under Adverse Reactions.

Population evidence

Pooled phase 3 program: mean hemoglobin change from baseline −1.4% on placebo versus +3.5% on ertugliflozin 5 mg and +3.5% on 15 mg. A hemoglobin increase of >2 g/dL above the upper limit of normal occurred in 0.0% (placebo), 0.2% (5 mg), and 0.4% (15 mg) of patients.

Mechanism

Osmotic diuresis and intravascular volume contraction (labeled elsewhere as a documented effect of SGLT2 inhibition) plausibly concentrate red-cell mass; a secondary renal erythropoietin-stimulating effect is described for the SGLT2 inhibitor class in the literature, though not confirmed for ertugliflozin specifically in a source this review could open (see Iron/UNGRADED note).

Counter-evidence held on record

This is a laboratory-threshold change over the trial's exposure window; the label does not report clinical polycythemia or thrombotic events tied to this finding for ertugliflozin. It should not be read as an oxygen-delivery deficiency; if anything it is the opposite. Framing caution: this is a retention/concentration effect, not evidence of anemia or iron deficiency requiring correction. It should not be used to justify iron or other hematinic supplementation, which would run the wrong direction and could compound the hemoconcentration in a volume-contracted patient.

ATP production

Yellow — Low

See study details

The same ertugliflozin-specific mouse studies report improved cardiac energetics and upregulated genes for oxidative phosphorylation and fatty-acid metabolism, a reverse-direction (protective) finding graded yellow because it is animal-only and cardiac-tissue-specific.

Full detail, limits and 2 references

What the grade means here: low/theoretical: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also context flags and reverse-direction/protective findings. Yellow

Limits on what this shows

  • At-risk subgroups: Not applicable; animal model only.

Regulatory status

Not addressed in the label; the label separately documents that ertugliflozin promotes a systemic shift toward lipolysis and ketogenesis, disclosed as a diabetic-ketoacidosis risk warning, which is the same fuel-shift mechanism underlying these animal energetics findings.

Population evidence

Croteau D et al., J Am Heart Assoc 2021 (PMID 34169737) and Biomed Pharmacother 2023 (PMID 36731341), both ertugliflozin-specific mouse studies of cardiac energetics described in the Mitochondrial burden entry above.

Mechanism

SGLT2 inhibition shifts systemic fuel utilization toward fatty-acid oxidation and ketogenesis; in these animal models this correlated with improved, not worsened, myocardial energetic status.

Counter-evidence held on record

The same fuel-shift mechanism (enhanced lipolysis/ketogenesis) that appears protective for cardiac ATP production in these models is the mechanism behind the label's diabetic ketoacidosis warning in vulnerable patients (insulin-deficient states, prolonged fasting, acute illness, surgery), so this is not a uniformly benign signal at the whole-body level even though the cardiac-tissue animal data are favorable. Framing caution: do not present this as evidence that ertugliflozin "boosts energy" for consumers. It is a preclinical, cardiac-specific finding tied to the same metabolic shift that carries a labeled ketoacidosis warning.

Claims checked and not supported

These circulate online for this medication. They are listed here only so they can be answered, never as findings, and they are not graded.

A claim with no supporting evidence is not necessarily disproven. Where evidence actually argues against a claim, that is stated below.

  • Bone mineral density / fracture risk (calcium–vitamin D–PTH axis)

    Where it comes from: Extrapolated from canagliflozin's CANVAS program, which showed reduced hip bone mineral density and an increased fracture signal, and from general "SGLT2 inhibitors weaken bones" consumer messaging that does not distinguish molecules within the class.

    Why it fails: Ertugliflozin's own dedicated trial, VERTIS MET (Diabetes Obes Metab 2018, PMID 28857451, n=621, 26-week randomized placebo-controlled design with ertugliflozin 5 mg and 15 mg arms), directly measured bone mineral density in this drug's own cohort and reported "no adverse impact on BMD at week 26." This is Tier A, drug-specific evidence that contradicts, rather than merely fails to confirm, the extrapolated class claim for ertugliflozin specifically.

  • Vitamin B12 depletion

    Where it comes from: Consumer drug-nutrient-depletion listings that associate diabetes medications broadly with B12 depletion (a mechanism well established for metformin), sometimes applied without distinction to ertugliflozin or to combination products containing it (e.g., metformin-containing combinations sold under related brand names).

    Why it fails: Ertugliflozin itself has no gastric-acid-suppressing or metformin-type ileal-malabsorption mechanism (Step 1 pharmacokinetic basis: no acid suppression, no B12-transporter interference documented). No Tier B or C evidence for an ertugliflozin-specific B12 effect was found. Where B12 depletion is a real concern in a combination product, it traces to the metformin component, not to ertugliflozin.

All references used above
  1. STEGLATRO (ertugliflozin) tablets, full prescribing information — FDA-approved label, DailyMed, Merck Sharp & Dohme, initial US approval 2017
  2. Pratley RE et al., "Effect of ertugliflozin on glucose control, body weight, blood pressure and bone density in type 2 diabetes mellitus inadequately controlled on metformin monotherapy (VERTIS MET)" — Randomized, double-blind, placebo-controlled trial, n=621, 26 weeks (78-week extension ongoing). Diabetes Obes Metab. 2018. PMID 28857451.
  3. Cianciolo G, De Pascalis A, Capelli I, Gasperoni L, Di Lullo L, Bellasi A, La Manna G, "Mineral and Electrolyte Disorders With SGLT2i Therapy" — Narrative review, class-level (empagliflozin, dapagliflozin, ertugliflozin, canagliflozin, ipragliflozin named). JBMR Plus. 2019. PMID 31768494.Not stratified by individual drug in the accessible abstract; graded Tier C, class-level only.
  4. Case report, "Improvement in Serum Magnesium Levels With Sodium-Glucose Cotransporter 2 Inhibitors" — Single-patient case report, empagliflozin. JCEM Case Reports. 2022. PMC10578385.Cohort excludes ertugliflozin (empagliflozin only); cited for class mechanism context only.
  5. Croteau D, Luptak I, Chambers JM, Hobai I, Panagia M, Pimentel DR, Siwik DA, Qin F, Colucci WS, "Effects of Sodium-Glucose Linked Transporter 2 Inhibition With Ertugliflozin on Mitochondrial Function, Energetics, and Metabolic Gene Expression in the Presence and Absence of Diabetes Mellitus in Mice" — Mouse model, ertugliflozin-specific. J Am Heart Assoc. 2021. PMID 34169737.Full abstract could not be opened (repeated rate-limiting); bibliographic details and title-confirmed drug/topic verified via PubMed search-listing content only.
  6. Croteau D, Baka T, Young S, He H, Chambers JM, Qin F, Panagia M, Pimentel DR, Balschi JA, Colucci WS, Luptak I, "SGLT2 inhibitor ertugliflozin decreases elevated intracellular sodium, and improves energetics and contractile function in diabetic cardiomyopathy" — Mouse model, ertugliflozin-specific, high-fat-diet diabetic cardiomyopathy. Biomedicine & Pharmacotherapy. 2023. PMID 36731341.
  7. Ertugliflozin, general pharmacology reference entry — Tertiary reference summarizing ATC classification (A10BK04), pharmacokinetics, and mechanism.
  8. PubMed search, "SGLT2 inhibitor copper" — Search performed to test for any copper-nutrient-status literature; returned only unrelated synthetic-chemistry papers and one dapagliflozin cuproptosis-pathway mechanistic study, not ertugliflozin and not a nutrient-status study.
  9. PubMed search, "SGLT2 inhibitor copper zinc trace element" (combined) — Zero results.
  10. PubMed search, "ertugliflozin fracture" — Search-listing summary referencing an ertugliflozin pooled safety analysis stating no increased fracture association, and canagliflozin's distinct fracture signal; specific pooled-analysis citation could not be independently opened and verified within this session and is therefore not relied upon in the graded entries above (VERTIS MET's direct BMD finding is used instead).