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GIP (native Infusion / GIP(3-30) Antagonist)

MARKETED

GIP receptor (native/physiology)

graded findings

effect domains

Evidence spread

High evidence 0Moderate evidence 1Low evidence 3Very low evidence 0

GIP (native Infusion / GIP(3-30) Antagonist) is shown as a marketed evidence record where applicable. Findings describe observed research and regulatory records; they do not provide treatment advice.

Thin or bounded evidence here means uncertainty remains visible. It is not evidence that an effect has been ruled out.

GIP (native Infusion / GIP(3-30) Antagonist) MARKETED

renal Not directional

Moderate evidence

No published study has measured a direct renal effect (natriuresis, sodium handling, GFR, renal blood flow) of selective/isolating GIP-receptor agonism, GIP infusion,...

Absence established via PubMed sweep (2026-06-21): no dual-agonist CV-outcome-trial recor... Source

Full findingNo published study has measured a direct renal effect (natriuresis, sodium handling, GFR, renal blood flow) of selective/isolating GIP-receptor agonism, GIP infusion, or GIPR antagonism in humans; renal GIP-receptor expression is sparse and the independent renal contribution of the GIP arm is unestablished. Honest gap record.

PopulationNarrative review (GIP in cardiovascular and kidney disease) attesting the absence/controversy; carries no positive attribution.

Fundingacademic / non-commercial (De Fano GIP review; no industry sponsor; disclosed)

Scope limitsanimal data; human relevance uncertain; surrogate/exploratory endpoint

GIP (native Infusion / GIP(3-30) Antagonist) MARKETED

renal No change

Low evidence

An oral sodium-load study in 10 lean healthy men found that adding 6 g NaCl to an oral glucose load selectively amplified postprandial plasma GLP-1 but did NOT change...

Asmar A et al., Physiol Rep 2020;8(15):e14519 Source

Full findingAn oral sodium-load study in 10 lean healthy men found that adding 6 g NaCl to an oral glucose load selectively amplified postprandial plasma GLP-1 but did NOT change the postprandial GIP response; the proposed acute feed-forward natriuretic gut-kidney signal was attributed to GLP-1, with GIP showing no sodium-sensitivity.

Population10 lean healthy male participants; crossover (75 g glucose + 6 g NaCl vs glucose alone).

Fundingacademic/independent analysis (manufacturer not study sponsor; per-study COI not individually audited)

Scope limitssmall sample (N~10) lean healthy men; mechanistic crossover; indirect (GIP secretion vs sodium stimulus, not a GIPR renal action)

Comparatorsglucose alone (no added NaCl)

Thin or bounded evidence here means uncertainty remains visible. It is not evidence that an effect has been ruled out.

GIP (native Infusion / GIP(3-30) Antagonist) MARKETED

heart-rate-chronotropy Increase

Low evidence

A systematic review of native GIP(1-42) administration in humans (67 studies, 30 min to 6 days) found that, among the 15% of studies reporting safety events, the most...

Helsted MM et al., Peptides 2024;177:171214 Source

Full findingA systematic review of native GIP(1-42) administration in humans (67 studies, 30 min to 6 days) found that, among the 15% of studies reporting safety events, the most frequent was a moderate and transient increase in heart rate; no correlation between achieved GIP concentration and reported events.

Populationsystematic review of 67 human native-GIP(1-42) administration studies

Fundingacademic/independent analysis (manufacturer not study sponsor; per-study COI not individually audited)

Scope limitsconference/abstract-level; surrogate/exploratory endpoint

Comparatorsplacebo

Thin or bounded evidence here means uncertainty remains visible. It is not evidence that an effect has been ruled out.

GIP (native Infusion / GIP(3-30) Antagonist) MARKETED

Insulin and beta-cell function Mixed

Low evidence

GIP is insulinotropic only at elevated glucose; the GIPR antagonist GIP(3-30)NH2 cut GIP-induced insulin secretion by 82%, confirming receptor specificity.

Gasbjerg LS et al., Diabetologia 2017 (GIP(3-30)NH2 antagonist) Source

PopulationHealthy humans and T2D (clamp/infusion studies)

Fundingacademic/independent analysis (manufacturer not study sponsor; per-study COI not individually audited)

Scope limitsReused from corpus L2-008 (antagonist), L2-010/L2-011 (PMID:21984584, glucose-dependence + glucagonotropic), L2-013 (PMID:21386059, T2D glucagon hypersecretion). Mixed direction: insulinotropic (beta) but glucagonotropic (alpha) — the GIPR islet paradox underlying the agonism-vs-antagonism debate. Individual sub-claim PMIDs carried in cross_ref notes. [CORRECTED 2026-06-20] The glucagonotropic / blunted-in-T2D claims rest on the cross-ref corpus records (L2-010/011/013), not this source.

Comparatorssaline; glucose-matched controls