Evidence reference only. Not medical advice, not a dosing guide, and not a recommendation to use any drug.
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GIP (native; Selective Acyl-GIP / CNS-Gipr-KO)

MARKETED

GIPR agonist (physiology)

1
graded findings
1
effect domains
Evidence spread
High evidence 0Moderate evidence 0Low evidence 0Very low evidence 1

GIP (native; Selective Acyl-GIP / CNS-Gipr-KO) 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; Selective Acyl-GIP / CNS-Gipr-KO) MARKETED
Appetite and food intake Decrease
Very low evidence

CNS-GIPR signalling regulates body weight and food intake: HFD-fed CNS-Gipr-KO and humanised-GIPR mice with CNS-hGIPR deletion show decreased body weight, and acute...

Zhang Q et al., Cell Metab 2021;33(4):833-844.e5 Source
Full findingCNS-GIPR signalling regulates body weight and food intake: HFD-fed CNS-Gipr-KO and humanised-GIPR mice with CNS-hGIPR deletion show decreased body weight, and acute central/peripheral acyl-GIP raises cFos in hypothalamic feeding centres coinciding with decreased food intake; the GLP-1/GIP co-agonist intake advantage is extinguished in CNS-Gipr-KO. This is the CNS-GIP appetite-suppression pole.
PopulationMice (genetic + acyl-GIP)
Fundingacademic/independent analysis (manufacturer not study sponsor; per-study COI not individually audited)
Scope limitsReused from corpus T9-GIPR-01. AGONISM pole of the GIP agonism-vs-antagonism appetite paradox. Mouse — does not license a human CNS-GIP-appetite attribution.
Comparatorsvehicle; GLP-1/GIP co-agonist