GIP
Glucose-Dependent Insulinotropic Polypeptide
An incretin hormone secreted by K-cells in the small intestine that potentiates glucose-stimulated insulin secretion, promotes fat storage, and modulates bone metabolism. GIP receptor agonism is a key component of tirzepatide's dual mechanism.
Mechanism of Action
GIP binds GIPR on pancreatic beta cells, potentiating glucose-stimulated insulin release via cAMP-PKA signaling. In adipose tissue, GIP promotes lipogenesis and fat storage. In bone, GIP has anabolic effects. The combination of GIP and GLP-1 receptor agonism (as in tirzepatide) produces superior weight loss compared to GLP-1 alone.
Health Claims & Evidence
Potentiates glucose-stimulated insulin secretion
Synergistic weight loss when combined with GLP-1 agonism
Anabolic effects on bone metabolism
Short-Term Effects
Improved postprandial glucose control and reduced appetite.
Long-Term Effects
Sustained weight loss and glycemic improvement with tirzepatide formulation.
Side Effects
Nausea, vomiting, diarrhea (as tirzepatide). Generally well-tolerated.
Contraindications
Personal or family history of medullary thyroid carcinoma, MEN2.
This profile is provided for educational research only. It is not a treatment recommendation or dosing guide. Human evidence, safety information and regulatory status vary by substance. Verify primary sources and consult a qualified healthcare professional for medical decisions.
Research Papers
GIP and GLP-1 in type 2 diabetes
Nauck et al. · Nature Reviews Endocrinology · 2021
Educational research only. This profile is not a treatment recommendation or dosing guide. Human evidence, safety information and regulatory status vary by substance. Consult a qualified healthcare professional for medical decisions.
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