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The glucose-dependent insulinotropic polypeptide (GIP) regulates body weight and food intake via CNS-GIPR signaling
How a gut hormone controls body weight and eating through brain signaling
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Abstract
HFD-fed CNS-Gipr KO mice show decreased body weight and improved glucose metabolism.
- The physiological relevance of GIPR in the central nervous system remains unclear.
- Acute administration of acyl-GIP increases neuronal activity in hypothalamic feeding centers, which is linked to reduced body weight and food intake.
- Chronic administration of acyl-GIP decreases body weight and food intake in wild-type mice but is less effective in CNS-Gipr KO mice.
- The enhanced metabolic effect of GLP-1/GIP co-agonism compared to GLP-1 alone is not observed in CNS-Gipr KO mice.
- CNS Gipr appears to play a crucial role in regulating energy metabolism.
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