GIP Receptor

GIP receptor, which stands for gastric inhibitory polypeptide receptor, a member of the glucagon receptor family that also includes glucagon, GLP-1, GLP-2, secretin and GHRH receptors, plays a key role in glucose homeostasis and lipid metabolism. GIP is secreted particularly in response to carbohydrate- and lipid-rich meals, and exerts its effects through binding to a specific G-protein-coupled GIP receptor (GIP-R) of the glucagon–secretin family of peptides.

[Pro3]-GIP (Mouse)
[Pro3]-GIP (Rat)
GIP (human)
100040-31-1
GIP (1-39)
725474-97-5

Background


An overview of GIP receptor

Glucose dependent insulinotropic peptide (GIP) receptor, which stands for gastric inhibitory polypeptide receptor, is a member of the glucagon receptor family that also includes glucagon, GLP-1, GLP-2, secretin and growth hormone-releasing hormone (GHRH) receptors, and plays a key role in glucose homeostasis and lipid metabolism. GIP is secreted particularly in response to carbohydrate- and lipid-rich meals, and exerts its effects through binding to a specific G-protein-coupled GIP receptor (GIP-R) of the glucagon–secretin family of peptides.

Activation of GIP receptor

DA-JC1 is an agonist of GIPR. It can improve the expression of TH positive cells, and can reduce the activation of astrocytes and microglia, inhibiting the inflammatory reaction.

GIP receptor and diseases

GIP combined with GIPR in adipose tissue, which can improve the activity of lipoprotein lipase (LPL), and regulate the release of LPL. The GIP level of obese people is significantly higher than that of healthy people. Long-term nutrient excess, especially the high fat content of food will lead to the hyperplasia hypertrophy of K-cells, so that the blood circulation in the GIP level rises, promoting food storage in the body's energy. When food intake decreases, GIP secretion will decrease. GIP can activate Akt, which increases the cell membrane glucose transporter 4 (GLUI4), increases the uptake of glucose by fat cells, promotes the conversion of glucose into fatty acids and assists the deposition of fatty acids in adipose tissue. In addition, GIP has insulin-like effect on peripheral adipose cells in rats, which can increase the absorption of nutrients in the small intestine, promote the re-esterification of free fatty acids and weaken the ability of isoproterenol to decompose fat. After giving a high-fat diet and not causing obesity, fat content decreases, and energy consumption increases in GIPR gene knockout mice. These studies have suggested that the GIP/GIPR signaling pathway plays an important role in the transformation and storage of energy, lipid metabolism and the occurrence of obesity.