gastric inhibitory polypeptide

GIP (3-42), human (Gastric Inhibitory Polypeptide (3-42) (human)) is a peptide that acts as a glucose-dependent proinsulinotropic polypeptide (GIP) receptor antagonist and regulates insulin secretion and the metabolic effects of GIP in vivo, which can be used to study type 2 diabetes.

Gastric Inhibitory Polypeptide (1-30), porcine, deficient in the 12 C-terminal amino acids of the natural gastric inhibitory polypeptide (GIP), demonstrates biological activity by enhancing the release of insulin and somatostatin [1].

Gastric Inhibitory Polypeptide (6-30) amide (human) is an incretin hormone used in diabetes research [1].

GIP (1-30) amide, porcine TFA is a high-affinity full agonist of the glucose-dependent insulinotropic polypeptide (GIP) receptor, with potency comparable to native GIP(1-42) [1]. It also exhibits potent insulin-stimulating properties and weakly inhibits gastric acid secretion.

[Tyr0] Gastric Inhibitory Peptide (23-42), human, is a glucose-dependent insulinotropic polypeptide (GIP) that modestly inhibits gastric acid secretion while enhancing insulin secretion, making it relevant for research on diabetes and obesity [1] [2].

Gastric Inhibitory Peptide (porcine), also known as a glucose-dependent insulinotropic polypeptide, is a 42-amino acid intestinal hormone that influences fat and glucose metabolism [1].

Acetyl Gastric Inhibitory Peptide (human), a fatty acid-derivatized analog of glucose-dependent insulinotropic polypeptide, exhibits enhanced antihyperglycemic and insulinotropic characteristics. This compound is utilized in diabetes, insulin resistance, and obesity research [1] [2] [3].

Acetyl Gastric Inhibitory Peptide (human) TFA, a fatty acid-derivatized analog of the glucose-dependent insulinotropic polypeptide, exhibits enhanced antihyperglycemic and insulinotropic properties. It is utilized in the research of diabetes, insulin resistance, and obesity [1] [2] [3].

GIP, rat TFA (glucose-dependent insulinotropic polypeptide), a 42-amino acid peptide secreted by K cells in the duodenum and jejunum, promotes insulin release from pancreatic beta cells, supports beta cell proliferation, and enhances their survival. This rat-origin bioactive peptide, along with GLP (gastric-like peptide), belongs to the intestinal insulinotropic hormone family and is implicated in lipid homeostasis and potentially in the pathogenesis of obesity. Recent research suggests GIP's multifaceted role in these metabolic processes.

GIP (rat) (Glucose-dependent Insulinotropic Polypeptide), also known as Gastric Inhibitory Polypeptide, is a biologically active 42-amino acid peptide secreted by the K cells of the duodenum and jejunum following food consumption. It belongs to the incretin hormone peptide family, which includes GLP (Gastric-like Peptide), and it not only stimulates insulin release from pancreatic islet β-cells but also may encourage β-cell proliferation and survival. Additionally, recent research indicates GIP may have a role in lipid regulation and could contribute to the development of obesity.