Introduction

Glucose-dependent insulinotropic (GIP) ^[1] is a gastric inhibitory polypeptide. It is categorized as a incretin, which is a gut-based hormone that is secreted upon the ingestion of food. It is found in K cells in the upper small intestines of humans.

History

The idea of incretin began in 1902 after the discovery of secretin by Bayliss and Starling. Inspired by their discovery, Moore et al. hypothesized that there must be some kind of gut hormone that regulates the endocrine pancreas. His experiments showed that gut extracts in patients with diabetes have reduced amounts of sugars in their urine as a result of endocrine stimulation. In 1929, a French scientist named La Barre was able to purify incretin from gut extracts. The name incretin comes from INtestine seCRETion INsulin.^[2]

Structure Overview

GIP is a G-coupled receptor. It is composed of the alpha, beta, and gamma . Function

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You may include any references to papers as in: the use of JSmol in Proteopedia ^[3] or to the article describing Jmol ^[4] to the rescue.

Function

Mechanism

The mechanism of GIP begins with the ingestion of food.

Disease

One of the most promising treatments to GIP malfunction is .

Sequence Comparison

Relevance

In GIP, the residue 2 is an but in Tirzepatide, the residue changes to

Structural highlights

Alanine converted to AIB

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