Long before GLP-1 became a household name, researchers noticed something odd: glucose taken by mouth triggers a much larger insulin response than the same amount of glucose delivered straight into a vein. The gut, it seemed, was sending its own signal to the pancreas.
A century-old idea
The concept of gut hormones dates to 1902, when William Bayliss and Ernest Starling described secretin. In 1932 the Belgian physiologist Jean La Barre coined the term “incretin” for a gut factor that lowers blood sugar. When reliable insulin assays arrived in the 1960s, the oral versus intravenous glucose experiments put hard numbers behind the idea, which became known as the incretin effect.
From GIP to the proglucagon gene
The first incretin identified was GIP (glucose-dependent insulinotropic polypeptide) in the 1970s. The second came from molecular biology. In the early 1980s, cloning of the proglucagon gene revealed that it encodes more than glucagon. It also carries two related sequences, later named glucagon-like peptide-1 and glucagon-like peptide-2.
Finding the active form
Work in the mid-1980s, including research by Svetlana Mojsov and Joel Habener in Boston and by Jens Juul Holst in Copenhagen, showed that a truncated form of GLP-1 strongly stimulates insulin release in a glucose-dependent way. Daniel Drucker and others helped map its wider biology, including effects on glucagon, gastric emptying and appetite.
The catch: a two-minute half-life
Natural GLP-1 is broken down by the enzyme DPP-4 within minutes, which made it nearly useless as a drug on its own. Solving that problem became the next chapter of the story. In 2024, Habener, Mojsov and Novo Nordisk scientist Lotte Bjerre Knudsen received the Lasker-DeBakey Clinical Medical Research Award for their roles in the discovery and development of GLP-1 based medicines.
This article is for educational purposes only and is not medical advice. Products sold by Cacti Research Solutions are for research/laboratory use only.
Leave a Reply