GLP-1 agonists
Antidiabetic Drugs

Author: Gianpiero Pescarmona
Date: 06/02/2016

Description

Dulaglutide Semaglutide Liraglutide are long-acting glucagon-like peptide-1 agonists (GLP-1 agonist an incretin)

GLP-1 exerts its main effect by stimulating glucose-dependent insulin release from the pancreatic islets. It has also been shown to slow gastric emptying, inhibit inappropriate post-meal glucagon release, and reduce food intake (table 1 and figure 1)

GLP-1 origin

Is the physiological release of GLP-1 associated to equimolar release of Glucagone?

Protein Aminoacids Percentage : INSULIN & GLUCAGON

Comments
2023-04-18T20:47:48 - Gianpiero Pescarmona

Minireview: Glucagon-Like Peptides Regulate Cell Proliferation and Apoptosis in the Pancreas, Gut, and Central Nervous System, 2004

GLP-1 o i suoi analoghi stabili aumentano la sintesi e il rilascio di insulina.

L'insulina non è solo un ormone che stimola l'entrata del glucoso nelle cellule muscolari, ma è anche un potente induttore della proliferazione cellular.
Nel diabete di Tipo II, caratterizzato da insulino resistenza dipendente dal calo di ormoni sessuali da andro/menopausa, si ha un iperinsulinismo e un aumento della frequenza dei tumori rispetto ad una popolazione analoga non diabetica.

glucagon+and+cell+proliferation

GIP Gastric inhibitory polypeptide

Potent stimulator of insulin secretion and relatively poor inhibitor of gastric acid secretion.

Interrupted Glucagon Signaling Reveals Hepatic α Cell Axis and Role for L-Glutamine in α Cell Proliferation, 2017

  • Decreasing glucagon action lowers the blood glucose and may be useful therapeutically for diabetes. However, interrupted glucagon signaling leads to α cell proliferation. To identify postulated hepatic-derived circulating factor(s) responsible for α cell proliferation, we used transcriptomics/proteomics/metabolomics in three models of interrupted glucagon signaling and found that proliferation of mouse, zebrafish, and human α cells was mTOR and FoxP transcription factor dependent. Changes in hepatic amino acid (AA) catabolism gene expression predicted the observed increase in circulating AAs. Mimicking these AA levels stimulated α cell proliferation in a newly developed in vitro assay with L-glutamine being a critical AA. α cell expression of the AA transporter Slc38a5 was markedly increased in mice with interrupted glucagon signaling and played a role in α cell proliferation. These results indicate a hepatic α islet cell axis where glucagon regulates serum AA availability and AAs, especially L-glutamine, regulate α cell proliferation and mass via mTOR-dependent nutrient sensing.
Attachments
fileuserdate
GIP_et_al_ch1.pnggp31/03/2024
GIP_et_al_ch2.pnggp31/03/2024
INS_GLUC_CH1B.pnggp18/03/2023
INS_GLUC_CH2.pnggp18/03/2023
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