Glucagon receptor family in GtoPdb v.2021.3

The glucagon family of receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on the Glucagon receptor family [162]) are activated by the endogenous peptide (27-44 aa) hormones glucagon, glucagon-like peptide 1, glucagon-like peptide 2, glucose-dependent insulinotropic polypeptide (also known as gastric inhibitory polypeptide), GHRH and secretin. One common precursor (GCG) generates glucagon, glucagon-like peptide 1 and glucagon-like peptide 2 peptides [119]. For a recent review on the current understanding of the structures of GLP-1 and GLP-1R, the molecular basis of their interaction, and the associated signaling events see de Graaf et al., 2016 [89].

Prediction of early response to liraglutide therapy in patients with obesity

BACKGROUND: The main goal of treating obesity is to reduce the risk of developing its complications and comorbid diseases, which requires a steady decrease in body weight by at least 510%. In Russia in 2016, the list of drugs for the treatment of obesity was supplemented by a glucagon-like peptide 1 receptor agonist (GLP-1) liraglutide . There is evidence that about one third of patients do not achieve a clinically significant decrease in body weight during treatment with liraglutide, while the factors that predict the so-called early response to treatment are currently unknown. AIM: To identify prognostic factors of an early response to complex therapy of exogenously constitutional obesity, including agonist of GLP-1 receptors liraglutide, and to evaluate the effect of this therapy on the dynamics of levels of endogenous peptide bioregulators of eating behavior (IB). MATERIALS AND METHODS: The study included 42 patients with exogenously constitutional obesity, which were divided into 2 groups, comparable by sex, age and body mass index (BMI). The first group (n=22) received treatment recommendations for the correction of nutrition and physical activity, as well as liraglutide 3.0 mg for 3 months. The second group (n=20) received only recommendations for the correction of nutrition and physical activity. At the start and after 3 months, anthropometric characteristics and laboratory parameters were evaluated in all patients, including the levels of endogenous peptide bioregulators of IB (leptin, ghrelin, obestatin and GLP-1), their dynamics was compared between groups. Depending on the therapeutic effect, the 1st group was divided into two subgroups: those who achieved (n = 14) and did not achieve (n = 8) a clinically significant decrease in body weight. In both subgroups, baseline characteristics were analyzed as possible prognostic factors for the effectiveness of complex therapy. RESULTS: To predict an early response to complex therapy, including liraglutide, a mathematical model has been developed that is implemented as a calculator in MS Excel and contains a combination of initial body weight and fasting plasma ghrelin. The dynamics of body weight and BMI in the group of complex therapy was statistically significantly higher than that in the group of isolated lifestyle modifications (ILM). CONCLUSIONS: The proportion of individuals with an early response to 3.0 mg liraglutide therapy is comparable to that of data from randomized clinical trials. The mathematical model, which includes a combination of initial body weight and plasma ghrelin, allows predicting the likelihood of a clinically significant decrease in body weight after 3 months of using liraglutide 3.0 mg in combination with ILM with a sensitivity of 86% [65%; 97%] and prognostic value of a positive result of 80% [60%; 95%].

A novel endogenous antimicrobial peptide CAMP211-225 derived from casein in human milk

A novel endogenous peptide CAMP211-225 up-regulated in preterm milk specifically kills E. coli and Y. enterocolitica through a membrane-disrupting mechanism.

Glucagon receptor family (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

The glucagon family of receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on the Glucagon receptor family [159]) are activated by the endogenous peptide (27-44 aa) hormones glucagon, glucagon-like peptide 1, glucagon-like peptide 2, glucose-dependent insulinotropic polypeptide (also known as gastric inhibitory polypeptide), GHRH and secretin. One common precursor (GCG) generates glucagon, glucagon-like peptide 1 and glucagon-like peptide 2 peptides [116]. For a recent review on review the current understanding of the structures of GLP-1 and GLP-1R, the molecular basis of their interaction, and the signaling events associated with it, see de Graaf et al., 2016 [87].