Secretion of incretin hormones in people having risk factors for type 2 diabetes mellitus
Autor: | E A Shestakova, A V Il'in, M V Shestakova, I I Dedov |
---|---|
Jazyk: | ruština |
Rok vydání: | 2014 |
Předmět: | |
Zdroj: | Терапевтический архив, Vol 86, Iss 10, Pp 10-14 (2014) |
Druh dokumentu: | article |
ISSN: | 0040-3660 2309-5342 |
Popis: | AIM. To study the secretion of glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and glucagon-like peptide 2 (GLP-2) in response to a carbohydrate load in people with risk factors for type 2 diabetes mellitus (DM2) in relation to the type of carbohydrate metabolic disturbances and age. MATERIALS AND METHODS. One hundred and twenty-seven patients having DM2 risk factors who had not previously received glucose-lowering therapy underwent an oral glucose tolerance test (OGTT). The plasma levels of glucose, insulin, glucagon, GLP-1, GIP, and GLP-2 were determined at 0, 30, and 120 minutes of the test. RESULTS. According to the findings, the patients were divided into 3 groups: 1) normal glucose tolerance; 2) prediabetic states (impaired glucose tolerance and/or impaired fasting glycemia); 3) new-onset DM2. OGTT showed that the secretion of GLP-1 was lower and that of GIP and GLP-2 was higher in patients with DM2. GLP-1 secretion decreased with patient age. CONCLUSION. During OGTT, there is a statistically significantly difference in the secretion of incretin hormones in persons with varying degrees of carbohydrate metabolic disturbances: the peak GLP-1 secretion is the highest in healthy individuals and lowest in the patients with DM2; on the contrary, the peak GLP2 and GIP secretions are the highest in the patients with DM2. This may suggest that GLP-1 and the two other hormones (GLP-2 and GIP) show opposite effect in the regulatory mechanisms of carbohydrate metabolism. GLP-1 secretion is decreased with age, which may be one of the reasons for the higher prevalence of DM2 among the elderly. |
Databáze: | Directory of Open Access Journals |
Externí odkaz: |