GLP-1 secretion by human enteroendocrine NCI-H716 cells is augmented in a dose-dependent manner by the addition of CPE.

METHODS: Human type II lung cells were incubated with GLP-1(7-36)amide (1-1000 nM). 3-isobutyl-1-methylxanthine (0.5 mM) was present during incubation to prevent cAMP hydrolysis. 24 After 1 hour, remove the culture medium and add 1 ml of cold ethanol to lyse the cells. After 1 hour of incubation at 4°C, the wells are scraped and the suspension is centrifuged at 10,000 × g for 10 minutes. The supernatant is removed and evaporated under vacuum. The residues were dissolved in assay buffer and cAMP was measured using a competition binding assay kit (Radiochemistry Center).
RESULTS GLP-1(7-36)amide increased cAMP concentration in human type II pneumocytes in a concentration-dependent manner, both in the short and long term. [2]

METHODS: Tail vein blood samples were collected from male mice each time 5 minutes before glucose infusion. After glucose infusion, GLP-1(7-36)amide [0.3-10 μ mol, intraventricular (i.c.v)] or normal saline (5 μl) was administered. , i.c.v).
RESULTS GLP-1(7-36)amide (0.3-10 nmol, i.c.v) dose-dependently reduced the blood glucose AUC0-50 value by 32.6%. [1]
METHODS: A 390-minute intravenous infusion of GLP-1-(7-36)amide was studied in 14 healthy volunteers. After 30 minutes, a solid test meal was provided, and gastric emptying was assessed. Blood was drawn for GLP-1 (total and intact), glucose, insulin, C-peptide, and glucagon measurements.
RESULTS Administration of GLP-1-(7-36)amide significantly increased total GLP-1 plasma levels. During infusion of GLP-1-(7-36)amide, plasma concentrations of intact GLP-1 increased to 21 +/- 5 pmol/l. GLP-1-(7-36)amide reduced fasting and postprandial glucose concentrations (P < 0.001) and delayed gastric emptying (P < 0.001). GLP-1-(7-36)amide reduces glucagon levels. [3]