Control

The impairment in insulin secretory responses to glucose (betacell function) in Late-Onset Autoimmune Diabetes (LADA) and Type 2 diabetes (T2) are presumed to have different aetiologies. Whether the stimulation of insulin secretion by Glueagori-like PeptideI (7-36 amide) (GLP-1), diffes in these two groups is not known . We have investigated the stimulation of C-peptide secretion by GLP-1 in 12 LADA (islet cell antibody titre > 5 or glutamic acid decarboxylase antibody titre >20) and 12 matched T2 patients, mean (SO) age 62 (6) and 59 (6) years, BMI 32.4 (7.2) and 35.0 (6.9) kg.m'2 , in LADA and T2 respectively, with 2 sulphonylurea vs I 0 insulin treated in each group. Subject~ had two stepped 90 min 5 mmol.rt and 90 min 13 mmol.l' 1 hyperglycaemic clamps with infusions of 1.2 pmol.kg·'.min·' GLP-1 or saline. RESULTS: The plasma C-peptide responses at 5 mmol.l'1 and 13 mmol.l' 1 during GLP-1 infusion correlated with those during saline infusion, Spearman Rank Rs = 0.91 and 0.96, in LADA and 0.92 and 0.85 in T2 respectively (all p<O.OOO I). The regression slopes were similar (p=0.7), with common slopes of2.1 (SE 0.3) and 3.0 (SE 0.5) i.e. GLP-1 stimulated secretion two fold and three fold at5 and 13 mmol.l'1, respectively. CONCLUSIONS: GLP-1 amplifies beta-cell response similarly in LADA and Type 2 diabetic patients, with moderate to severe levels of .beta-cell dysfunction.