Diabetes, obesity & metabolism · 2025
Glucose-dependent insulinotropic polypeptide reduces postprandial glucose excursions but does not protect from hypoglycaemia in persons with type 1 diabetes-A randomised placebo-controlled study.
СтатьяРандомизированное исследованиеНазвание и аннотация: Перевод в очереди
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Hoe Bjørn, Heimbürger Sebastian M N, Gasbjerg Lærke S, Lanng Amalie R, Lynggaard Mads B, Lund Asger B, Dela Flemming, Faber Jens, Skov-Jeppesen Kirsa, Engberg Susanne, Hartmann Bolette, Holst Jens J, Vilsbøll Tina, Christensen Mikkel B, Dejgaard Thomas F, Knop Filip K
Аннотация
AIMS: In type 1 diabetes, glucose-dependent insulinotropic polypeptide (GIP) increases glucagon secretion during low plasma glucose and improves time in the glycaemic range during daytime. To explore the glucose-stabilising potential of GIP in type 1 diabetes, we evaluated the effects of exogenous and endogenous GIP on plasma glucose excursions in a setting of excess prandial insulin and physical activity after meal ingestion.
MATERIALS AND METHODS: In a randomised, placebo-controlled, double-blind crossover design, 12 men with type 1 diabetes underwent three separate study days involving a 4.5-h continuous intravenous infusion of GIP, the GIP receptor antagonist GIP(3-30)NH2, and placebo, respectively, during which ingestion of a standardised mixed meal with subcutaneous injection of excess prandial insulin (125% of normal dose) was followed by 30 min of intermediate resistance bicycling (to increase the risk of postprandial hypoglycaemia).
RESULTS: The GIP infusion did not protect against hypoglycaemia, but compared to GIP(3-30)NH2 infusion, it attenuated postprandial maximum plasma glucose by 1.5 ± 0.5 mmol/L (mean ± standard error of the mean) (p = 0.048). GIP(3-30)NH2 did not exacerbate glucose excursions or risk of hypoglycaemia compared with placebo. The amount of glucose infused to avoid plasma glucose <2.5 mmol/L was similar on all three study days. No differences were found in C-peptide, insulin or glucagon levels.
CONCLUSION: GIP did not prevent hypoglycaemia following excess prandial insulin and physical activity after meal ingestion in males with type 1 diabetes, but it reduced peak postprandial plasma glucose compared to GIP(3-30)NH2.
MATERIALS AND METHODS: In a randomised, placebo-controlled, double-blind crossover design, 12 men with type 1 diabetes underwent three separate study days involving a 4.5-h continuous intravenous infusion of GIP, the GIP receptor antagonist GIP(3-30)NH2, and placebo, respectively, during which ingestion of a standardised mixed meal with subcutaneous injection of excess prandial insulin (125% of normal dose) was followed by 30 min of intermediate resistance bicycling (to increase the risk of postprandial hypoglycaemia).
RESULTS: The GIP infusion did not protect against hypoglycaemia, but compared to GIP(3-30)NH2 infusion, it attenuated postprandial maximum plasma glucose by 1.5 ± 0.5 mmol/L (mean ± standard error of the mean) (p = 0.048). GIP(3-30)NH2 did not exacerbate glucose excursions or risk of hypoglycaemia compared with placebo. The amount of glucose infused to avoid plasma glucose <2.5 mmol/L was similar on all three study days. No differences were found in C-peptide, insulin or glucagon levels.
CONCLUSION: GIP did not prevent hypoglycaemia following excess prandial insulin and physical activity after meal ingestion in males with type 1 diabetes, but it reduced peak postprandial plasma glucose compared to GIP(3-30)NH2.