Diabetes, obesity & metabolism · 2026
Dose-Response Effect of Glucagon on Glucose, Beta-Cell Secretion and Metabolism in Healthy Individuals.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Brock Sophie Betty, Hansen Nina Lerberg, Sturlaugsson Jóhönnuson Elvar Már, Kjeldsen Sasha Alexandra Sampson, Wewer Albrechtsen Nicolai J
Аннотация
AIM: Glucagon is a key regulator of glucose and energy metabolism, yet the dose-response effects of glucagon on markers of metabolism in humans are not fully characterised. We investigated the dose-dependent effects of glucagon on glucose metabolism, β-cell secretion and markers of hepatic metabolism in healthy adults.
MATERIALS AND METHODS: Fifteen healthy, lean adults underwent a 180-min stepwise intravenous infusion of native human glucagon at six increasing doses (0.01, 0.1, 0.5, 1, 10 and 50 ng × kg-1 × min-1). Plasma glucose, insulin, C-peptide, cyclic AMP (cAMP), non-esterified fatty acids, triglycerides, total amino acids and urea were measured repeatedly throughout the study.
RESULTS: Plasma glucose increased in a dose-dependent manner, with significant stepwise elevations observed from intermediate infusion rates and reaching peak levels at supraphysiological glucagon levels. Insulin and C-peptide levels rose markedly, reflecting β-cell activation. Plasma cAMP increased only during the highest glucagon infusion rate, despite earlier metabolic responses. Plasma non-esterified fatty acids, triglycerides and total amino acids declined at higher glucagon doses, whilst plasma urea decreased gradually from the second infusion rate onward.
CONCLUSION: Infusion of glucagon results in dose-dependent metabolic effects in healthy humans. The differential timing of glucose, lipid and amino acid responses relative to systemic cAMP elevations could be consistent with pathway-specific activation thresholds rather than uniform signalling. These findings provide new insights into human glucagon physiology with potential relevance for metabolic diseases.
MATERIALS AND METHODS: Fifteen healthy, lean adults underwent a 180-min stepwise intravenous infusion of native human glucagon at six increasing doses (0.01, 0.1, 0.5, 1, 10 and 50 ng × kg-1 × min-1). Plasma glucose, insulin, C-peptide, cyclic AMP (cAMP), non-esterified fatty acids, triglycerides, total amino acids and urea were measured repeatedly throughout the study.
RESULTS: Plasma glucose increased in a dose-dependent manner, with significant stepwise elevations observed from intermediate infusion rates and reaching peak levels at supraphysiological glucagon levels. Insulin and C-peptide levels rose markedly, reflecting β-cell activation. Plasma cAMP increased only during the highest glucagon infusion rate, despite earlier metabolic responses. Plasma non-esterified fatty acids, triglycerides and total amino acids declined at higher glucagon doses, whilst plasma urea decreased gradually from the second infusion rate onward.
CONCLUSION: Infusion of glucagon results in dose-dependent metabolic effects in healthy humans. The differential timing of glucose, lipid and amino acid responses relative to systemic cAMP elevations could be consistent with pathway-specific activation thresholds rather than uniform signalling. These findings provide new insights into human glucagon physiology with potential relevance for metabolic diseases.