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This version published online on May 22, 2007
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2007-0244
A more recent version of this article appeared on August 1, 2007
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Submitted on February 1, 2007
Accepted on May 14, 2007

Meal-stimulated glucagon release is associated with postprandial blood glucose level and does not interfere with glycemic control in children and adolescents with new onset type 1 diabetes

Sven Pörksen*, Lotte B. Nielsen, Anne Kaas, Mirjana Kocova, Francesco Chiarelli, Cathrine Ørskov, Jens J. Holst, Kenneth B. Ploug, Philip Hougaard, Lars Hansen, Henrik B. Mortensen, and the Hvidøre Study Group on Childhood Diabetes

Pediatric Department, Glostrup University Hospital, Glostrup, Denmark, Pediatric Clinic, Department of Endocrinology and Genetics, Skopje, Republic of Macedonia Clinica Pediatrica, Ospedale Policlinico, Chieti, Italy, Medical Anatomy, The Panum Institute, Copenhagen, Denmark, Medical Physiology, The Panum Institute, Copenhagen, Denmark, Department of Neurology, Glostrup University Hospital, Glostrup, Denmark, Statistics, University of Southern Denmark, Odense, Denmark, Development Projects, Novo Nordisk A/S, Bagsværd, Denmark

* To whom correspondence should be addressed. E-mail: svepor01{at}glo.regionh.dk.

Context: The role of glucagon in hyperglycemia in type 1 diabetes is unresolved and in vitro studies suggest that increasing blood glucose might stimulate glucagon secretion.

Objective: To investigate the relationship between postprandial glucose and glucagon level during the first 12 months after diagnosis of childhood type 1 diabetes.

Design: Prospective, non-interventional, 12 months follow-up study conducted in 22 centers in 18 countries.

Patients: 257 children and adolescents < 16 years with newly diagnosed type 1 diabetes. 204 completed the 12 months follow-up.

Setting: Pediatric outpatient clinic.

Main outcome measures: Residual beta cell function (C-peptide), HbA1c, blood glucose, glucagon- and GLP-1 release in response to a 90 minute meal stimulation (BOOST) at 1, 6, and 12 months after diagnosis.

Results: Compound symmetric repeated measurements models including all 3 visits showed: Postprandial glucagon increased by 17% during follow up (P=0.001). Glucagon levels were highly associated with postprandial blood glucose levels as a 10 mmol/L increase in blood glucose corresponded to 20% increase in glucagon release (p=0.0003). Glucagon levels were also associated with GLP-1 release as a 10% increase in GLP-1 corresponded to a 2% increase in glucagon release (p=0.0003). Glucagon levels were not associated (coefficient -0.21, p=0.07) with HbA1c, adjusted for insulin dose. Immunohistochemical staining confirmed the presence of Kir6.2/SUR1 in human alpha cells.

Conclusion: Our study supports the recent in vitro data showing a stimulation of glucagon secretion by high glucose levels. Postprandial glucagon levels were not associated with HbA1c, adjusted for insulin dose, during the first year after onset of childhood type 1 diabetes.




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