Endocrine Abstracts (2010) 22 P142

Insulin mediates the glucagon-induced decrease in atrial natriuretic peptide: a randomized controlled trial

Ayman Arafat1, Natalia Rudovich1, Aikaterini Adamidou1, Joachim Spranger1, Martin Weickert1,2, Matthias Möhlig1 & Andreas Pfeiffer1

1Department of Endocrinology, Diabetes and Nutrition, Charité-University Medicine Berlin, Campus Benjamin Franklin, Berlin, Germany; 2Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism, University Hospitals Coventry and Warwickshire, Coventry, UK.

Objectives: Atrial natriuretic peptide (ANP) is a cardiac hormone that is known to play an essential role in regulation of blood pressure and vascular endothelial function. However, the metabolic regulation of ANP is not fully understood. In patients suffering from metabolic syndrome hypertension, hyperinsulinemia and postprandial hyperglucagonemia are common features. It was the aim of the present study to evaluate the impact of glucagon on proANP and the possible mechanisms underlying this effect.

Methods: We studied the endocrine and metabolic responses to intramuscular glucagon or placebo administration in 13 patients with type 1 diabetes mellitus (DM1) (6/7 males/females; BMI 24.8±0.95 kg/m2), in 14 lean (LS) (6/8; 21.6±0.5 kg/m2) and in 12 obese healthy subjects (OS) (6/6; 33.9±1.6 kg/m2).

Results: Age, fasting glucose, glucagon and proANP levels were comparable between groups.

Glucagon significantly decreased proANP in LS (proANP-AUC240: 205.8±2.6 (glucagon) vs 245.8±9.2 (placebo), P<0.001) and OS (203.4±4.8 vs 226.6±6.9, P<0.001) but failed to affect proANP concentrations in DM1 (P=0.737).

After glucagon administration, glucagon levels increased in all study groups and were comparable between groups. Insulin levels increased in LS and OS (P<0.001) and were comparable between both groups, whereas no significant change in insulin in DM1 was observed (P>0.05).

Conclusions: We show that glucagon significantly decreases proANP in both lean and obese healthy subjects, but fails to affect it in type 1 diabetic patients pointing out to the role of insulin in mediating this effect.

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