BSPED2013 Poster Presentations (1) (89 abstracts)
Altered plasma incretin concentrations in patients with non-typical forms of congenital hyperinsulinism
Yanqin Shi 1 , Hima B Avatapalle 2 , Mars S Skae 2 , Raja Padidela 2 , Melanie Newbould 3 , Lindsey Rigby 2 , Sarah E Flanagan 4 , Sian Ellard 4 , Jacques Rahier 5 , Peter E Clayton 6 , Indraneel Banerjee 2 , Mark J Dunne 1 & Karen E Cosgrove 1
1Faculty of Life Sciences, University of Manchester, Manchester, UK; 2Department of Paediatric Endocrinology, Royal Manchester Children’s Hospital, Manchester, UK; 3Department of Paediatric Histopathology, Royal Manchester Children’s Hospital, Manchester, UK; 4Royal Devon and Exeter NHS Foundation Trust, Peninsula College of Medicine and Dentistry, Exeter, UK; 5Department of Pathology, Cliniques Universitaires Saint Luc, Brussels, Belgium; 6Faculty of Medicine and Human Sciences, Manchester Academic Health Sciences Centre, University of Manchester, Manchester, UK.
Introduction: Congenital hyperinsulinism (CHI) may arise due to loss-of-function mutations in ABCC8 and KCNJ11 genes which encode subunits of ATP-sensitive potassium (KATP) channels. KATP channels couple nutrient metabolism with insulin secretion in pancreatic β-cells but are also located in enteroendocrine L- and K-cells and may play a role in the control of GLP-1 and GIP secretion respectively. More than 70% of patients with CHI have no identified mutations in known CHI-associated genes and this includes many patients with transient CHI which spontaneously resolves.
Aims: We hypothesized that CHI patients with KATP channel gene mutations may have altered plasma profiles of GLP-1 (7–36) and GIP compared with other groups of CHI patients.
Methods: Thirteen patients with CHI were recruited from a single referral centre. Fasting and post-prandial GLP-1 (7–36) and GIP were measured in patient plasma using ELISA. Data were compared between patients with ABCC8/KCNJ11 mutation-positive CHI (CHI-F and CHI-D, focal and diffuse, n=6), mutation-negative persistent CHI (CHI-UV, unclassified variant, n=2), and mutation-negative transient CHI (n=5) using ANOVA and post-hoc tests.
Results: Our data revealed no differences in plasma incretin concentrations between transient CHI and ABCC8/KCNJ11 mutation-positive patients, but demonstrated marked differences in plasma incretin concentrations in CHI-UV patients compared with all other groups (P<0.05).
Conclusion: These data provide evidence that measurement of plasma GLP-1 (7–36) and GIP may aid the identification and diagnosis of a novel sub-group of CHI patients, and suggest that KATP channels do not play a significant role in nutrient sensing in enteroendocrine cells.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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