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Molecular mechanisms of protein induced hyperinsulinaemic hypoglycaemia

World Journal of Diabetes 2014年第5期5卷 666-677页

作者： suresh chandran Fabian Yap Khalid Hussain Department of Neonatology KK Women’s and Children’s Hospital Singapore 229899 Singapore Yong Loo Lin School of Medicine National University of Singapore Singapore 117598 Singapore Duke-NUS Graduate Medical School Singapore 169857 Singapore Lee Kong Chian School of Medicine Nanyang Technological University Singapore 308232 Singapore Department of Paediatric Endocrinology KK Wom-en’s and Children’s Hospital Singapore 229899 Singapore Departments of Paediatric Endocrinology Great Ormond Street Hospital for Children NHS Foundation Trust London WC1N 3JH United Kingdom Developmental Endocrinology Research Group Molecular Genetics Unit Institute of Child Health University College London London WC1N 1EH United Kingdom

The interplay between glucose metabolism and that of the two other primary nutrient classes, amino acids and fatty acids is critical for regulated insulin secretion. Mitochondrial metabolism of glucose, amino acid and fatty acids generates metabolic coupling factors(such as ATP, NADPH, glutamate, long chain acyl-CoA and diacylglycerol) which trigger insulin secretion. The observation of protein induced hypoglycaemia in patients with mutations in GLUD1 gene, encoding the enzyme glutamate dehydrogenase(GDH) and HADH gene, encoding for the enzyme short-chain 3-hydroxyacyl-CoA dehydrogenase has provided new mechanistic insights into the regulation of insulin secretion by amino acid and fatty acid metabolism. Metabolic signals arising from amino acid and fatty acid metabolism converge on the enzyme GDH which integrates both signals from both pathways and controls insulin secretion. Hence GDH seems to play a pivotal role in regulating both amino acid and fatty acid metabolism.

关键词： Hyperinsulinaemic hypoglycaemia KATP channel Glutamate dehydrogenase Hyperinsulinism/Hyperammonaemia syndrome Short-chain-3-hydroxyacyl-CoA dehydrogenase Glutamine

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