Low levels of glucose transporters and K+ ATP channels in human pancreatic beta cells early in development

Richardson, C .C. and Hussain, K. and Jones, P. M. and Persaud, S. and Lobner, K. and Boehm, A. and Clark, A. and Christie, Michael R. (2007) Low levels of glucose transporters and K+ ATP channels in human pancreatic beta cells early in development. Diabetologia, 50 (5). pp. 1000-1005. ISSN 0012-186X

Full content URL: http://link.springer.com/article/10.1007%2Fs00125-...

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Low levels of glucose transporters and K+ ATP channels in human pancreatic beta cells early in development

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Abstract

Aims/hypothesis: Although cells expressing insulin are detected early in human fetal development, islets isolated from fetal pancreases show poor insulin secretory responses to glucose, which may be the result of deficient glucose sensing. We have used dual and triple immunolabelling of human fetal and adult pancreas sections to investigate the presence of proteins that participate in glucose sensing in the pancreatic beta cell, namely glucose transporter 1 (GLUT 1, also known as SLC2A1), glucose transporter 2 (GLUT2, also known as SLC2A2), glucokinase (GCK) and inwardly rectifying K+ channel (KIR6.2, also known as KCNJ11) and sulphonylurea receptor 1 (SUR1, also known as ABCC8) subunits of ATP-sensitive K+ channels (K+ ATP channels). Materials and methods: Pancreases obtained with ethical approval from human fetuses from 11 to 36 weeks of gestation, from infants and from adults were formalin-fixed and embedded in paraffin. Sections were labelled with antibodies to proteins of interest. Co-production of antigens was examined by dual and triple immunolabelling. Results: GLUT2 and K+ ATP channel labelling was detected in the 11-week pancreas, but largely within the pancreatic epithelium, whereas no labelling for GLUT1 was observed. From 15 weeks, GLUT1, GCK and K+ ATP channel labelling was detected in an increasing proportion of insulin-positive cells and epithelial labelling with K+ ATP channel antibodies diminished. GLUT2 was seen in the majority of beta cells only after 7 months of age. Conclusions/ interpretation: The results demonstrate that only a subpopulation of beta cells in the human fetal pancreas produce all key elements of the glucose-sensing apparatus, which may contribute to poor secretory responses in early life. © 2007 Springer-Verlag.

Keywords:adenosine triphosphate, formaldehyde, glucokinase, glucose transporter, glucose transporter 1, glucose transporter 2, inwardly rectifying potassium channel subunit Kir6.2, paraffin, potassium channel, antibody labeling, article, cell population, development, epithelium, ethics, fetus, gestation period, glucose transport, human, human tissue, pancreas, pancreas islet beta cell, priority journal, Adult, Fetal Development, Gestational Age, Glucose Transport Proteins, Facilitative, Glucose Transporter Type 1, Glucose Transporter Type 2, Humans, Infant, Insulin-Secreting Cells, Potassium Channels, Inwardly Rectifying
Subjects:B Subjects allied to Medicine > B120 Physiology
Divisions:College of Science > School of Life Sciences
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ID Code:18121
Deposited On:31 Jul 2015 09:16

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