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Deletion of the gene encoding the islet-specific glucose-6-phosphatase catalytic subunit-related protein autoantigen results in a mild metabolic phenotype
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Deletion of the gene encoding the islet-specific glucose-6-phosphatase catalytic subunit-related protein autoantigen results in a mild metabolic phenotype
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Deletion of the gene encoding the islet-specific glucose-6-phosphatase catalytic subunit-related protein autoantigen results in a mild metabolic phenotype
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Journal Article
Deletion of the gene encoding the islet-specific glucose-6-phosphatase catalytic subunit-related protein autoantigen results in a mild metabolic phenotype
2007
Overview
Aims/hypothesis Islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP, now known as glucose-6-phosphatase, catalytic, 2 [G6PC2]) has recently been identified as a major autoantigen in mouse and human type 1 diabetes. Strategies designed to suppress expression of the gene encoding G6PC2 might therefore be useful in delaying or preventing the onset of this disease. However, since the function of G6PC2 is unclear, the concern with such an approach is that a change in G6PC2 expression might itself have deleterious consequences. Methods To address this concern and assess the physiological function of G6PC2, we generated G6pc2-null mice and performed a phenotypic analysis focusing principally on energy metabolism. Results No differences in body weight were observed and no gross anatomical or behavioural changes were evident. In 16-week-old animals, following a 6-h fast, a small but significant decrease in blood glucose was observed in both male (-14%) and female (-11%) G6pc2 -/- mice, while female G6pc2 -/- mice also exhibited a 12% decrease in plasma triacylglycerol. Plasma cholesterol, glycerol, insulin and glucagon concentrations were unchanged. Conclusions/interpretation These results argue against the possibility of G6PC2 playing a major role in pancreatic islet stimulus secretion coupling or energy homeostasis under physiological conditions imposed by conventional animal housing. This indicates that manipulating the expression of G6PC2 for therapeutic ends may be feasible.
Publisher
Berlin/Heidelberg : Springer-Verlag,Springer,Springer Nature B.V
Subject
/ Animals
/ Biological and medical sciences
/ Diabetes
/ Diabetes. Impaired glucose tolerance
/ Endocrine pancreas. Apud cells (diseases)
/ Etiopathogenesis. Screening. Investigations. Target tissue resistance
/ Female
/ Glucose
/ Glucose-6-Phosphatase - metabolism
/ Glucose-6-Phosphate - metabolism
/ Humans
/ Insulin
/ Islet
/ Islets of Langerhans - metabolism
/ Male
/ Mice
/ Plasma
/ Proteins
