Searching across hundreds of databases

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Deletion of the gene encoding the islet-specific glucose-6-phosphatase catalytic subunit-related protein autoantigen results in a mild metabolic phenotype.

Diabetologia | Apr 5, 2007

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.

Pubmed ID: 17265032 RIS Download

Mesh terms: Alleles | Animals | Autoantigens | Body Weight | Catalysis | Catalytic Domain | Female | Gene Deletion | Glucose-6-Phosphatase | Glucose-6-Phosphate | Humans | Islets of Langerhans | Male | Mice | Mice, Transgenic | Proteins

Research resources used in this publication

None found

Research tools detected in this publication

Data used in this publication

None found

Associated grants

  • Agency: NIDDK NIH HHS, Id: P60 DK020593
  • Agency: NCI NIH HHS, Id: P30 CA68485-06
  • Agency: NIDDK NIH HHS, Id: DK061645
  • Agency: NIDDK NIH HHS, Id: P30 DK57516
  • Agency: NIDDK NIH HHS, Id: DK59637
  • Agency: NIDDK NIH HHS, Id: DK076027
  • Agency: NIDDK NIH HHS, Id: P60 DK20593
  • Agency: NIDDK NIH HHS, Id: P60 DK20593-24
  • Agency: NIDDK NIH HHS, Id: DK064877
  • Agency: NIDDK NIH HHS, Id: U24 DK059637

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

This is a list of tools and resources that we have found mentioned in this publication.

National Mouse Metabolic Phenotyping Centers

The mission is to advance medical and biological research by providing the scientific community with standardized, high quality metabolic and physiologic phenotyping services for mouse models of diabetes, diabetic complications, obesity and related disorders.


View all literature mentions