ArticleDiabetologia2007
Defective IGF2 and IGF1R protein production in embryonic pancreas precedes beta cell mass anomaly in the Goto-Kakizaki rat model of type 2 diabetes.
Article in Diabetologia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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31 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
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- Epidemiological Investigation of Type 2 Diabetes and Alzheimer's Disease in a Pakistani Population.International journal of environmental research and public health · 2018Article
- IGF2 stimulates fetal growth in a sex- and organ-dependent manner.Pediatric research · 2018Article
- Comparison of Goto-Kakizaki rats and high fat diet-induced obese rats: Are they reliable models to study Type 2 Diabetes mellitus?PloS one · 2017Article
- The association of soluble IGF2R and IGF2R gene polymorphism with type 2 diabetes.Journal of diabetes research · 2015Article
- Effects of genetics and in utero diet on murine pancreatic development.The Journal of endocrinology · 2014Article
- Defective prolactin signaling impairs pancreatic β-cell development during the perinatal period.American journal of physiology. Endocrinology and metabolism · 2013Article
- Transcription factor ZBED6 affects gene expression, proliferation, and cell death in pancreatic beta cells.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- A euglycaemic/non-diabetic perinatal environment does not alleviate early beta cell maldevelopment and type 2 diabetes risk in the GK/Par rat model.Diabetologia · 2013Article
- Fine-mapping diabetes-related traits, including insulin resistance, in heterogeneous stock rats.Physiological genomics · 2012Article
- Transgenerational glucose intolerance with Igf2/H19 epigenetic alterations in mouse islet induced by intrauterine hyperglycemia.Diabetes · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisThe Goto-Kakizaki (GK) rat is a spontaneous model of type 2 diabetes. Defective beta cell mass detectable in late fetal age precedes the onset of hyperglycaemia. Our hypothesis was that an embryonic IGF production deficiency might be involved in beta cell mass anomaly in the diabetic GK rat. To test this, we evaluated during pancreatic organogenesis: (1) the beta cell development in GK rats on embryonic day (E) 13.5 and E18.5; (2) IGF2 and IGF1 receptor (IGF1R) pancreatic protein production on E13.5 and E18.5; (3) the in vitro development of GK pancreatic rudiment on E13.5; and (4) the in vitro effect of IGF2 addition on beta cell mass. MATERIALS AND
methodsBeta cell quantitative analyses were determined by immunohistochemistry and morphometry. IGF2 and IGF1R pancreatic protein production was evaluated using western blot analyses. Dorsal pancreatic rudiments were dissected on E13.5, separated from surrounding mesenchyme and cultured for 7 days without or with recombinant IGF2.
resultsWhile beta cell mass was already decreased on E18.5, the differentiation of the first beta cells was in fact normal in E13.5 GK pancreas. Moreover, defective IGF2 and IGF1R protein production was detected in GK pancreatic rudiment as early as E13.5. The isolated GK pancreatic rudiment as maintained in vitro mimics the GK beta cell deficiency observed in vivo. This last approach enabled us to show that GK beta cells were fully responsive to IGF2 as far as their net growth is concerned. CONCLUSIONS/
interpretationIn diabetic GK rat, defective IGF2 and IGF1R protein production in embryonic pancreas precedes beta cell mass anomaly. IGF2 supplementation expands the pool of beta cells.
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