ArticleMedical molecular morphology2006
Immunohistochemical and electron-microscopic observation of beta-cells in pancreatic islets of spontaneously diabetic Goto-Kakizaki rats.
Article in Medical molecular morphology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Vitamin D alleviates type 2 diabetes by promoting autophagy and inhibiting inflammation via the NLRP3 inflammasome pathway.Open life sciences · 2026Article
- Advanced Imaging Techniques for the Characterization of Subcellular Organelle Structure in Pancreatic Islet β Cells.Comprehensive Physiology · 2023Article
- Single-cell RNA-seq transcriptomic landscape of human and mouse islets and pathological alterations of diabetes.iScience · 2022Article
- Null mutation of the endothelin receptor type B gene causes embryonic death in the GK rat.PloS one · 2019Article
- Nkx6.1 decline accompanies mitochondrial DNA reduction but subtle nucleoid size decrease in pancreatic islet β-cells of diabetic Goto Kakizaki rats.Scientific reports · 2017Article
- Delta Cell Hyperplasia in Adult Goto-Kakizaki (GK/MolTac) Diabetic Rats.Journal of diabetes research · 2015Article
- Scanning and transmission electron microscopic observation of femoral head feeding vessels in stroke-prone spontaneously hypertensive rats.Medical molecular morphology · 2011Article
- Article
- Reduction of retinaldehyde dehydrogenase 1 expression and production in estrogen-induced prolactinoma of rat.Medical molecular morphology · 2008Article
- Increased pancreatic islet mass is accompanied by activation of the insulin receptor substrate-2/serine-threonine kinase pathway and augmented cyclin D2 protein levels in insulin-resistant rats.International journal of experimental pathology · 2008Article
- Fetal and neonatal nicotine exposure in Wistar rats causes progressive pancreatic mitochondrial damage and beta cell dysfunction.PloS one · 2008Article
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Authors and funding
6 authors.
Funding
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Abstract
The Goto-Kakizaki (GK) rat offers a genetic model of type 2 diabetes and displays profoundly defective insulin secretion leading to basal hyperglycemia. This animal is widely used for studying type 2 diabetes. However, the morphological characteristics of the pancreatic islets of Langerhans in GK rats are not fully understood. The present study sought to clarify this issue using immunohistochemical and electron microscopic techniques. GK rats were killed at 7, 14, 21, and 35 weeks of age. Structural islet changes were not observed at 7 weeks old. At 14 and 21 weeks of age, GK rats displayed histopathological islet changes. The general shape of islets became irregular, and immunoreaction of beta-cells against antiinsulin appeared diffusely weakened. Electron microscopy revealed that the numbers of so-called beta-granules decreased and the numbers of immature granules increased. The Golgi apparatus of beta-cells was developed and the cisternae of rough endoplasmic reticulum were often dilated, indicating hyperfunction of the cells. However, at 35 weeks old, immunoreactivities of dispersed beta-cells into the exocrine portion recovered, and numbers of secretory granules increased again and features of the cell organelles did not display hyperfunction. These results suggest that insulin deficiency in GK rats is not caused by simple dysfunction and/or degeneration of beta-cells but rather by more complicated events within cells.
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