ArticleFrontiers in genetics2018
Integrative Analysis of Genome and Expression Profile Data Reveals the Genetic Mechanism of the Diabetic Pathogenesis in Goto Kakizaki (GK) Rats.
Article in Frontiers in genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 8 citations in OpenAlex.
- Histopathological and Transcriptomic Alterations in Metabolic Organs: A Case Study from a Spontaneously Diabetic Rhesus Macaque.International journal of molecular sciences · 2026Article
- DNA methylation in the association between pesticide exposures and type 2 diabetes.World journal of diabetes · 2025Article
- Unveiling disulfidptosis-linked lncRNA signatures: insights into the immune microenvironment and drug responsiveness in oral squamous cell carcinoma.Frontiers in genetics · 2025Article
- Identification of key ubiquitination-related genes in gestational diabetes mellitus: A bioinformatics-driven study.Health science reports · 2024Article
- Article
- Identification of reference genes for real-time polymerase chain reaction gene expression studies in Nile rats fed Water-Soluble Palm Fruit Extract.Molecular biology reports · 2020Article
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7 authors at 1 institution in 1 country.
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Abstract
The Goto Kakizaki (GK) rats which can spontaneously develop type 2 diabetes (T2D), are generated by repeated inbreeding of Wistar rats with glucose intolerance. The glucose intolerance in GK rat is mainly attributed to the impairment in glucose-stimulated insulin secretion (GSIS). In addition, GK rat display a decrease in beta cell mass, and a change in insulin action. However, the genetic mechanism of these features remain unclear. In the present study, we analyzed the population variants of GK rats and control Wistar rats by whole genome sequencing and identified 1,839 and 1,333 specific amino acid changed (SAAC) genes in GK and Wistar rats, respectively. We also detected the putative artificial selective sweeps (PASS) regions in GK rat which were enriched with GK fixed variants and were under selected in the initial diabetic-driven derivation by homogeneity test with the fixed and polymorphic sites between GK and Wistar populations. Finally, we integrated the SAAC genes, PASS region genes and differentially expressed genes in GK pancreatic beta cells to reveal the genetic mechanism of the impairment in GSIS, a decrease in beta cell mass, and a change in insulin action in GK rat. The results showed that
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