Project description:The Goto-Kakizak (GK) rat, a nonobese animal model of Type 2 diabetes (T2D), were developed by repeated inbreeding of glucose-intolerent individuals selected from Wistar rats. During their development, GK rats suffer from reduced beta-cell mass and insulin resistance spontaneously (T2D phenotype), which are supposed to be caused by loci holding different genotypes between GK and Wistar rats. This array CGH experiment can detect loci which show different copy numbers (genotype) between GK and Wistar rats. These loci serve as a valuable repository for mining candidates contributing to the pathogenesis of T2D.
Project description:The Goto-Kakizak (GK) rat, a nonobese animal model of Type 2 diabetes (T2D), were developed by repeated inbreeding of glucose-intolerent individuals selected from Wistar rats. During their development, GK rats suffer from reduced beta-cell mass and insulin resistance spontaneously (T2D phenotype), which are supposed to be caused by loci holding different genotypes between GK and Wistar rats. This array CGH experiment can detect loci which show different copy numbers (genotype) between GK and Wistar rats. These loci serve as a valuable repository for mining candidates contributing to the pathogenesis of T2D. The genomic DNA taken from 3 male GK rats as 3 test samples while pooled genomic DNA from 8 male Wistar rats as the common referrence. For each of the hybridization, a dye-swap was designed as well.
Project description:MicroRNAs (miRNAs), which are a newly identified class of small single-stranded non-coding RNAs, regulate their target genes via post-transcriptional pathway. It has been proved that miRNAs play important roles in many biological processes. To better understand miRNA function with type 2 diabetes, we have used an oligonucleotide microarray to monitor miRNA expression profiles of GK and Wistar rats’ muscle. We found 7 miRNAs were down-expressed and 2 were over-expressed in the muscle of GK rats. Among them, miR-24 showed the most prominent change. P38 MAPK, which is a direct target of miR-24 also showed expression difference. All the data give a clue that miR-24 might be associated with diabetes through down regulation of p38 MAPK.
Project description:To explored the mechanism of pharmacokinetic perturbation in chronic unpredicted mild stress (CUMS) resulting depression, CUMS-induced depression animal model with spontaneous diabetic GK rats were established. The expression profile in GK rats' livers were screened using Affymetrix Rat 230 2.0 Array.
Project description:Gene expression along the crypt-villus (C-V) axis was analyzed using cryostat sectioning to isolate fractions representing the crypts (bottom) and villus tops (top). These fractions were used for analyzing gene expression in iron replete Wistar rats (++), iron deficient Wistar rats (low iron), and in iron deficient Wistar rats fed iron for 3 and 6 days (iron-fed). Differences were observed between the crypts and villus tops in the expression of genes associated with Wnt and BNP signaling, cell proliferation and apoptosis, lipid and iron transport and metabolism. Gene expression in villus crypts and tops was also compared between Wistar and Belgrade rats (bb) and Belgrade rats fed iron (iron-fed) particularly as related to iron absorption and metabolism to define the affects of the mutation in DMT1 in the Belgrade rat on the expression of genes related to iron absorption and metabolism and the response to iron feeding. Keywords: iron stress response
