Project description:This SuperSeries is composed of the following subset Series: GSE17058: MiRNA expression in adipose tissue and liver from a spontaneous rat model of Type 2 diabetes GSE17059: Gene expression in adipose tissue and liver from a spontaneous rat model of Type 2 diabetes Refer to individual Series
Project description:MicroRNAs (miRNAs) are non-coding RNA molecules involved in post-transcriptional control of gene expression of a wide number of genes, including those involved in glucose homeostasis. Type 2 diabetes (T2D) is characterized by hyperglycaemia and defects in insulin secretion and action at target tissues. Using a miRNA microarray platform, we sought to establish differences in miRNA expression in two insulin-target tissues (liver and adipose tissue) from seven-month-old spontaneously diabetic (Goto-Kakizaki [GK]) and non-diabetic (Brown-Norway [BN]) rats. MiRNA data were integrated with gene expression data from the same rats to investigate how differentially expressed miRNAs affected the expression of their predicted target genes. Two-colour experiment comparing GK and BN rat strains for two different tissues. Biological replicates: 4 GK and 4 BN rats; adipose tissue and liver extracted from each rat. Two samples were hybridised to each array (one of each strain, same tissue)
Project description:To evaluate functional consequences of insulin-deficient diabetes mellitus for adipose tissue, we used a genetically engineered pig model of mutant INS gene induced diabetes of youth (MIDY). Adipose tissue samples of MIDY pigs and wild-type (WT) littermate controls were analyzed by label-free proteomics to reveal pathways and key drivers significantly affected by chronic insulin deficiency and hyperglycemia.
Project description:Fat metabolism is also peturbed after the diagnosis of type 1 diabetes. Patients have less fat in the liver (4) and increased fasting lipid oxidation (5) compared to controls. Similarly, in a BioBreeding rat model of type 1 diabetes, the diabetes-prone animals develop a reduced respiratory quotient compared to non-diabetic rats before the onset of hyperglycemia, consistent with an increased use of fatty acids relative to carbohydrates as an energy substrate (6). We hypothesized that a lack of insulin reaching the liver contributes to the metabolic shift towards lipid oxidation observed in humans with type 1 diabetes and rodent models of the disease. To test our hypothesis, we measured changes in the hepatic gene expression and serum metabolome of a BioBreeding rat model of type 1 diabetes before and after the onset of hyperglycemia.
Project description:Obesity is a strong risk factor for the development of type 2 diabetes. We have previously reported that in adipose tissue of obese (ob/ob) mice, the expression of adipogenic genes is decreased. When made genetically obese, the BTBR mouse strain is diabetes susceptible and the C57BL/6J (B6) strain is diabetes resistant. We used DNA microarrays and RT-PCR to compare the gene expression in BTBR-ob/ob versus B6-ob/ob mice in adipose tissue, liver, skeletal muscle, and pancreatic islets. Our results show: 1) there is an increased expression of genes involved in inflammation in adipose tissue of diabetic mice; 2) lipogenic gene expression was lower in adipose tissue of diabetes-susceptible mice, and it continued to decrease with the development of diabetes, compared with diabetes-resistant obese mice; 3) hepatic expression of lipogenic enzymes was increased and the hepatic triglyceride content was greatly elevated in diabetes-resistant obese mice; 4) hepatic expression of gluconeogenic genes was suppressed at the prediabetic stage but not at the onset of diabetes; and 5) genes normally not expressed in skeletal muscle and pancreatic islets were expressed in these tissues in the diabetic mice. We propose that increased hepatic lipogenic capacity protects the B6-ob/ob mice from the development of type 2 diabetes. Diabetes 52:688–700, 2003 Keywords: Genetic modifications
Project description:Functional enrichment analysis of differentially expressed genes reveals alteration of visceral adipose tissue resembling type 2 diabetes signatures in a mouse model of Friedreich’s ataxia
