Salivary Transcriptomic Biomarkers for Insulin Resistance
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE67738 | GEO | 2015/04/10
SECONDARY ACCESSION(S): PRJNA280775
REPOSITORIES: GEO
Similar Datasets
Project description:We have performed gene expression microarray analysis to profile transcriptomic signatures between insulin resistance high risk subjects and insulin resistance low risk subjects Participants enrolled in this study were recruited in the overnight fasted state, then the collection and processing of glucose (fasting, 30, 60 and 120 minutes) and insulin from blood samples, hemoglobin A1c (HbA1c) , assessment of medical history, socio-demographic characteristics, lifestyle factors, blood pressure and anthropometric and body composition measurements were conducted. During baseline visit, participants were asked to refrain from eating, drinking and oral hygiene procedures for at least 1-hour prior to saliva collection.5 ml of unstimulated whole saliva samples were consistently collected, stabilized and preserved, the sample supernatants were reserved at -80°C prior to assay. Based on the homeostasis model assessment of insulin resistance (HOMA-IR), using the formula [HOMA-IR= (fasting glucose*fasting insulin)/405], participants were divided into 2 groups: IR high risk group (HOMA-IR value ?2.5) and IR low risk group (HOMA-IR value <2.5). Total RNA was extracted from saliva and subjected to gene expression microarray analysis using Affymetrix human genome 2.0 plus array
2015-04-10 | E-GEOD-67738 | biostudies-arrayexpress
Project description:Insulin resistance, the defective regulation of glucose metabolism by insulin, increases the risk of type 2 diabetes and cardiovascular disease. It is not yet known how insulin resistance remodels signalling networks in human tissues. Here, we define the signalling architecture of insulin resistance in skeletal muscle. We measured phenotypes and phosphoproteomes of insulin resistant and insulin sensitive subjects as they responded to exercise and an insulin infusion, quantifying more than 26,000 phosphosites in 114 skeletal muscle biopsies. Incorporating a temporal component to personalised phosphoproteomics identified signalling linked with the range of insulin sensitivity across the participants.
2024-11-22 | PXD032948 | Pride
Project description:Cellular and tissue defects associated with insulin resistance are coincident with transcriptional abnormalities and are improved after insulin sensitization with thiazolidinedione (TZD) PPARγ ligands. We transcriptionally profiled 364 biopsies gathered from 72 human subjects harvested before and after hyperinsulinemic-euglycemic clamp, at baseline and after three-month TZD treatment. Subjects range from insulin-sensitive to insulin-resistant. Insulin resistant subjects responded to TZD treatment with varied improvements in insulin sensitivity, thus they were ranked by their degree of TZD response to define responder and non-responder subgroups.
2010-05-17 | GSE13070 | GEO
Project description:Cellular and tissue defects associated with insulin resistance are coincident with transcriptional abnormalities and are improved after insulin sensitization with thiazolidinedione (TZD) PPAR? ligands. We transcriptionally profiled 364 biopsies gathered from 72 human subjects harvested before and after hyperinsulinemic-euglycemic clamp, at baseline and after three-month TZD treatment. Subjects range from insulin-sensitive to insulin-resistant. Insulin resistant subjects responded to TZD treatment with varied improvements in insulin sensitivity, thus they were ranked by their degree of TZD response to define responder and non-responder subgroups. Skeletal muscle biopsies were obtained from vastus lateralis before and after hyperinsulinemic-euglycemic clamp, at baseline and after three-month TZD treatment. Adipose tissue biopsies were obtained from abdominal subcutaneous before clamp, at baseline and after three-month TZD treatment. *** CEL files not provided for 40 Samples. ***
2010-05-17 | E-GEOD-13070 | biostudies-arrayexpress
Project description:We aim to identify a novel pathway to regulate insulin resistance from transcriptional profiles of skeletal muscles from patients with diabetes and to demonstrate its role in experimental models of insulin resistance. We performed transcriptional profiling of skeletal muscles from subjects with or without diabetes. Through an integrative analysis of our dataset with four previous datasets, we identified the core gene sets associated with insulin resistance.
2015-09-01 | E-MTAB-3420 | biostudies-arrayexpress
Project description:We have developed novel molecular methodology utilizing a stool sample, which contains intact sloughed colon cells, in order to quantify colonic gene expression profiles. In this study, our goal was to identify diagnostic gene sets (combinations) for the noninvasive classification of different phenotypes. For this purpose, the effects of a legume enriched, low glycemic index, high fermentable fiber diet was evaluated in subjects with four possible combinations of risk factors, including insulin resistance (IR) and a history of adenomatous polyps. In a randomized crossover design controlled feeding study each participant (a total of 23, 5-12/group) consumed the experimental diet (1.5 cups of cooked dry beans) and a control diet (isocaloric average American diet) for 4 wk with a 3 wk washout period between diets. Using prior biological knowledge, the complexity of feature selection was reduced in order to perform an exhaustive search on all allowable feature (gene) sets of size 3, and among these, 27 had (unbiased) error estimates of 0.15 or less. Linear discriminant analysis (LDA) was successfully used to identify the best single genes and two- to three-gene combinations for distinguishing subjects with IR, a history of polyps or exposure to a chemoprotective legume-rich diet. These results support our premise that gene products (RNA) isolated from stool have diagnostic value in terms of assessing colon cancer risk. Keywords: Exfoliated cells, legumes, insulin resistance, polyps
2010-02-11 | GSE14797 | GEO
Project description:Postoperative insulin resistance refers to the phenomenon that the body’s glucose uptake stimulated by insulin is reduced due to stress effects such as trauma or the inhibitory effect of insulin on liver glucose output is weakened after surgery.
There is a clear link between postoperative insulin resistance and poor perioperative prognosis. Therefore, exploring interventions to reduce postoperative stress insulin resistance, stabilize postoperative blood glucose, and reduce postoperative complications are clinical problems that need to be solved urgently. In recent years, research on branched-chain amino acids and metabolic diseases has become a hot spot. Studies have found that in the rat model, preoperatively given a high branched-chain amino acid diet can inhibit postoperative insulin resistance and stabilize blood glucose levels. This research plan is to try to add branched-chain amino acids before surgery to observe the occurrence of postoperative insulin resistance in patients.
| 2744698 | ecrin-mdr-crc
Project description:Global transcript profiling to identify differentially expressed skeletal muscle genes in insulin resistance, a major risk factor for Type II (non-insulin-dependent) diabetes mellitus. Compared gene expression profiles of skeletal muscle tissues from 18 insulin-sensitive versus 17 insulin-resistant equally obese, non-diabetic Pima Indians. Keywords: other
2002-12-17 | GSE121 | GEO
Project description:Insulin resistance is considered to be a pathogenetic mechanism in several and diverse diseases (e.g. type 2 diabetes, atherosclerosis) often antedating them in apparently healthy subjects. The aim of this study was to investigate whether IR per se is characterized by a specific pattern of gene expression. We analyzed the transcriptomic profile of peripheral blood mononuclear cells in two groups (10 subjects each) of healthy individuals, with extreme insulin resistance or sensitivity, matched for BMI, age and gender, selected within the MultiKnowledge Study cohort (n=148). Data were analyzed with an ad-hoc rank-based classification method. 321 genes composed the gene set distinguishing the insulin resistant and sensitive groups, within which the “Adrenergic signaling in cardiomyocytes” Kegg pathway was significantly represented, suggesting a pattern of increased intracellular cAMP and Ca2+, and apoptosis in the IR group. The same pathway allow to discriminate between insulin resistance and insulin sensitive subjects with BMI >25, supporting his role as a biomarker of IR. Moreover, ASCM pathway harbored biomarkers able to distinguish healthy and diseased subjects (from publicly available data sets) in IR-related diseases involving excitable cells: type 2 diabetes, chronic heart failure, and Alzheimer’s disease. Altered gene expression profile of the ASCM pathway is an early molecular signature of IR and could provide a common molecular pathogenetic platform for IR-related disorders, possibly representing an important aid in the efforts aiming at preventing, early detecting and optimally treating IR-related diseases.
2017-08-18 | GSE87005 | GEO
Project description:Rationale: Physical inactivity is a risk factor for insulin resistance. We examined the effect of nine days of bed rest on basal and insulin stimulated expression of genes potentially involved in insulin action by applying hypothesis-generating microarray in parallel with candidate gene real-time PCR approaches in 20 healthy, young men. Furthermore, we investigated whether bed rest affected DNA methylation in the promoter region of the peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PPARGC1A) gene. Subjects were re-examined after four weeks of retraining. Findings: Bed rest induced insulin resistance and altered the expression of more than 4,500 genes. These changes were only partly normalized after four weeks of retraining. Pathway analyses revealed significant down-regulation of 34 pathways, predominantly those of genes associated with mitochondrial function including PPARGC1A. Despite induction of insulin resistance, bed rest resulted in a paradoxically increased response to acute insulin in the general expression of genes, particularly those involved in inflammation and endoplasmatic reticulum (ER) stress. Furthermore, bed rest changed gene expressions of several insulin resistance and diabetes candidate genes. We also observed a trend toward increased PPARGC1A DNA methylation after bed rest. Conclusions: Impaired expression of PPARGC1A and other genes involved in mitochondrial function as well as a paradoxically increased response to insulin of genes involved in inflammation and ER stress may contribute to the development of insulin resistance induced by bed rest. Lack of complete normalization of changes after four weeks of exercise retraining underscores the importance of maintaining a minimum of daily physical activity. 50 samples were collected (5 samples from 10 subjects) and included in this study. Ten technical repeats were also performed in this analysis
2010-09-21 | E-GEOD-24215 | biostudies-arrayexpress