Similar Datasets
Project description:Transcriptional profiling of mProx24 in control, high glucose, high FFAs, hypoxia, triple stimuli and triple stimuli + Rapamycin
2018-12-15 | GSE76044 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2018-12-15 | GSE76046 | GEO
Project description:mProx24 cell: control vs diabetic condition
| PRJNA306051 | ENA
Project description:Obesity and type 2 diabetes mellitus are global emergencies and long noncoding RNAs (lncRNAs) are regulatory transcrips with elusive functions in metabolism. Here we report that an unexpectedly high fraction of lncRNAs, but not protein-coding mRNAs, is repressed during diet-induced obesity (DIO) and refeeding, whilst nutrient deprivation specifically induced lncRNAs in mouse liver. Similarly, lncRNAs were lost in diabetic humans. LncRNA promoter analyses, global cistrome and gain-of-function analyses confirmed that increased MAFG signaling during DIO curbs lncRNA expression. Silencing Mafg in primary hepatocytes and in vivo elicited a fasting-like expression profile, improved glucose metabolism, derepressed lncRNAs and prevented mammalian target of rapamycin (mTOR)-driven protein translation. We found that obesity-repressed lincIRS2 is controlled by MAFG and observed that genetic and RNAi-mediated lincIRS2 loss causes hyperglycemia, insulin resistance and aberrant glucose output in lean mice. Taken together, we identify a novel MAFG-lncRNA axis controlling hepatic glucose metabolism in health and metabolic disease.
2019-12-18 | GSE121344 | GEO
Project description:Background: Hypoxia can affect aerobic organisms profoundly. Biological responses to extreme hypoxia have been well studied. However, it is not well characterized how living organisms respond to mild hypoxia, and how they distinguish different levels of hypoxia. Results: We examined the transcriptional responses of locusts using microarrays to reveal their strategies to cope with mild hypoxia. Mitochondrial activities were systemically suppressed, mainly involving energy production and mitochondrial biogenesis. The functions of endoplasmic reticulum were activated to clear the dysfunctional proteins and rescue newly synthesized proteins. Glucose in cytosol was shunted from glycolysis to pentose phosphate pathway probably to tackle the oxidative stress by enhancing the production of reductive forces. Conclusions: Locusts’ responses to mild hypoxia differ from that to severe hypoxia . In severe hypoxia, glucose resources are shunted to glycolysis to produce ATP and tackle energy crisis; however, in mild hypoxia, they are diverted to produce reductive forces and deal with oxidative stress. Locusts are capable of distinguishing different levels of hypoxia and initiating proper defenses.
2012-12-12 | GSE33898 | GEO
Project description:Brännmark2013 - Insulin signalling in human adipocytes (diabetic condition)
The paper describes insulin signalling in human adipocytes under normal and diabetic states using mathematical models based on experimental data. This model corresponds to insulin signalling under diabetic condtion
This model is described in the article:
Insulin Signaling in Type 2 Diabetes: EXPERIMENTAL AND MODELING ANALYSES REVEAL MECHANISMS OF INSULIN RESISTANCE IN HUMAN ADIPOCYTES.
Brännmark C, Nyman E, Fagerholm S, Bergenholm L, Ekstrand EM, Cedersund G, Strålfors P.
J Biol Chem. 2013 Apr 5;288(14):9867-80.
Abstract:
Type 2 diabetes originates in an expanding adipose tissue that for unknown reasons becomes insulin resistant. Insulin resistance reflects impairments in insulin signaling, but mechanisms involved are unclear because current research is fragmented. We report a systems level mechanistic understanding of insulin resistance, using systems wide and internally consistent data from human adipocytes. Based on quantitative steady-state and dynamic time course data on signaling intermediaries, normally and in diabetes, we developed a dynamic mathematical model of insulin signaling. The model structure and parameters are identical in the normal and diabetic states of the model, except for three parameters that change in diabetes: (i) reduced concentration of insulin receptor, (ii) reduced concentration of insulin-regulated glucose transporter GLUT4, and (iii) changed feedback from mammalian target of rapamycin in complex with raptor (mTORC1). Modeling reveals that at the core of insulin resistance in human adipocytes is attenuation of a positive feedback from mTORC1 to the insulin receptor substrate-1, which explains reduced sensitivity and signal strength throughout the signaling network. Model simulations with inhibition of mTORC1 are comparable with experimental data on inhibition of mTORC1 using rapamycin in human adipocytes. We demonstrate the potential of the model for identification of drug targets, e.g. increasing the feedback restores insulin signaling, both at the cellular level and, using a multilevel model, at the whole body level. Our findings suggest that insulin resistance in an expanded adipose tissue results from cell growth restriction to prevent cell necrosis.
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2024-09-02 | BIOMD0000000449 | BioModels
Project description:To define the contribution of CDK8 versus CDK19 to gene expression control, we performed a series of microarray assays for cells where each kinase was stably knocked down. Toward this end, we subjected HCT116 cells to three different stress stimuli: 5-fluorouracil (5FU), glucose deprivation, and hypoxia. We found that CDK8, but not CDK19, functions as a widespread coactivator of HIF1A target genes in hypoxia.
2013-03-01 | GSE38061 | GEO
Project description:We have hypothesized that carbonic anhydrases (CAs) play a role in stabilizing both intracellular and extracellular pH to a value that favors cancer progression and metastasis. This is likely in cooperation with the ion transport family. Here, we examined the expression pattern of selected ion transporters, glucose transporters, and carbonic anhydrases in a triple negative cell model of human breast cancer (UFH-001) and the effect of hypoxia. Heat map analysis of RNA transcripts from normoxic and hypoxic cells were significantly different. Additionally, our results show that transcription of the MCT1 monocarboxylate transporter, but not that of MCT4, was sensitive to hypoxia. Both MCT1 and MCT4 were robustly expressed at the protein level, but neither were significantly upregulated by hypoxia. Only low levels of the vATPase and NHE1 transcripts were detected, which is consistent with little to no detectable signal at the protein level. Our data also show high transcript levels of the GLUT1-glucose transporter, CAII and CAIX. Only GLUT1 and CAIX transcription were significantly increased by exposure to hypoxia. CAXII transcripts levels were very low, confirming the lack of expression at the protein level. Yet, CAXII transcription was significantly increased by hypoxia. Overall protein levels of our proteins of interest matched transcription patterns. These studies show a coordinate expression at both the transcriptional and translational levels of the monocarboxylate transporters, the GLUT1 transporter and CAIX in the aggressive triple negative UFH-001 breast cancer cells.
2019-12-01 | GSE123856 | GEO
Project description:The prevalence of type 2 diabetes mellitus (T2D) is increasing constantly and various risk factors such as obesity, aging, nutritional states and physical inactivity, in addition to genetic pre-dispositions in different populations has been identified. The consequences of high blood glucose include damaged blood vessels, leading to arteriosclerosis and chronic diabetic microangiopathies. These changes lead to occlusive angiopathy, altered vascular permeability, or tissue hypoxia, resulting in complications such as heart disease, strokes, kidney disease, blindness, impaired wound healing, chronic skin ulcers, or amputations. We isolated dermal endothelial cells from diabetic patients (Pat) and control individuals (Ctrl) and performed RNASeq to compare differentially expressed genes.
2018-01-08 | GSE92724 | GEO
Project description:Background: Hypoxia can affect aerobic organisms profoundly. Biological responses to extreme hypoxia have been well studied. However, it is not well characterized how living organisms respond to mild hypoxia, and how they distinguish different levels of hypoxia. Results: We examined the transcriptional responses of locusts using microarrays to reveal their strategies to cope with mild hypoxia. Mitochondrial activities were systemically suppressed, mainly involving energy production and mitochondrial biogenesis. The functions of endoplasmic reticulum were activated to clear the dysfunctional proteins and rescue newly synthesized proteins. Glucose in cytosol was shunted from glycolysis to pentose phosphate pathway probably to tackle the oxidative stress by enhancing the production of reductive forces. Conclusions: LocustsM-bM-^@M-^Y responses to mild hypoxia differ from that to severe hypoxia . In severe hypoxia, glucose resources are shunted to glycolysis to produce ATP and tackle energy crisis; however, in mild hypoxia, they are diverted to produce reductive forces and deal with oxidative stress. Locusts are capable of distinguishing different levels of hypoxia and initiating proper defenses. Simulated 4km altitude hypoxia treatment vs. normoxia control;direct comparison on 6 separate microarrays; each microarray compares one biological replicate of treatment and control; each biological replicate contains 10 individuals
2012-12-12 | E-GEOD-33898 | biostudies-arrayexpress