Whole exome sequencing of Severe Insulin Resistant patients
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ABSTRACT:
PROVIDER: EGAS00001000025 | EGA |
REPOSITORIES: EGA
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Project description:Illumina paired-end sequencing of whole- exome pulldown DNA from Severe Insulin Resistant patients.
| EGAS00001000041 | EGA
Project description:insulin resistant duodenum vs. non-insulin resistant duodenum
| PRJNA615363 | ENA
Project description:Objective: To study if diabetic and insulin-resistant states lead to mitochondrial dysfunction in the liver, or alternatively, if there is adaption of mitochondrial function to these states in the long-term range. Results: High-fat diet (HFD) caused insulin resistance and severe hepatic lipid accumulation, but respiratory chain parameters were unchanged. Livers from insulin-resistant IR/IRS-1+/- mice had normal lipid contents and normal respiratory chain parameters, however showed mitochondrial uncoupling. Livers from severely hyperglycemic and hypoinsulimic, streptozotocin (STZ)-treated mice had massively depleted lipid levels, but respiratory chain abundance was unchanged. However, their mitochondria showed increased abundance and activity of the respiratory chain, which was better coupled compared to controls. Conclusions: Insulin resistance, either induced by obesity or by genetic manipulation, does not cause mitochondrial dysfunction in the liver of mice. However, severe insulin deficiency and high blood glucose levels in mice cause an enhanced performance of the respiratory chain, probably in order to maintain the high energy requirement of the unsuppressed gluconeogenesis. We performed gene expression microarray analysis on liver tissue derived from mice treated with STZ or standard diet (control).
2013-12-10 | E-GEOD-39752 | biostudies-arrayexpress
Project description:Objective: To study if diabetic and insulin-resistant states lead to mitochondrial dysfunction in the liver, or alternatively, if there is adaption of mitochondrial function to these states in the long-term range. Results: High-fat diet (HFD) caused insulin resistance and severe hepatic lipid accumulation, but respiratory chain parameters were unchanged. Livers from insulin-resistant IR/IRS-1+/- mice had normal lipid contents and normal respiratory chain parameters, however showed mitochondrial uncoupling. Livers from severely hyperglycemic and hypoinsulimic, streptozotocin (STZ)-treated mice had massively depleted lipid levels, but respiratory chain abundance was unchanged. However, their mitochondria showed increased abundance and activity of the respiratory chain, which was better coupled compared to controls. Conclusions: Insulin resistance, either induced by obesity or by genetic manipulation, does not cause mitochondrial dysfunction in the liver of mice. However, severe insulin deficiency and high blood glucose levels in mice cause an enhanced performance of the respiratory chain, probably in order to maintain the high energy requirement of the unsuppressed gluconeogenesis.
2013-12-10 | GSE39752 | GEO
Project description:Insulin resistance is accompanied by chronic hyperinsulinemia and is associated with type 2 diabetes and other metabolic syndromes in a substantial portion of the population. The risk factors and features of insulin resistance have been thoroughly described but its mechanistic triggers are still under study. Here we consider a condensate model for insulin receptor (IR) function in normal conditions and when dysregulated in chronic hyperinsulinemia-induced insulin resistance. We find that IR is incorporated into liquid-like condensates at the plasma membrane, in the cytoplasm and in the nucleus of liver cells, and provide evidence for insulin-dependent IR function in condensates. Insulin stimulation promotes further incorporation of IR into these dynamic condensates in insulin sensitive cells, which form and dissolve on short, sub-minute time-scales. In contrast, insulin stimulation does not promote further incorporation of IR into condensates in insulin resistant cells, where IR molecules within condensates exhibit less dynamic behavior. Metformin treatment of insulin resistant cells rescues IR condensate dynamics and insulin responsiveness. Insulin resistant cells experience high levels of oxidative stress, which causes reduced condensate dynamics, and treatment of these cells with metformin reduces ROS levels and returns condensates to their normal dynamic behavior. The condensate model we propose can account for features of normal and dysregulated insulin response and has implications for improved therapeutic approaches to insulin resistance.
2023-07-28 | GSE181096 | GEO
Project description:Illumina paired-end sequencing of whole- exome pulldown DNA from Severe Insulin Resistant patients.
| EGAD00001000381 | EGA
Project description:Illumina paired-end sequencing of whole- exome pulldown DNA from Severe Insulin Resistant patients.
| EGAD00001000380 | EGA
Project description:Muscle sample pool #5 from 2 insulin resistant subjects. Keywords: parallel sample
2002-08-26 | GSE73 | GEO
Project description:Muscle sample pool #4 from 3 insulin resistant subjects. Keywords: parallel sample
2002-08-26 | GSE72 | GEO
Project description:Muscle sample pool #3 from 4 insulin resistant subjects. Keywords: parallel sample
2002-08-26 | GSE71 | GEO