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Towards epigenetic understanding and therapy of insulin resistance by intranuclear insulin [human cell line gene expression]

ABSTRACT: There is evidence indicating the involvement of DNA methylation memory in maintaining gene expression patterns associated with insulin resistance. Although the exact mechanism remains unknown, it has been proved that insulin resistance is correlated to low heat shock protein (HSP) expression. We reveal that intranuclear insulin can reduce HSP DNA methylation level to up-regulate HSP protein expression and result in long term cure of hyperglycemia. Insulin resistance HepG2 cell were selected in our experiments.Three conditions were compared with three replicates each. These are:(1) Insulin resistance HepG2(R-HepG2) (2) Insulin treated HepG2(Insulin); (3) Biomineralized insulin treated HepG2 (BI).

ORGANISM(S): Homo sapiens

SUBMITTER: Yun Xiao

PROVIDER: E-GEOD-57893 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Towards epigenetic understanding and therapy of insulin resistance by intranuclear insulin [DNA methylation]

Project description:There is evidence indicating the involvement of DNA methylation memory in maintaining gene expression patterns associated with insulin resistance. Although the exact mechanism remains unknown, it has been proved that insulin resistance is correlated to low heat shock protein (HSP) expression. We reveal that intranuclear insulin can reduce HSP DNA methylation level to up-regulate HSP protein expression and result in long term cure of hyperglycemia. Insulin resistance HepG2 cell were selected in our experiments.Two conditions were compared with three replicates each. These are:(1) Insulin resistance HepG2(R-HepG2) and (2) Biomineralized insulin treated HepG2 (BI).

2014-05-23 | E-GEOD-57894 | biostudies-arrayexpress

Effects of the insulin degrading enzyme silencing on the transcriptome of HepG2 cells

Project description:Insulin degrading enzyme (IDE) is a major enzyme responsible for insulin degradation in the liver. The modulation of insulin degrading enzyme activity is hypothesized to be a link between T2DM and liver cancer. Results provide insight into role of IDE in proliferation and other cell functions. HepG2 cells were transfected with 96nM siRNA for IDE or AllStars Negative Control siRNA (Qiagen) using Lipofectamine 2000 (Invitrogen). 16 h after transfection, cells were treated with 10 nM insulin (Sigma Aldrich) or vehicle for 24 h in serum starvation condition. Total RNA was extracted. For each of the 4 conditions, 3 biological replicates were included.

2014-09-06 | E-GEOD-61142 | biostudies-arrayexpress

Towards epigenetic understanding and therapy of insulin resistance by intranuclear insulin [DNA methylation]

2014-05-23 | GSE57894 | GEO

Towards epigenetic understanding and therapy of insulin resistance by intranuclear insulin [mouse liver gene expression]

2014-05-21 | GSE57817 | GEO

Towards epigenetic understanding and therapy of insulin resistance by intranuclear insulin [human cell line gene expression]

2014-05-23 | GSE57893 | GEO

Towards epigenetic understanding and therapy of insulin resistance by intranuclear insulin [mouse liver gene expression]

Project description:There is evidence indicating the involvement of DNA methylation memory in maintaining gene expression patterns associated with insulin resistance. Although the exact mechanism remains unknown, it has been proved that insulin resistance is correlated to low heat shock protein (HSP) expression. We reveal that intranuclear insulin can reduce HSP DNA methylation level to up-regulate HSP protein expression and result in long term cure of hyperglycemia. Type 2 diabetes KKAy mouse were selected in our experiments.Three conditions were compared with three replicates each. These are:(1) Untreated KKAy mouse (2) Insulin treated KKAy mouse(Insulin); (3) Biomineralized insulin treated KKAy mouse(BI).

2014-05-21 | E-GEOD-57817 | biostudies-arrayexpress

Towards epigenetic understanding and therapy of insulin resistance by intranuclear insulin

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-05-23 | E-GEOD-57928 | biostudies-arrayexpress

the Effect of Fatty Acids in Hepatic Insulin resistance-part2

Project description:Monounsaturated fatty acid (MUFA) oleic acid (OA) has been reported to reverse saturated fatty acid palmitic acid (PA)-induced hepatic insulin resistance (IR). However, the detailed molecular mechanism remains elusive. In addition, previous research also showed that -3 polyunsaturated fatty acid (PUFA) eicosapentaenoic acid (EPA), exerted opposite effects to PA in muscle IR, but whether it plays the same role in hepatic IR and the possible mechanism involved needs to be further explored. Here, we confirmed that EPA reversed PA-induced IR in HepG2 cells and compared the proteome change after different free fatty acids (FFAs) treatments. For MUFA, 234 proteins were identified as differentially expressed proteins, and their functions were mainly related to response to stress and endogenous stimuli, lipid metabolic process and protein binding. For PUFA, the PA-induced expression change of 1326 proteins could be reversed by EPA and 415 of them were mitochondrial proteins, which covered most of the functional proteins in oxidative phosphorylation (OXPHOS) and tricarboxylic acid cycle (TCA). Mechanism study revealed that c-Jun and ROS played a role in OA- and EPA-reversed PA-induced IR, respectively. EPA or OA alleviated PA-induced abnormal ATP production, ROS generation, and calcium content. Importantly, H2O2-activated production of ROS increased the expression of c-Jun, further resulting in IR of HepG2 cells. Besides, we provided more feasible candidates as potential c-Jun-targeted “responders” for FFAs treatments. Taken together, we demonstrated that ROS/c-Jun is a common pathway to different FFAs-regulated IR in HepG2 cells.

2019-07-11 | PXD012066 | Pride

Comprehensive analysis of different in vitro insulin resistance models

Project description:Diet-induced obesity (DIO) predisposes individuals to insulin resistance, and adipose tissue has a major role in the disease. Insulin resistance can be induced in cultured adipocytes by a variety of treatments, but what aspects of the in vivo responses are captured by these models remains unknown. We use global RNA sequencing to investigate changes induced by TNF-a, hypoxia, dexamethasone, high insulin, and a combination of TNF-a and hypoxia, comparing the results to the changes in white adipose tissue from DIO mice. We found that different in vitro models capture distinct features of DIO adipose insulin resistance, and a combined treatment of TNF-a and hypoxia is most able to mimic the in vivo changes. Using genome-wide DNase I hypersensitivity followed by sequencing, we further examined the transcriptional regulation of TNF-a-induced insulin resistance, and we found that C/EPBM-CM-^_ key regulator of adipose insulin resistance. RNA-seq for 6 insulin resistance conditions and 2 control conditions, Dnase hypersensitivity-seq of 4 conditions and 1 control condition, ChIP-seq on p65 after TNFa treatment.

2013-10-18 | E-GEOD-35724 | biostudies-arrayexpress

FKBP5 expression in human adipose tissue increases following dexamethasone exposure and is associated with insulin resistance.

Project description:Glucocorticoid excess is linked to central obesity, adipose tissue insulin resistance and type 2 diabetes mellitus. The aim of our study was to investigate the effects of dexamethasone on gene expression in human subcutaneous and omental adipose tissue, in order to identify potential novel mechanisms and biomarkers for glucocorticoid-induced insulin resistance in adipose tissue. Dexamethasone changed the expression of 527 genes in both subcutaneous and omental adipose tissue. FKBP5 and CNR1 were the most responsive genes in both depots (~7-fold increase). Dexamethasone increased FKBP5 gene and protein expression in a dose-dependent manner in both depots, but FKBP5 protein levels were 10-fold higher in omental than subcutaneous adipose tissue. FKBP5 gene expression in subcutaneous adipose tissue was positively correlated with serum insulin, HOMA-IR and subcutaneous adipocyte diameter, while fold change in gene expression by dexamethasone was negatively correlated with clinical markers of insulin resistance, i.e. HbA1c, BMI, HOMA-IR and serum insulin. Only one gene, SERTM1, clearly differed in response to dexamethasone between the two depots. Dexamethasone at high concentrations, influences gene expression in both subcutaneous and omental adipose tissue in a similar pattern and promotes gene expression of FKBP5, a gene that may be implicated in glucocorticoid-induced insulin resistance. Paired human subcutaneous (sc) and omental (om) adipose tissue samples obtained from 4 non-diabetic adipose tissue donors (4 M; BMI: 20.8-27.5 Kg/m2) were incubated without (Ctr) or with dexamethasone (Dex, 3 M-NM-<M) for 24 h.

2014-08-18 | E-GEOD-42902 | biostudies-arrayexpress

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