Similar Datasets
Project description:Treatment of insulin resistant 3T3-L1 adipose cells with MnTBAP
| PRJNA416094 | ENA
Project description:3T3-L1 adipose cells were grown, differentiated and insulin resistance was stimulated by addition of TNF or treatment inlcuding chronic insulin and dexamethasone.
2018-01-31 | GSE87853 | GEO
Project description:3T3-L1 adipose cells were grown, differentiated and insulin resistance was stimulated by addition of Glucose Oxidase.
2018-02-14 | GSE106270 | GEO
Project description:Obesity is associated with insulin resistance and type 2 diabetes, implying a role for adipose tissue in the etiology of these disorders. We used cDNA microarrays to obtain expression profiles of adipocyte by the treatment of insulin and anti-diabetic drug rosiglitazone at both high and low glucose level. Mouse 3T3-L1 mature adipocytes were treated 2 days 1) with or without 1 µM insulin at low and high glucose level, 2) with or without 0.5 μM rosiglitazone at low and high glucose and insulin level. 1) The comparison between the insulin and non-insulin treatment at the same glucose level showed minor changes in the transcriptome. The expressions of some processing enzymes for extracellular matrix components were regulated by insulin. 2) Transcriptome data indicates that an altered energy metabolism is induced by rosiglitazone in mature adipocytes. In addition, rosiglitazone represses adipokine expression, except adiponectin and ApoE. Moreover, transcriptome changes indicate that a general repression of secreted protein encoding genes occurs. Keywords: homone and drug response
2006-11-21 | GSE4683 | GEO
Project description:Murine 3T3-L1 progenitor adipocytes cell cultures, treated and untreated (Control) with resveratrol before the induction of differentiation and the effects on adipogenesis and insulin signaling was investigated. Keywords: Treatment response
2012-12-25 | GSE7111 | GEO
Project description:Adipocytes play a major role in whole body fuel homeostasis. Integrated proteomic analysis of adipose from insulin resistant versus healthy humans or mice or in 3T3-L1 adipocytes revealed defects in the mevalonate/coenzyme Q (CoQ) biosynthesis pathway as a unifying feature of adipocyte insulin resistance. CoQ was decreased selectively in mitochondria in all insulin resistant conditions and this was associated with a selective increase in mitochondrial oxidative stress. CoQ supplementation lowered mitochondrial oxidative stress and reversed insulin resistance in vitro and in vivo. Decreasing mitochondrial CoQ by genetic or pharmacological means caused insulin resistance by increasing mitochondrial oxidants from complex II. Our data suggest that loss of mitochondrial CoQ is a proximal driver of mitochondrial oxidative stress and insulin resistance. These findings may explain why statin use is associated with insulin resistance, and suggest that mitochondrial CoQ may be an effective therapeutic target for treating insulin resistance in humans.
2018-02-09 | PXD006891 | Pride
Project description:Murine 3T3-L1 progenitor adipocytes cell cultures, treated and untreated (Control) with resveratrol before the induction of differentiation and the effects on adipogenesis and insulin signaling was investigated. Keywords: Treatment response 3 Replicates of treated and untreated (Control) cell cultures
2012-12-25 | E-GEOD-7111 | biostudies-arrayexpress
Project description:Diabetes mellitus (DM) is a metabolic disorder with chronic hyperglycemia featured by metabolic outcomes owing to insufficient insulin secretion and/or insulin effect defect. It is critical to investigate new therapeutic approaches for T2DM and alternative, natural agents that target molecules in potential signal pathways. Medicinal plants are significant resources in the research of alternative new drug active ingredients. Bolanthus spergulifolius (B. spergulifolius) is one of the genera of the family Caryophyllaceae. In this study, it was explored the potential anti-diabetic effects in vitro of B. spergulifolius extracts on 3T3-L1 adipocytes. The total phenolic contents (TPC) of methanolic (MeOH), ethyl acettate (EA) and aqueous extracts of B. spergulifolius were evaluated via Folin-Ciocateau. B. spergulifolius extracts showing highly TPC (Aqueous< MeOH< EA) and their different concentrations were carried out on preadipocytes differentiated in to mature 3T3-L1 adipocytes to investigate their half-maximal (50%) inhibitory concentration (IC50) value by using Thiazolyl blue tetrazolium bromide (MTT) assay. The IC50 of MeOH, EA and Aqueous extracts were observed as 305.7 ± 5.583 μg/mL, 567.4 ± 3.008 μg/mL, and 418.3 ± 4.390 μg/mL and used for further experiments. A live/dead assay further confirmed the cytotoxic effects of MeOH, EA and Aqueous extracts (respectively, 69.75 ± 1.70%, 61.75 ± 1.70%, 70 ± 4.24%, and for all p< 0.05). Also, effects of extracts on lipid accumulation in mature 3T3-L1 adipocytes were evaluated by Oil-Red O staining assay. The extracts effectively decreased lipid-accumulation compared to untreated adipocytes (for all p< 0.05). Moreover, effect of extracts on apoptosis regulated by the Bax and Bcl-2 was investigated by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The extracts significantly induced apoptosis by up-regulating pro-apoptotic Bax expression but down-regulated anti-apoptotic Bcl-2 gene expression compared to untreated adipocytes (for all p< 0.05). The Glut-4 expression linked with insulin resistance was determined by qRT-PCR, Western-blot analysis, and immunofluorescence staining. In parallel, the expression of Glut-4 in adipocytes treated with extracts was significantly higher compared to untreated adipocytes (for all p< 0.05). Extracts significantly suppressed cell migration after 30 h of wounding in a scratch-assay (for all p< 0.05). Cell morphology and diameter were further evaluated by phase-contrast microscopy, scanning electron microscopy, Immunofluorescence with F-Actin and Giemsa staining. The adipocytes treated with extracts partially lost spherical morphology and showed smaller cell-diameter compared to untreated adipocytes (for all p< 0.05). In conclusion, these results suggest that extracts of B. spergulifolius cause to an induce apoptosis, decrease lipid-accumulation, wound healing, up-regulating Glut-4 level and might contribute to reducing of insulin-resistance in DM.
| S-EPMC8208533 | biostudies-literature
Project description:Insulin is a potent regulator of protein metabolism. Here we describe a time-resolved map of insulin-regulated protein turnover in 3T3-L1 adipocytes using metabolic pulse-chase labelling and high-resolution mass spectrometry.
2016-10-07 | PXD003696 | Pride
Project description:Microbiota contributes to induction of type 2 diabetes by high-fat/high-sugar (HFHS), but which organs/pathways are impacted by microbiota remains unknown. Using multi-organ network and transkingdom analyses, we found that microbiota-dependent. impairment of OXPHOS /mitochondria in white adipose tissue (WAT) plays a primary role in regulating systemic glucose metabolism. The follow-up analysis established that Mmp12+ macrophages link microbiota-dependent inflammation and OXPHOS damage in WAT. Moreover, the molecular signature of Mmp12+ macrophages in WAT was associated with insulin resistance in obese patients. Next, we tested functional effects of MMP12 and found that Mmp12 genetic deficiency or MMP12 inhibition improved glucose metabolism in conventional, but not in germfree mice. MMP12 treatment induced insulin resistance in adipocytes. TLR2-ligands present in Oscillibacter valericigenes bacteria, which are expanded by HFHS, induce Mmp12 in WAT macrophages in a MYD88-ATF3-dependent manner. Thus, HFHS induces Mmp12+ macrophages and MMP12, representing a microbiota-dependent bridge between inflammation and mitochondrial damage in WAT and causing insulin resistance. doi: https://doi.org/10.1084/jem.20220017
2022-05-27 | GSE203489 | GEO