Mus musculus
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ABSTRACT:
PROVIDER: PRJNA347985 | ENA |
REPOSITORIES: ENA
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Project description:The chronic inflammatory state that accompanies obesity is a major contributor to insulin resistance and other metabolic dysfunction features. Despite recent advances in our understanding of the cellular and secreted factors that promote the inflammatory milieu of obesity, we have much less insight into the transcriptional pathways that drive these processes. While most attention has focused on the canonical inflammatory transcription factor NF-KB, other potentially important factors exist, including members of the interferon regultory factor (IRF) family. Here we show that IRF3 expression is upregulated in the adipocytes of obese mice and humans. TLR3/TLR4 activation induces insulin resistance in adipocytes, which can be prevented by IRF3 knockdown. Furthermore, Irf3KO mice display improved insulin sensitivity, associated with reduced intra-adipose and systemic inflammation in the high-fat fed state, enhanced browning of subcutaneous fat, and increased adipose expression of Glut4. Taken together, our data indicates that IRF3 is a major transcriptional regulator of adipose inflammation to maintain systemic glucose and energy homeostasis. Transcriptional profiling of murine 3T3-L1 adipocytes with altered expression of IRF3. Overexpression or knockdown of IRF3 was achieved by lentivirus transduction for 6 days. 3T3-L1 adipocytes with IRF3 knockdown were further treated in the absence or presence of LPS for 6 days. Samples consist of triplicate replica with appropriate control.
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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.
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Project description:Gestational diabetes mellitus (GDM) is considered as the early stage of type 2 diabetes mellitus. In this study, we compared the demographic and clinical data between six GDM and six NGT (healthy controls) and found the HOMA-IR was increased in GDM. Previously, many researches had proved that omental adipose tissues dysfunction could induce insulin resistance. Thus, in order to investigate the cause of the insulin resistance in GDM, label-free proteomics was used to discover differentially expressed proteins in omental adipose tissues between GDM and NGT. A total of 3529 proteins identified, including 66 significantly changed proteins. Adipocyte plasma membrane associated protein (APMAP also called C20orf3) was one of changed proteins and down regulated in GDM omental adipose tissues. Further, mature 3T3-L1 adipocytes were used to simulate omental adipocytes and we found that inhibited the expression of APMAP by RNAi would impaired the insulin signaling and activated the NFkB signaling in adipocytes. These results indicated that the decreased of APMAP in mental adipose tissues may be important in process of the insulin resistance in GDM.
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