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Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes

ABSTRACT: Accumulation of visceral white adipose tissue (WAT) associates with insulin resistance, adipose tissue inflammation, and metabolic syndrome, whereas accumulation of subcutaneous WAT may be protective. We aimed to identify molecular mechanisms that might provide mechanistic insights underlying the phenotypic differences in these tissues. Membrane Metallo-Endopeptidase (MME/Neprislyin) is an extracellular, membrane-bound protease enriched in subcutaneous WAT that can target degradation of a variety of peptides, including insulin, IL6, and β-amyloids. We hypothesized that MME contributes to adipose depot-specific metabolic properties.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE117353 | GEO | 2019/02/25

REPOSITORIES: GEO

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Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes (Microarray Expression)

Project description:Accumulation of subcutaneous white adipose tissue (WAT) is associated with increased insulin sensitivity, low levels of inflammation and a generally metabolically-healthy state, whereas accumulation of visceral adipose tissue is associated with insulin resistance, adipose tissue inflammation and metabolic syndrome. Membrane Metallo-Endopeptidase (MME/Neprislyin) is an extracellular, membrane-bound protease enriched in subcutaneous WAT that can target degradation of a variety of peptides, including insulin, IL6, and β-amyloids. Here, we show that MME in white preadipocytes is differently expressed in subcutaneous vs visceral WAT, and favors insulin signaling and a low inflammatory response. Thus, knockdown of MME in preadipocytes increases the inflammatory response to substance P and amyloidβ aggregates. This is associated with increased basal insulin signaling and decreased insulin-stimulated signaling. Moreover, MME differentially regulates the internalization and turnover of the α/β subunits of the insulin receptor. Thus, MME is a novel regulator of the insulin receptor in adipose tissue and may serve as a therapeutic target to increase insulin sensitivity and decrease inflammatory susceptibility.

2019-02-25 | GSE117352 | GEO

Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes (RNA-Seq)

2019-02-25 | GSE117270 | GEO

The epigenetic signature of systemic insulin resistance in obese women [BL]

Project description:Impaired ability of insulin to stimulate cellular glucose uptake and regulate metabolism, that is insulin resistance (IR), links adiposity to metabolic disorders such as type 2 diabetes (T2D), dyslipidemia and cardiovascular disease (Langenberg, 2012). Both genetic and epigenetic factors are implicated in development of systemic IR (Vaag, 2001). IR is characterized by elevated levels of fasting insulin in the general circulation. The aim of this study is to explore whether white adipose tissue (WAT) epigenetic dysregulation is associated with systemic IR by global CpG methylation and gene expression profiling in subcutaneous and visceral adipose tissue. A secondary aim is to determine whether the DNA methylation signature in peripheral blood mononuclear cells reflect WAT methylation, and can be used as marker for systemic IR. DNA methylation was analyzed in DNA extracted from SAT (subcutaneous adipose tissue) and VAT (visceral adipose tissue) pieces, as well as PBMCs (peripheral blood mononuclear cells), using the Infinium Human Methylation 450 BeadChip assay. This data is from PBMCs.

2016-08-01 | E-GEOD-76285 | biostudies-arrayexpress

The epigenetic signature of systemic insulin resistance in obese women [SC]

2016-08-01 | E-GEOD-76398 | biostudies-arrayexpress

The epigenetic signature of systemic insulin resistance in obese women [OM]

2016-08-01 | E-GEOD-76394 | biostudies-arrayexpress

Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes

Project description:Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White Preadipocytes

| PRJNA481868 | ENA

The epigenetic signature of systemic insulin resistance in obese women [SC]

2016-08-01 | GSE76398 | GEO

The epigenetic signature of systemic insulin resistance in obese women [OM]

2016-08-01 | GSE76394 | GEO

The epigenetic signature of systemic insulin resistance in obese women [BL]

2016-08-01 | GSE76285 | GEO

Regulation of gene expression in murine liver by IL-6

Project description:STEAP4 is a plasma membrane metallo-reductase involved in the transport of iron and copper. Recently, STEAP4 was implicated in promoting insulin sensitivity by acting in white adipose tissue (WAT) to control the production of inflammatory cytokines such as IL-6. Indeed, the loss of STEAP4 expression in mice leads to increased production of inflammatory cytokines in visceral WAT and systemic insulin resistance. In this report, we demonstrate that in mouse liver STEAP4 is produced at significant levels and that STEAP4 transcription is induced by IL-6. We further demonstrate that the STEAP4 gene is a direct target of phosphorylated STAT3 in mouse liver. In addition, hepatic STEAP4 expression is regulated by feeding and fasting, and obesity leads to the induction of STEAP4 expression in the liver. Interestingly, the regulation of STEAP4 in both feeding and fasting and the obese state appears to require the transcription factor C/EBPalpha that may act in concert with STAT3 as they both bind to the proximal STEAP4 promoter in vivo. Taken together these data suggest the transcriptional regulation of hepatic STEAP4 may play a critical role in the response to nutritional and inflammatory stress and contribute to the protective effect of STEAP4 in vivo. 10-week old male C57BL6 mice were fasted for 16 h overnight and then given either saline or IL-6 (100 ng/mouse) injections intraperitoneally for 1 h. Mice were euthanized using CO2, and the livers were collected and snap-frozen in liquid nitrogen and stored at -800C until further use.

2010-04-08 | E-GEOD-21060 | biostudies-arrayexpress

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