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Systemic approaches reveal anti-adipogenic signals at the onset of obesity–related inflammation in white adipose tissue

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE132885 | GEO | 2020/03/18

REPOSITORIES: GEO

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Systemic approaches reveal anti-adipogenic signals at the onset of obesity–related inflammation in white adipose tissue [RNA-seq]

Project description:HFD feeding induces a rapid adipocyte progenitors (APs) proliferation in visceral adipose tissue (vWAT), followed by a block of differentiation. In contrast, subcutaneous adipose tissue (scWAT), in obesity, undergoes trans-differentiation of beige adipocytes to white and, consequently, a hyperplastic growth at later stages. We performed RNA-seq to investigate the global transcriptomic changes induced by HFD feeding

2020-03-19 | GSE132706 | GEO

Systemic approaches reveal anti-adipogenic signals at the onset of obesity–related inflammation in white adipose tissue [ChIP-seq]

Project description:HFD feeding induces a rapid adipocyte progenitors (APs) proliferation in visceral adipose tissue (vWAT), followed by a block of differentiation. In contrast, subcutaneous adipose tissue (scWAT), in obesity, undergoes trans-differentiation of beige adipocytes to white and, consequently, a hyperplastic growth at later stages. We performed ChIP-seq to profile RNA pol II recruitment and the global epigenetic changes of H3K4me1 and H3K27Ac induced by HFD feeding.

2020-03-19 | GSE132726 | GEO

Anti-adipogenic signals at the onset of obesity-related inflammation in white adipose tissue.

Project description:Chronic inflammation that affects primarily metabolic organs, such as white adipose tissue (WAT), is considered as a major cause of human obesity-associated co-morbidities. However, the molecular mechanisms initiating this inflammation in WAT are poorly understood. By combining transcriptomics, ChIP-seq and modeling approaches, we studied the global early and late responses to a high-fat diet (HFD) in visceral (vWAT) and subcutaneous (scWAT) AT, the first being more prone to obesity-induced inflammation. HFD rapidly triggers proliferation of adipocyte precursors within vWAT. However, concomitant antiadipogenic signals limit vWAT hyperplastic expansion by interfering with the differentiation of proliferating adipocyte precursors. Conversely, in scWAT, residing beige adipocytes lose their oxidizing properties and allow storage of excessive fatty acids. This phase is followed by tissue hyperplastic growth and increased angiogenic signals, which further enable scWAT expansion without generating inflammation. Our data indicate that scWAT and vWAT differential ability to modulate adipocyte number and differentiation in response to obesogenic stimuli has a crucial impact on the different susceptibility to obesity-related inflammation of these adipose tissue depots.

| S-EPMC7867564 | biostudies-literature

Systemic approaches reveal anti-adipogenic signals at the onset of obesity–related inflammation in white adipose tissue

Project description:Systemic approaches reveal anti-adipogenic signals at the onset of obesity–related inflammation in white adipose tissue

| PRJNA549551 | ENA

Systemic approaches reveal anti-adipogenic signals at the onset of obesity–related inflammation in white adipose tissue [RNA-seq]

Project description:Systemic approaches reveal anti-adipogenic signals at the onset of obesity–related inflammation in white adipose tissue [RNA-seq]

| PRJNA548796 | ENA

Systemic approaches reveal anti-adipogenic signals at the onset of obesity–related inflammation in white adipose tissue [ChIP-seq]

Project description:Systemic approaches reveal anti-adipogenic signals at the onset of obesity–related inflammation in white adipose tissue [ChIP-seq]

| PRJNA548815 | ENA

CXCR3 modulates obesity-induced visceral adipose inflammation and systemic insulin resistance.

Project description:Chemokine (C-X-C motif) receptor 3 (CXCR3) is a chemokine receptor involved in the regulation of immune cell trafficking and activation. Increased CXCR3 expression in the visceral adipose of obese humans and mice was observed. A pathophysiologic role for CXCR3 in diet-induced obesity (DIO) was hypothesized.Wild-type (WT) C57B/L6J and chemokine receptor 3 knockout (CXCR3(-/-) ) mice were fed a high-fat diet (HFD) for 20 weeks followed by assessment of glucose metabolism and visceral adipose tissue (VAT) inflammation.CXCR3(-/-) mice exhibited lower fasting glucose and improved glucose tolerance compared with WT-HFD mice, despite similar body mass. HFD-induced VAT innate and adaptive immune cell infiltration, including immature myeloid cells (CD11b(+) F4/80(lo) Ly6C(+) ), were markedly ameliorated in CXCR3(-/-) mice. In vitro IBIDI and in vivo migration assays demonstrated no CXCR3-mediated effect on macrophage or monocyte migration, respectively. CXCR3(-/-) macrophages, however, had a blunted response to interferon-?, a TH 1 cytokine that induces macrophage activation.A previously unreported role for CXCR3 in the development of HFD-induced insulin resistance (IR) and VAT macrophage infiltration in mice was demonstrated. Our results support pharmaceutical targeting of the CXCR3 receptor as a potential treatment for obesity/IR.

| S-EPMC4167757 | biostudies-literature

Adipose saturation reduces lipotoxic systemic inflammation and explains the obesity paradox.

Project description:Obesity sometimes seems protective in disease. This obesity paradox is predominantly described in reports from the Western Hemisphere during acute illnesses. Since adipose triglyceride composition corresponds to long-term dietary patterns, we performed a meta-analysis modeling the effect of obesity on severity of acute pancreatitis, in the context of dietary patterns of the countries from which the studies originated. Increased severity was noted in leaner populations with a higher proportion of unsaturated fat intake. In mice, greater hydrolysis of unsaturated visceral triglyceride caused worse organ failure during pancreatitis, even when the mice were leaner than those having saturated triglyceride. Saturation interfered with triglyceride's interaction and lipolysis by pancreatic triglyceride lipase, which mediates organ failure. Unsaturation increased fatty acid monomers in vivo and aqueous media, resulting in greater lipotoxic cellular responses and organ failure. Therefore, visceral triglyceride saturation reduces the ensuing lipotoxicity despite higher adiposity, thus explaining the obesity paradox.

| S-EPMC7846167 | biostudies-literature

Systemic Correlates of White Adipose Tissue Inflammation in Early-Stage Breast Cancer.

Project description:PurposeObesity, insulin resistance, and elevated levels of circulating proinflammatory mediators are associated with poorer prognosis in early-stage breast cancer. To investigate whether white adipose tissue (WAT) inflammation represents a potential unifying mechanism, we examined the relationship between breast WAT inflammation and the metabolic syndrome and its prognostic importance.Experimental designWAT inflammation was defined by the presence of dead/dying adipocytes surrounded by macrophages forming crown-like structures (CLS) of the breast. Two independent groups were examined in cross-sectional (cohort 1) and retrospective (cohort 2) studies. Cohort 1 included 100 women undergoing mastectomy for breast cancer risk reduction (n = 10) or treatment (n = 90). Metabolic syndrome-associated circulating factors were compared by CLS-B status. The association between CLS of the breast and the metabolic syndrome was validated in cohort 2, which included 127 women who developed metastatic breast cancer. Distant recurrence-free survival (dRFS) was compared by CLS-B status.ResultsIn cohorts 1 and 2, breast WAT inflammation was detected in 52 of 100 (52%) and 52 of 127 (41%) patients, respectively. Patients with breast WAT inflammation had elevated insulin, glucose, leptin, triglycerides, C-reactive protein, and IL6 and lower high-density lipoprotein cholesterol and adiponectin (P < 0.05) in cohort 1. In cohort 2, breast WAT inflammation was associated with hyperlipidemia, hypertension, and diabetes (P < 0.05). Compared with patients without breast WAT inflammation, the adjusted HR for dRFS was 1.83 (95% CI, 1.07-3.13) for patients with inflammation.ConclusionsWAT inflammation, a clinically occult process, helps to explain the relationship between metabolic syndrome and worse breast cancer prognosis. Clin Cancer Res; 22(9); 2283-9. ©2015 AACR.

| S-EPMC4854755 | biostudies-literature

Glutamine Links Obesity to Inflammation in Human White Adipose Tissue

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-11-15 | GSE140426 | GEO