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Gene expression differences in omental mesothelial cells from lean and obese human donors

ABSTRACT: Visceral adipose tissue inflammation correlates with metabolic dysfunction in obesity. However, critical cell types that trigger and contribute to inflammation in this depot are not completely understood. Mesothelial cells line the omental fat depot and are thought to contribute to several intraperitoneal inflammatory conditions. Whether adipose-associated mesothelial cell inflammation is a feature of pathologic obesity is unclear. This study was performed to delineate a contribution of omental adipose mesothelial cells to visceral adipose tissue dysfunction in pathologic obesity. We performed a cross-sectional case-control study from two separate cohorts of patients undergoing abdominal surgery with varying degrees of obesity and metabolic disease. Whole-genome expression profiling was conducted on mesothelial cells isolated from lean and obese surgical patients to determine differences in relevant pathways related to obesity and metabolic disease.

ORGANISM(S): Homo sapiens

PROVIDER: GSE128021 | GEO | 2019/03/08

REPOSITORIES: GEO

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Project description:Maternal obesity is linked with increased adverse outcomes for mother and fetus. However, the metabolic impact of excessive fat accumulation within the altered hormonal context of pregnancy is not well understood. We used a murine model of obesity, the high fat diet-fed C57BL/6J mouse to determine adipose tissue-mediated molecular mechanisms driving metabolic dysfunction throughout pregnancy. Remarkably, obese mice exhibited a normalization of visceral fat accumulation at late-stage pregnancy (-53%, P<0.001 E18.5) to achieve levels comparable in mass (per gram of body weight) to that of non pregnant, control diet fed mice. Moreover, whilst obese pregnant mice showed a marked glucose intolerance and apparent insulin resistance at mid-stage pregnancy (E14.5), glucose homeostasis converged with that of lean pregnant mice at late-stage pregnancy, suggesting an unexpected amelioration of the worsening metabolic dysfunction in obese pregnant mice. Transcriptomic analysis of the late-stage visceral fat indicated reduced de novo lipogenic drive (Me1, Fasn, Scd1, Dgat2), retinol metabolism (Rdh11, Rbp4) and inflammation (Mcp1, Tnfα) in obese pregnant mice that was confirmed functionally by their lower adipose proinflammatory macrophage density. Elevated expression of estrogen receptor a (ERα) in visceral adipose tissue was identified as potential unifying mechanism for the transcriptional changes and reduced adiposity of late stage obese pregnancy. Support for a role for ERα was provided by experiments showing that the ERα selective agonist PPT suppressed lipogenesis in primary mouse adipocytes and suppressed Me1, Fasn, SCD1 and Dgat2 mRNA levels in mature female human ChubS7 clonal fat cells. Our data reveal a novel role for elevated visceral adipocyte estrogen signaling as a protective mechanism against visceral fat hypertrophy and inflammation in late pregnancy. Pregnant high fat, pregnant control fat, non pregnant high fat, non pregnant control fat. Five biologial replictes each (20 samples).

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Gene expression differences in omental mesothelial cells from lean and obese human donors

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