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Single-cell transcriptional profiles in the visceral adipose tissue from obese and lean C57BL6 mice

ABSTRACT: Cellular senescence has been reported to play an important role in insulin resistance. While the molecular mechanism remains unclear. Here we applied the scRNA-seq analysis for the visceral fat from the obese mice with 2 month of high-fat diet. Visceral fat was digested by type II collagenase. Stromal Vascular Fraction was collected, incubated with hashing antibody and then subjected to the 10X Chromium. 8180 cells were found from the obese mice and 14,502 cells were from the lean mice. 14 clusters and 9 cell types were identified. The key senescence marker P21 were found highly expressed in the obese group, when compared to the lean group. However, the other senescence marker P16 were unchanged. P21+ cells are mainly preadipocytes, macrophage and endothelial cells. More than 300 different expressed genes were found among the P21+ cells. The NF-kB pathway was activate according to the GO analysis, which is strongly associated with insulin resistance and diabetes

ORGANISM(S): Mus musculus

PROVIDER: GSE161872 | GEO | 2021/12/03

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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Single-cell transcriptional profiles in the visceral adipose tissue from obese and lean C57BL6 mice

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