Human visceral adipose tissue RT-PCR in individuals with obesity
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ABSTRACT:
PROVIDER: PRJNA1190933 | ENA |
REPOSITORIES: ENA
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Project description:Distinct characteristics of adipose tissue at different localization of human body has shown greater significance in development of metabolic disorders. Visceral adipose tissue in particular is known to be associated with obesity related metabolic complications that include type II diabetes. In this experiment, we attempt to profile transcriptome signatures of adipocyte, stromal vascular fraction (SVF) and adipose tissue from subcutaneous and visceral adipose tissue from obese individuals.
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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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Project description:As a serious public health problem nowadays, obesity and its complications are receiving gradually more attention, especially on how food-induced obesity causes the expansion of adipose tissue and leads to the occurrence of metabolic inflammation and infiltration of immune cells. It's still worth mentioning that numerous genes in adipose tissue which differ between obese and normal individuals in food-induced obesity were not insufficiently studied. Applying machine learning methods and natural language processing methods on transcriptome datasets and PubMed abstracts, we investigated 8 genes with differential expression and high association with macrophages in the visceral and subcutaneous adipose tissue between obese and normal individuals, and meanwhile low correlation with leptin. Compared with normal group, Quantitative Real-time Polymerase Chain Reaction, Western Blot, immunohistochemistry, immunofluorescence and other subsequent animal experiments on the 8 filtered genes were applied in the adipose tissue of C57BL/6J and OB/OB mice, we found that the expression of glycoprotein IX (GP9), MHC class I polypeptide related sequence B (MICB), CDGSH iron sulfur domain 1 (CISD1) and Pre-mRNA-processing factor 19 (PRPF19) in protein level were down-regulated in visceral fat of obese mice induced by high-fat diet. And these obese mice showed decreased levels of mannosidase alpha class 2B member 1 (MAN2B1) and TYRO protein tyrosine kinase binding protein (TYROBP) in their subcutaneous adipose tissue, while phosphate and tension homology deleted on chromosome pten (PTEN) and eukaryotic translation initiation factor 4E binding protein 1 (EIF4EBP1) had been sufficiently studied. The pattern in OB/OB mouse was dramatically different with these patterns. Through double immunofluorescence staining, it was found that all genes were co-localized with CD206, which was the marker of M1 and M2 macrophage in adipose tissue. Further interacting drugs for the genes were calculated and subsequently circumin and beta-catonin were proved to be interacting with these genes and functioned in inhibiting food-induced obesity. Further knowledge gragh was constructed to illustrate the relationship between obesity, filtered genes, drugs and related concepts. To summarize our findings, we discovered some new differential genes in adipose tissue which could potentially establish a new connection between adipose tissue macrophages and food-induced obesity. Furthermore, they offered unique insights into exploring the mechanism of adipose tissue genes related to food-induced obesity and related diseases.
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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.
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