Abstract:
Background:Genome-wide association studies have found an obesity-related single-nucleotide polymorphism rs10938397 near the glucosamine-6-phosphate deaminase 2 gene (GNPDA2) encoding, an enzyme that catalyzes the deamination of the glucosamine-6-phosphate involved in the hexosamine signaling pathway, but the molecular mechanisms underlying the missing link between GNPDA2 and obesity remain elusive. Methods:As obesity is accompanied by an increase in the size and the number of adipocytes, the present study investigates the possible mechanism of the GNPDA2 in adipogenesis using GeneChip® Human Transcriptome Array 2.0 in human adipose-derived mesenchymal stem cells. Results:We found that overexpression of GNPDA2 enhanced accumulation of lipid droplets, and knocking down the gene decreased accumulation of lipid droplets. GO term enrichment analysis indicated that most differentially expressed genes (DEGs) affected by deficiency of GNPDA2 have functions to lipid and glucose metabolism. Further KEGG enrichment analysis showed that the greatest proportion of DEGs are involved in thermogenesis, peroxisome proliferator-activated receptor (PPAR) signaling pathway, carbon metabolism, and fatty acid metabolism including fatty acid degradation, elongation, and biosynthesis. Conclusion:These findings suggest that GNPDA2 may be a critical gene for lipid and glucose metabolism, and the expression level of GNPDA2 alters the transcriptome profile of human adipose-derived mesenchymal stem cells.
journal_name
Int J Endocrinoljournal_title
International journal of endocrinologyauthors
Wu L,Ma F,Zhao X,Zhang MX,Wu J,Mi Jdoi
10.1155/2019/9145452subject
Has Abstractpub_date
2019-08-01 00:00:00pages
9145452eissn
1687-8337issn
1687-8345journal_volume
2019pub_type
杂志文章abstract:Background:Gonadal injury following chemotherapy is of increasing importance with the continuous improvement of survival rates. The protection of gonadotropin hormone antagonist (GnRHant) in long-term adult survivors of adolescent cancers and some autoimmune diseases has not yet been evaluated. Methods:The present stu...
journal_title:International journal of endocrinology
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journal_title:International journal of endocrinology
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journal_title:International journal of endocrinology
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journal_title:International journal of endocrinology
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journal_title:International journal of endocrinology
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journal_title:International journal of endocrinology
pub_type: 杂志文章
doi:10.1155/2017/8724869
更新日期:2017-01-01 00:00:00
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journal_title:International journal of endocrinology
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doi:10.1155/2012/516718
更新日期:2012-01-01 00:00:00
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journal_title:International journal of endocrinology
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