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Adverse Effects of Methylglyoxal on Transcriptome and Metabolic Changes in Visceral Adipose Tissue in a Prediabetic Rat Model
M. Hüttl, I. Markova, D. Miklankova, P. Makovicky, T. Pelikanova, O. Šeda, L. Šedová, H. Malinska,
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články
Grantová podpora
Institute for Clinical and Experimental Medicine - IKEM, IN 00023001
Ministerstvo Zdravotnictví Ceské Republiky
RVO VFN64165, General University Hospital in Prague
Ministerstvo Zdravotnictví Ceské Republiky
NLK
Directory of Open Access Journals
od 2012
PubMed Central
od 2012
Europe PubMed Central
od 2012
ProQuest Central
od 2012-03-01
Open Access Digital Library
od 2012-01-01
Open Access Digital Library
od 2012-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2012
PubMed
32878255
DOI
10.3390/antiox9090803
Knihovny.cz E-zdroje
- Publikační typ
- časopisecké články MeSH
Excessive methylglyoxal (MG) production contributes to metabolic and vascular changes by increasing inflammatory processes, disturbing regulatory mechanisms and exacerbating tissue dysfunction. MG accumulation in adipocytes leads to structural and functional changes. We used transcriptome analysis to investigate the effect of MG on metabolic changes in the visceral adipose tissue of hereditary hypetriglyceridaemic rats, a non-obese model of metabolic syndrome. Compared to controls, 4-week intragastric MG administration impaired glucose tolerance (p < 0.05) and increased glycaemia (p < 0.01) and serum levels of MCP-1 and TNFα (p < 0.05), but had no effect on serum adiponectin or leptin. Adipose tissue insulin sensitivity and lipolysis were impaired (p < 0.05) in MG-treated rats. In addition, MG reduced the expression of transcription factor Nrf2 (p < 0.01), which controls antioxidant and lipogenic genes. Increased expression of Mcp-1 and TNFα (p < 0.05) together with activation of the SAPK/JNK signaling pathway can promote chronic inflammation in adipose tissue. Transcriptome network analysis revealed the over-representation of genes involved in insulin signaling (Irs1, Igf2, Ide), lipid metabolism (Nr1d1, Lpin1, Lrpap1) and angiogenesis (Dusp10, Tp53inp1).
Diabetes Centre Institute for Clinical and Experimental Medicine 140 21 Prague Czech Republic
Faculty of Education Department of Biology J Selye University 94501 Komarno Slovakia
Citace poskytuje Crossref.org
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