Metabolomic profiling of urinary changes in mice with monosodium glutamate-induced obesity
Jazyk angličtina Země Německo Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
26577083
DOI
10.1007/s00216-015-9133-0
PII: 10.1007/s00216-015-9133-0
Knihovny.cz E-zdroje
- Klíčová slova
- Diabetes, Metabolomics, Monosodium glutamate (MSG) induced obesity, Mouse model, NMR, Urine,
- MeSH
- glutamát sodný škodlivé účinky MeSH
- inzulin metabolismus MeSH
- játra metabolismus MeSH
- krevní glukóza metabolismus MeSH
- lidé MeSH
- metabolismus lipidů MeSH
- metabolomika * MeSH
- moč chemie MeSH
- myši MeSH
- obezita etiologie genetika metabolismus moč MeSH
- receptory aktivované proliferátory peroxizomů genetika metabolismus MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- glutamát sodný MeSH
- inzulin MeSH
- krevní glukóza MeSH
- receptory aktivované proliferátory peroxizomů MeSH
Obesity with related complications represents a widespread health problem. The etiopathogenesis of obesity is often studied using numerous rodent models. The mouse model of monosodium glutamate (MSG)-induced obesity was exploited as a model of obesity combined with insulin resistance. The aim of this work was to characterize the metabolic status of MSG mice by NMR-based metabolomics in combination with relevant biochemical and hormonal parameters. NMR analysis of urine at 2, 6, and 9 months revealed altered metabolism of nicotinamide and polyamines, attenuated excretion of major urinary proteins, increased levels of phenylacetylglycine and allantoin, and decreased concentrations of methylamine in urine of MSG-treated mice. Altered levels of creatine, citrate, succinate, and acetate were observed at 2 months of age and approached the values of control mice with aging. The development of obesity and insulin resistance in 6-month-old MSG mice was also accompanied by decreased mRNA expressions of adiponectin, lipogenetic and lipolytic enzymes and peroxisome proliferator-activated receptor-gamma in fat while mRNA expressions of lipogenetic enzymes in the liver were enhanced. At the age of 9 months, biochemical parameters of MSG mice were normalized to the values of the controls. This fact pointed to a limited predictive value of biochemical data up to age of 6 months as NMR metabolomics confirmed altered urine metabolic composition even at 9 months.
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