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Gene expression in diet-induced obesity resistent (DIO non-responder) and diet-induced obesity susceptible (DIO responder) C57BL/6J mouse strain

ABSTRACT: Inbred C57BL/6J mice differ in their susceptibility to diet-induced obesity. Comparison of the liver transcriptomes leads to genes that are involved in the development as well as the maintenance of fatty liver during the onset of obesity upon high fat diet feeding. Genes being upregulated in DIO responder can be seen as drivers of fatty liver development, while genes upregulated in DIO non-responder are most likely involved in the protection against fatty liver diseases.

ORGANISM(S): Mus musculus

PROVIDER: GSE74542 | GEO | 2018/10/30

REPOSITORIES: GEO

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Project description:Introduction: Obestatin is a controversial gastrointestinal peptide purported to have metabolic actions. Objectives: This study investigated whether treatment with a stable obestatin analogue (PEG-OB(Cys10, Cys13) changed plasma metabolite levels firstly in lean and subsequently in diet-induced obesity (DIO) C57BL6/J mice. Method: Untargeted LC-HRMS metabolomics experiments were carried out in ESI+ mode with plasma extracts from both groups of animals. Data were normalised, multivariate and univariate statistical analysis performed and metabolites of interest putatively identified. Result: In lean mice, 39 metabolites were significantly changed by obestatin treatment and the majority of these were increased, including various C16 and C18 moieties of phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine and monoacylglycerol, along with vitamin A, vitamin D3, tyrosine, acetylcarnitine and 2alpha-(hydroxymethyl)-5alpha-androstane-3beta,17beta-diol. Decreased concentrations of glycolithocholic acid, 3-dehydroteasterone and various phospholipids were observed. In DIO mice, 25 metabolites were significantly affected and strikingly, the magnitudes of changes here were generally much greater in DIO mice than in lean mice, and in contrast, the majority of metabolite changes were decreases. Four metabolites affected in both groups included glycolithocholic acid, and three different long-chain (C18) phospholipid molecules (phosphatidylethanolamine, platelet activating factor (PAF), and monoacylglycerol). Metabolites exclusively affected in DIO mice included various phosphatidylcholines, lysophosphatidylcholines and fatty acyls, as well as creatine and oxidised glutathione. Conclusion: This investigation demonstrates that obestatin treatment affects phospholipid turnover and influences lipid homeostasis, whilst providing convincing evidence that obestatin may be acting to ameliorate diet-induced impairments in lipid metabolism, and it may influence steroid, bile acid, PAF and glutathione metabolism.

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Gene expression in diet-induced obesity resistent (DIO non-responder) and diet-induced obesity susceptible (DIO responder) C57BL/6J mouse strain

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