Skip to main content
Fig. 2 | Alzheimer's Research & Therapy

Fig. 2

From: Targeting soluble tumor necrosis factor as a potential intervention to lower risk for late-onset Alzheimer’s disease associated with obesity, metabolic syndrome, and type 2 diabetes

Fig. 2

Liver metabolic profile associated with HFHC diet consumption and solTNF neutralization with XPro1595. a Untargeted high-resolution metabolomics of hepatic tissues showed a significant metabolic response to diet and solTNF treatment. HFHC showed the greatest number of metabolic changes, with 1111 m/z features differentially expressed in association with diet. Targeting solTNF promoted marked liver metabolic alterations and resulted in differential expression of 768 m/z features. A large number of these showed interaction with diet or were also associated with hepatic changes following HFHC diet consumption. Venn diagram quantities represent the number of mass spectral features with FDR < 5% prior to metabolite annotation. b Mummichog pathway enrichment of m/z features associated with HFHC showed changes in inflammatory, lipid, oxidative stress, cofactor, branched-chain amino acid, biopterin, and purine pathways. solTNF treatment showed association with a number of these pathways, including inflammatory, oxidative stress, and fatty acid pathways. Interaction between solTNF and HFHC suggests solTNF neutralization could mediate diet-induced changes in inflammation and oxidative stress in hepatic tissues. Analysis using two-way ANOVA with post hoc analysis at false discovery rate (FDR) threshold ≤ 5%, n = 12 animals/group

Back to article page