Project description:This study investigates the impact of Plin4 gene deletion on lipid metabolism in mouse liver and plasma under different dietary conditions using untargeted lipidomics. Female wild-type (Plin4+/+) and knockout (Plin4-/-) mice were fed either a control diet or a Western diet high in fat, fructose, and cholesterol. Samples included liver tissue and plasma (n = 5 per tissue type per group, total n = 40). Lipids were extracted using isopropanol, with pooled quality control samples prepared and injected regularly for signal correction. Lipidomic analysis was performed using ultra-high-performance liquid chromatography coupled to Orbitrap mass spectrometry (UHPLC-MS), with data acquired using Xcalibur and processed in Compound Discoverer and LipidSearch. Features were normalized using the SERRF algorithm, and lipid identifications were based on MS/MS fragmentation matching. This dataset provides global lipid profiles for evaluating the metabolic effects of Plin4 deletion in both normal and diet-induced obese states.
Project description:Diets influence metabolism and susceptibility to disease. We have previously demonstrated that a ketogenic diet alleviates cardiac pathology, with its cardioprotective effects linked to increased lysine acetylation in the heart. To identify acetylated proteins associated with this diet, we conducted a proteomic analysis using liquid chromatography-tandem mass spectrometry in the hearts of mice fed either a ketogenic diet or a normal chow diet under hypertension. We identified 966 acetylated peptides corresponding to 320 acetylated proteins in the hearts of mice fed a normal chow diet (group A), while 1597 acetylated peptides corresponding to 425 acetylated proteins were identified in the hearts of mice fed a ketogenic diet (group M).
Project description:Humoral immunological memory is essential for the protection against pathogens post primary infection or vaccination. This protection relies on the long-term survival of pathogen-specific memory B cells and lone-lived plasma cells. We found that ketogenic diet (KD) impairs the humoral immunological memory by depleting the plasma cells. We performed functional analysis of these bone marrow plasma cells from control mice or KD-treated mice.
Project description:Specific pathogen free wild-type C57Bl/6 male mice fed ketogenic diet (Bio-Serv AIN-76-A) for 4 weeks Keywords: RNA Expression Array Hearts from 12 week-old mice that were maintained on a standard polysacchardide-rich chow until the age of 8 weeks, at which time they were switched to a ketogenic diet (ad libitum) and maintained for 4 additional weeks prior to collection of tissues
Project description:Analysis of liver gene transcription during feeding of a ketogenic diet. Ketogenic diets may alter physiologic and metabolic profiles in a direction that favors weight loss. C57BL/6J mice were maintained for six weeks on either chow or ketogenic diet. Mice eating KD had lower weights, 90% reduction in insulin levels and increased energy expenditure compared to animals fed chow. Despite consumpiton of a very high fat diet serum lipids remained normal. Here we show that consumption of KD shifted liver metabolism to drastically increased fatty acid oxidation. Concurrently, expression of genes involved in fatty acid synthesis were markedly suppressed. Keywords: Hepatic profile
Project description:Untargeted lipidomics of liver samples from female and male DBA/2J or C57BL/6J mice fed a control diet, Western diet, or high- or low-isoleucine Western diet. Both positive and negative mode are included.
Project description:To comprehensively elucidate the possible mechanism of short-term administration of emodin on the metabolic disturbance in vivo, our study utilized both LC/MS and NMR platforms for untargeted metabolomics studies. These analyses aimed to identify potential biomarkers associated with emodin-induced metabolic disturbances in mice. Subsequently, we delved into lipidomics to explore lipid metabolism systematically and determined the position of C=C double bonds in unsaturated lipids.