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PXD010272

PXD010272 is an original dataset announced via ProteomeXchange.

Dataset Summary
TitlePro-inflammatory remodeling of high density lipoprotein (HDL) precedes development of dyslipidemia and hepatic steatosis upon exposure to four weeks of high fat diet
DescriptionLong-term high fat feeding leads to hepatic steatosis, dyslipidemia, and a pro-inflammatory state. In a previous study, we observed this dysregulated metabolic phenotype when C57BL/6 mice were fed a high fat diet (HFD) for sixteen weeks. Additionally, a five-fold increase in liver gene expression of serum amyloid A-1 (SAA-1), an acute phase response protein that associates with high density lipoprotein (HDL), was observed. Inflammation induced changes composition may alter HDL functions, including anti-oxidant, anti-inflammatory and reverse cholesterol transport properties. Diet-induced onset and progression of HDL dysfunction is poorly understood. To examine the relationship between high fat diet and HDL dysfunction, we performed a short-term diet study. Four-week high fat feeding caused an increase in total plasma cholesterol compared with mice fed normal control diet (ND). No change in plasma triglycerides or development of hepatic steatosis was observed. These mice did however show evidence for increase in acute phase reactants, with a 3.25-fold increase in SAA-1 expression in liver. Heavy water labelling was used to determine the turnover rates of proteins associated with HDL. High fat diet resulted in increased fractional catabolic rate (HFD vs ND) of several acute phase response proteins involved ininnate immunity , including – Complement C3 (7.06 ± 0.99 vs 5.20 ± 0.56 %/h, p < 0.005), complement factor B (6.17 ± 0.59 vs 5.09 ± 0.87 %/h, p < 0.05), complement Factor H (4.16 ± 0.41 vs 3.56 ± 0.36 %/h, p < 0.05), and Complement factor I (3.50 ± 0.26 vs 2.75 ± 0.14 %/h, p < 0.005). Our findings suggest that early immune response-induced inflammatory remodeling of HDL precedes the diet-induced steatosis and dyslipidemia. Early HDL dysfunction reflected on impaired reverse cholesterol transport likely results in increase in plasma cholesterol in the absence of other lipid abnormalities.
HostingRepositoryPRIDE
AnnounceDate2024-10-22
AnnouncementXMLSubmission_2024-10-22_05:25:36.920.xml
DigitalObjectIdentifier
ReviewLevelPeer-reviewed dataset
DatasetOriginOriginal dataset
RepositorySupportUnsupported dataset by repository
PrimarySubmitterSerguei Ilchenko
SpeciesList scientific name: Mus musculus (Mouse); NCBI TaxID: 10090;
ModificationListiodoacetamide derivatized histidine; monohydroxylated residue; acetylated residue
InstrumentQ Exactive
Dataset History
RevisionDatetimeStatusChangeLog Entry
02018-06-29 02:34:47ID requested
12021-09-08 08:09:35announced
22024-10-22 05:25:39announced2024-10-22: Updated project metadata.
Publication List
Sadana P, Lin L, Aghayev M, Ilchenko S, Kasumov T, O-Metabolic Labeling-Based Kinetic Approach. Int J Mol Sci, 21(20):(2020) [pubmed]
10.3390/ijms21207472;
Keyword List
submitter keyword: high, inflammation, lipoprotien, liver, fat, steatosis, density,diet,plasma, dyslipidemia, hepatic
Contact List
Takhar Kasumov
contact affiliationDepartment of Pharmaceutical Sciences Northeast Ohio Medical University Rootstown, OH, USA MTD project_title Proteome dynamics in dogs with heart failure
contact emailTkasumov@neomed.edu
lab head
Serguei Ilchenko
contact affiliationNeomed
contact emailsilchenko@neomed.edu
dataset submitter
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