PXD010272

PXD010272 is an original dataset announced via ProteomeXchange.

Title	Pro-inflammatory remodeling of high density lipoprotein (HDL) precedes development of dyslipidemia and hepatic steatosis upon exposure to four weeks of high fat diet
Description	Long-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.
HostingRepository	PRIDE
AnnounceDate	2024-10-22
AnnouncementXML	Submission_2024-10-22_05:25:36.920.xml
DigitalObjectIdentifier
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Unsupported dataset by repository
PrimarySubmitter	Serguei Ilchenko
SpeciesList	scientific name: Mus musculus (Mouse); NCBI TaxID: 10090;
ModificationList	iodoacetamide derivatized histidine; monohydroxylated residue; acetylated residue
Instrument	Q Exactive

Revision	Datetime	Status	ChangeLog Entry
0	2018-06-29 02:34:47	ID requested
1	2021-09-08 08:09:35	announced
⏵ 2	2024-10-22 05:25:39	announced	2024-10-22: Updated project metadata.

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;

submitter keyword: high, inflammation, lipoprotien, liver, fat, steatosis, density,diet,plasma, dyslipidemia, hepatic

Takhar Kasumov
contact affiliation	Department of Pharmaceutical Sciences Northeast Ohio Medical University Rootstown, OH, USA MTD project_title Proteome dynamics in dogs with heart failure
contact email	Tkasumov@neomed.edu
lab head
Serguei Ilchenko
contact affiliation	Neomed
contact email	silchenko@neomed.edu
dataset submitter

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PRIDE project URI

• PRIDE
  1. PXD010272
     1. Label: PRIDE project
     2. Name: Pro-inflammatory remodeling of high density lipoprotein (HDL) precedes development of dyslipidemia and hepatic steatosis upon exposure to four weeks of high fat diet