PLTP Activity Kit (plasma phospholipid transfer protein)
- Known as:
- PLTP Activity Kit (plasma phospholipid transfer protein)
- Catalog number:
- ELI-6279
- Product Quantity:
- 100 Tests
- Category:
- -
- Supplier:
- Nal Von Minden
- Gene target:
- PLTP Activity Kit (plasma phospholipid transfer protein)
Related genes to: PLTP Activity Kit (plasma phospholipid transfer protein)
- Gene:
- PLTP NIH gene
- Name:
- phospholipid transfer protein
- Previous symbol:
- -
- Synonyms:
- BPIFE
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1994-09-16
- Date modifiied:
- 2014-11-18
Related products to: PLTP Activity Kit (plasma phospholipid transfer protein)
Related articles to: PLTP Activity Kit (plasma phospholipid transfer protein)
- Necrotizing enterocolitis (NEC) is a life-threatening gastrointestinal disease of neonates. This study aimed to identify Lipopolysaccharide-binding protein (LBP) as a potential biomarker for the diagnosis of NEC through multi-omics analyses and validation. - Source: PubMed
Publication date: 2026/05/26
Zou PengjianHou LonglongWei PengfeiSong KaiLu JietingZeng JiahaoLiu YingyanZhong XinChen LizhuHuang YaqiOuyang YuNong TaoTian YanLi WeinianLi LinHe QiumingXia HuiminZhong WeiLiu ZipengLan Chaoting - Growing evidence implicates neuroinflammation, gut-derived endotoxemia, and dysregulated lipid metabolism in the pathogenesis of Parkinson's disease (PD). However, the relationships among circulating lipopolysaccharide (LPS), LPS-handling proteins, systemic inflammatory activation, and lipid fractions remain insufficiently characterized. The aim of this study was to compare LPS levels, LPS-related inflammatory mediators, and plasma lipid parameters between PD patients and matched controls, and to explore correlations among these biomarkers. Twenty PD patients and twenty matched controls underwent fasting venous sampling. Circulating LPS, lipopolysaccharide binding protein (LBP), soluble cluster of differentiation 14 (sCD14), high-sensitivity C-reactive protein (hsCRP), and phospholipid transfer protein (PLTP) were quantified via LAL assay and ELISAs. Serum cholesterol, HDL cholesterol (HDL-C), phospholipids (PLs), HDL-PLs and triacylglycerols (TAGs) were assessed using validated biochemical techniques. LPS concentrations did not differ between groups. However, PD patients showed elevated sCD14 and hsCRP levels, reduced LBP, and increased PLTP. Lipid profiling revealed lower total cholesterol and reduced HDL-associated cholesterol and phospholipids in PD, while TAG levels remained unchanged. Correlation analyses indicated coordinated associations between inflammatory markers and lipid fractions, with distinct interaction patterns in PD compared with controls. These findings support a mechanistic interplay among endotoxemia, innate immune activation, and lipid dysregulation in the pathophysiology of PD. - Source: PubMed
Publication date: 2026/04/22
Della Porta MatteoBarichella MichelaPezzoli GianniCazzola Roberta - Accumulating evidence indicates that exogenous toxins can induce lipid metabolic disorders by influencing the gut microbiome. However, the effects of ammonia nitrogen on the gut microbiota and hepatic lipid metabolism of the burbot (lota lota) remain unknown. Therefore, we integrated biochemical measurements, 16S rDNA sequencing, and transcriptomic analysis to evaluate the impact of 96 h of ammonia nitrogen exposure on oxidative stress, the immune response, lipid metabolism, and gut microbiota in the liver and intestine of lota lota. In this study, lota lota exhibited oxidative damage and immunosuppression following ammonia nitrogen exposure, as evidenced by decreased antioxidant and immune enzyme activities and a concomitant increase in malondialdehyde (MDA) content. Furthermore, ammonia nitrogen exposure altered gut microbial diversity: the abundance of Proteobacteria decreased, whereas that of Bacteroidota and Firmicutes increased. In addition, transcriptomic analysis revealed that the expression of genes related to fatty acid metabolism (fabp, elovl6, pltp) and gut barrier dysfunction (collagen, ecm) was altered. Notably, lipopolysaccharide (LPS) was identified as a key microbial-derived signal triggered by ammonia nitrogen, as demonstrated by ELISA. The translocation of LPS from gut to liver, resulting from compromised intestinal barrier integrity, activated the gut-liver axis and contributed to hepatic lipid metabolic disorders. Overall, the current study elucidates the gut-liver axis-mediated mechanism of ammonia nitrogen toxicity and provides valuable information for understanding the toxic effects of ammonia nitrogen on lota lota and conserving this threatened cold-water species. - Source: PubMed
Publication date: 2026/05/11
Zhai CunhuaLi YutaoHan HaoxiangMa Bo - PCOS is the most common disorder encompassing reproductive, metabolic, and endocrine abnormalities, and has an increased risk of adverse pregnancy and neonatal complications, such as miscarriage, gestational diabetes mellitus, and preterm birth. Many studies suggested that oocyte quality is compromised in patients with PCOS compared to those without PCOS. To systematically characterize the follicular fluid (FF) proteomic landscape and identify potential biomarkers for oocyte quality assessment, we conducted a label-free proteomics analysis between patients with and without PCOS. - Source: PubMed
Publication date: 2026/04/16
Hong LingHuang ChunyuMo MeilanWang XuejinSun QingZhang RuitengLiu Su - Phospholipid transfer protein (PLTP) is a lipid transfer protein classically studied in the context of plasma lipoprotein metabolism, high-density lipoprotein (HDL) remodeling, and cardiovascular disease risk. PLTP facilitates phospholipid transfer between lipoproteins and regulates HDL particle size and composition through interactions with apolipoprotein A-I and apolipoprotein A-II. While its systemic roles in cholesterol handling, reverse cholesterol transport, and inflammatory signaling are well established, the cell-autonomous functions of PLTP within cardiomyocytes remain poorly defined, particularly in human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). Extensive experimental and clinical studies demonstrate that PLTP enhances ABCA1-dependent cholesterol efflux primarily by stabilizing ABCA1 at the plasma membrane and by promoting the generation of lipid-poor apolipoprotein A-I and pre-β HDL particles, which serve as efficient cholesterol acceptors; the magnitude of these effects depends on cellular context, PLTP expression levels, and the availability of lipid acceptors. PLTP expression is metabolically regulated and widely distributed across tissues, including macrophages and other non-hepatic cells, supporting roles beyond circulating lipoprotein remodeling. Altered PLTP activity has been linked to atherosclerosis, cardiovascular disease, and inflammatory pathways, underscoring its relevance to cardiac pathophysiology. Emerging evidence further suggests that intracellular cholesterol distribution, rather than total cholesterol content alone, critically influences mitochondrial membrane composition, bioenergetics, and stress signaling in cardiomyocytes. These observations raise the possibility that PLTP-regulated lipid flux may indirectly shape mitochondrial function by modulating cellular cholesterol homeostasis. This review synthesizes current knowledge of PLTP biology, cholesterol metabolism, and lipoprotein remodeling, and integrates these concepts with emerging frameworks in cardiomyocyte lipid metabolism and mitochondrial physiology. We highlight human iPSC-derived cardiomyocytes as a strategic and translationally relevant platform to investigate PLTP's non-canonical, cell-intrinsic roles, identify critical knowledge gaps, and propose future directions for elucidating how PLTP may influence mitochondrial function in human cardiac cells. - Source: PubMed
Publication date: 2026/04/18
Shahannaz Dhienda CSugiura Tadahisa