High-density lipoprotein metabolism, composition, function, and deficiency

Schaefer, Ernst J.; Anthanont, Pimjai; Asztalos, Bela F.

doi:10.1097/mol.0000000000000074

Cited by 50 publications

(38 citation statements)

References 25 publications

(43 reference statements)

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“…The present study showed that treatment with glibenclamide resulted in increased HDL level as reported by Santana et al (2004) and supported by YKi-Jarvinen (2004). It is widely known that there is an inverse relation between the level of HDL and the cardiovascular risk (Schaefer et al 2014). In this study glibenclamide causes a significant elevation in HDL that will reduce the risk of cardiovascular diseases.…”

Section: Discussion:-supporting

confidence: 69%

Influence of oral hypoglycemic agent (Glibenclamide)on Biochemical parameters.

Alblihed¹

2016

IJAR

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Objective: In vivo study was carried out to investigate the effect of oral glibenclamide on biochemical laboratory findings. Methods: 30 subjects (17 males and 13 females) with an average age of (45 ±16 years) and average weight (80 ± 18 kg) were participated in this study. They were newly diagnosed with non-insulin dependent diabetes mellitus. 20 healthy volunteers of comparable age and weight (47 ± 13 years ; 77 ± 12 kg) were used as control sample. Two venous blood samples were taken from each subject, first blood sample was taken before glibenclamide therapy (5 mg/daily) and the second blood sample was taken 14 weeks after drug therapy. The two samples were analysed for glucose, HbA1c, total cholesterol, Triglyceride, LDL and HDL.

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Section: Discussion:-supporting

confidence: 69%

Influence of oral hypoglycemic agent (Glibenclamide)on Biochemical parameters.

Alblihed¹

2016

IJAR

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“…Previous proteomic studies have revealed more than 100 proteins on HDL particles including structure proteins, enzymes, complement components and proteinase inhibitors. It became clear that the protective role of HDL against atherogenesis may relate to its composition as much as to its concentration in the plasma [18] . By contrast, there is no accepted gold standard to measure the physical and functional properties of HDL particles, although several tests and assays have been reported in the last few decades [1] .…”

Section: Discussionmentioning

confidence: 99%

HDL subfraction distribution and HDL function in untreated dyslipidemic patients

Harangi¹,

Szentpéteri²,

Nádró³

et al. 2017

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Aim:The protective role of high-density lipoprotein (HDL) against atherosclerosis is well known. However, both structural and functional changes of the HDL particles may affect its protective efficacy. Increased levels of HDL-associated myeloperoxidase (MPO) and decreased HDL-linked paraoxonase-1 (PON1) activity have been reported in dyslipidemic patients. Some changes in HDL subfraction distributions were also studied previously, but data on structural and functional changes in dyslipidemia are not complete. Therefore, the authors aimed to evaluate these qualitative and quantitative markers of HDL in dyslipidemic patients and healthy control subjects. Methods: Anthropometric parameters, serum levels of lipoproteins and MPO, as well as PON1 activities were investigated in 81 untreated dyslipidemic patients and in 32 healthy gender-matched controls. Additionally, HDL subfractions were detected by an electrophoretic method on polyacrylamide gel (Lipoprint). Results: Significantly higher glucose, hemoglobin A1c, total cholesterol, low-density lipoprotein-cholesterol, triglyceride, lipoprotein(a), apolipoprotein B, C-reactive protein, and MPO levels were found in patients compared to the healthy subjects. There were no significant differences in PON1 paraoxonase and arylesterase activities between the two study groups, but MPO/PON1 ratio was significantly higher in patients. There was a shift towards the smaller HDL subfractions, but only the intermediate HDL ratio was significantly lower in patients compared to controls. Conclusion:The results highlight the importance of HDL-associated pro-and antioxidant enzymes suggesting the possible clinical benefit of MPO/PON1 calculation and confirm that quantification of HDL-C level alone provides limited data regarding HDL's cardioprotective effect. Calculation of MPO/PON1 ratio may be a useful cardiovascular marker in dyslipidemia. Key words:High-density lipoprotein, subfraction, paraoxonase, myeloperoxidase, dyslipidemia ABSTRACTArticle history:

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“…Mammalian LCATs are primarily expressed in the liver and secreted to the plasma where they circulate in association with HDL (8). These enzymes are components of the reverse cholesterol transport pathway by which cholesterol from peripheral cells is delivered to the liver for excretion (9). LCAT deficiency syndromes (e.g.…”

mentioning

confidence: 99%

A Lipolytic Lecithin:Cholesterol Acyltransferase Secreted by Toxoplasma Facilitates Parasite Replication and Egress

Pszenny

Ehrenman

Romano

et al. 2016

Journal of Biological Chemistry

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The protozoan parasite Toxoplasma gondii develops within a parasitophorous vacuole (PV) in mammalian cells, where it scavenges cholesterol. When cholesterol is present in excess in its environment, the parasite expulses this lipid into the PV or esterifies it for storage in lipid bodies. Here, we characterized a unique T. gondii homologue of mammalian lecithin:cholesterol acyltransferase (LCAT), a key enzyme that produces cholesteryl esters via transfer of acyl groups from phospholipids to the 3-OH of free cholesterol, leading to the removal of excess cholesterol from tissues. TgLCAT contains a motif characteristic of serine lipases "AHSLG" and the catalytic triad consisting of serine, aspartate, and histidine (SDH) from LCAT enzymes. TgL-CAT is secreted by the parasite, but unlike other LCAT enzymes it is cleaved into two proteolytic fragments that share the residues of the catalytic triad and need to be reassembled to reconstitute enzymatic activity. TgLCAT uses phosphatidylcholine as substrate to form lysophosphatidylcholine that has the potential to disrupt membranes. The released fatty acid is transferred to cholesterol, but with a lower transesterification activity than mammalian LCAT. TgLCAT is stored in a subpopulation of dense granule secretory organelles, and following secretion, it localizes to the PV and parasite plasma membrane. LCAT-null parasites have impaired growth in vitro, reduced virulence in animals, and exhibit delays in egress from host cells. Parasites overexpressing LCAT show increased virulence and faster egress. These observations demonstrate that TgLCAT influences the outcome of an infection, presumably by facilitating replication and egress depending on the developmental stage of the parasite.The phospholipase A 2 (PLA 2 ) 2 family of serine lipases comprises more than 30 enzymes in mammals. The PLA 2 members hydrolyze the sn-2 ester of phospholipids, yielding lysophospholipid and releasing a fatty acid (1). Approximately one-third of the PLA 2 family members are secreted from cells and display various localizations post-secretion, reflecting their specialized biological functions (2). Among the secretory PLA 2 , lecithin: cholesterol acyltransferase (LCAT; EC 2.3.1.43) is characterized by dual activity, PLA 2 and acyltransferase. In mammals, this enzyme catalyzes the transacylation of the sn-2 fatty acid liberated from various phospholipids (e.g. phosphatidylcholine or phosphatidylethanolamine) to the 3-␤-hydroxyl group on the A-ring of cholesterol, thereby forming cholesteryl esters (3-5). The primary sequence of LCAT is well conserved between mammalian species (6). A structural model for LCAT predicts the conformation of a catalytic triad formed by SerAsp-His residues involved in the phospholipase reaction (7). Mammalian LCATs are primarily expressed in the liver and secreted to the plasma where they circulate in association with HDL (8). These enzymes are components of the reverse cholesterol transport pathway by which cholesterol from peripheral cells is delivered to the liver f...

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High-density lipoprotein metabolism, composition, function, and deficiency

Cited by 50 publications

References 25 publications

Influence of oral hypoglycemic agent (Glibenclamide)on Biochemical parameters.

Influence of oral hypoglycemic agent (Glibenclamide)on Biochemical parameters.

HDL subfraction distribution and HDL function in untreated dyslipidemic patients

A Lipolytic Lecithin:Cholesterol Acyltransferase Secreted by Toxoplasma Facilitates Parasite Replication and Egress

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