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  1. Article ; Online: Genetic causes of high and low serum HDL-cholesterol.

    Weissglas-Volkov, Daphna / Pajukanta, Päivi

    Journal of lipid research

    2010  Volume 51, Issue 8, Page(s) 2032–2057

    Abstract: ... heritability. Comprehensive investigation of the genetic factors conferring to low and high HDL-C levels using ... summarize what is known about HDL metabolism, monogenic disorders associated with both low and high HDL-C ... Plasma levels of HDL cholesterol (HDL-C) have a strong inherited basis with heritability estimates ...

    Abstract Plasma levels of HDL cholesterol (HDL-C) have a strong inherited basis with heritability estimates of 40-60%. The well-established inverse relationship between plasma HDL-C levels and the risk of coronary artery disease (CAD) has led to an extensive search for genetic factors influencing HDL-C concentrations. Over the past 30 years, candidate gene, genome-wide linkage, and most recently genome-wide association (GWA) studies have identified several genetic variations for plasma HDL-C levels. However, the functional role of several of these variants remains unknown, and they do not always correlate with CAD. In this review, we will first summarize what is known about HDL metabolism, monogenic disorders associated with both low and high HDL-C levels, and candidate gene studies. Then we will focus this review on recent genetic findings from the GWA studies and future strategies to elucidate the remaining substantial proportion of HDL-C heritability. Comprehensive investigation of the genetic factors conferring to low and high HDL-C levels using integrative approaches is important to unravel novel pathways and their relations to CAD, so that more effective means of diagnosis, treatment, and prevention will be identified.
    MeSH term(s) Animals ; Cholesterol, HDL/biosynthesis ; Cholesterol, HDL/blood ; Cholesterol, HDL/chemistry ; Cholesterol, HDL/genetics ; Genetic Diseases, Inborn/blood ; Genetic Diseases, Inborn/genetics ; Genome-Wide Association Study ; Heredity ; Humans ; Life Style ; Multifactorial Inheritance/genetics ; Phenotype
    Chemical Substances Cholesterol, HDL
    Language English
    Publishing date 2010-04-26
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 80154-9
    ISSN 1539-7262 ; 0022-2275
    ISSN (online) 1539-7262
    ISSN 0022-2275
    DOI 10.1194/jlr.R004739
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Genetic causes of high and low serum HDL-cholesterol

    Weissglas-Volkov, Daphna / Pajukanta, Päivi

    Journal of lipid research JLR. 2010 Aug., v. 51, no. 8

    2010  

    Abstract: ... heritability. Comprehensive investigation of the genetic factors conferring to low and high HDL-C levels using ... summarize what is known about HDL metabolism, monogenic disorders associated with both low and high HDL-C ... Plasma levels of HDL cholesterol (HDL-C) have a strong inherited basis with heritability estimates ...

    Abstract Plasma levels of HDL cholesterol (HDL-C) have a strong inherited basis with heritability estimates of 40-60%. The well-established inverse relationship between plasma HDL-C levels and the risk of coronary artery disease (CAD) has led to an extensive search for genetic factors influencing HDL-C concentrations. Over the past 30 years, candidate gene, genome-wide linkage, and most recently genome-wide association (GWA) studies have identified several genetic variations for plasma HDL-C levels. However, the functional role of several of these variants remains unknown, and they do not always correlate with CAD. In this review, we will first summarize what is known about HDL metabolism, monogenic disorders associated with both low and high HDL-C levels, and candidate gene studies. Then we will focus this review on recent genetic findings from the GWA studies and future strategies to elucidate the remaining substantial proportion of HDL-C heritability. Comprehensive investigation of the genetic factors conferring to low and high HDL-C levels using integrative approaches is important to unravel novel pathways and their relations to CAD, so that more effective means of diagnosis, treatment, and prevention will be identified.
    Language English
    Dates of publication 2010-08
    Size p. 2032-2057.
    Publishing place American Society for Biochemistry and Molecular Biology
    Document type Article
    ZDB-ID 80154-9
    ISSN 1539-7262 ; 0022-2275
    ISSN (online) 1539-7262
    ISSN 0022-2275
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: Genetic association of serum lipids and lipid-modifying targets with endometriosis: Trans-ethnic Mendelian-randomization and mediation analysis.

    Zhang, Hongling / Fan, Yawei / Li, Huijun / Feng, Xiaoqing / Yue, Daoyuan

    PloS one

    2024  Volume 19, Issue 5, Page(s) e0301752

    Abstract: ... Methods: Genome-wide association study data for high-density lipoprotein cholesterol (HDL-C ... low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), and total cholesterol (TC) from European (EUR) and East Asian (EAS ... datasets. Univariable Mendelian randomization (MR) examined causal links between serum lipids and EMS ...

    Abstract Background: Prior observational research identified dyslipidemia as a risk factor for endometriosis (EMS) but the causal relationship remains unestablished due to inherent study limitations.
    Methods: Genome-wide association study data for high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), and total cholesterol (TC) from European (EUR) and East Asian (EAS) ancestries were sourced from the Global Lipids Genetics Consortium. Multi-ancestry EMS data came from various datasets. Univariable Mendelian randomization (MR) examined causal links between serum lipids and EMS. Multivariable and mediation MR explored the influence of seven confounding factors and mediators. Drug-target MR investigates the association between lipid-lowering target genes identified in positive results and EMS. The primary method was inverse-variance weighted (IVW), with replication datasets and meta-analyses reinforcing causal associations. Sensitivity analyses included false discovery rate (FDR) correction, causal analysis using summary effect estimates (CAUSE), and colocalization analysis.
    Results: IVW analysis in EUR ancestry showed a significant causal association between TG and increased EMS risk (OR = 1.112, 95% CI 1.033-1.198, P = 5.03×10-3, PFDR = 0.03), supported by replication and meta-analyses. CAUSE analysis confirmed unbiased results (P < 0.05). Multivariable and mediation MR revealed that systolic blood pressure (Mediation effect: 7.52%, P = 0.02) and total testosterone (Mediation effect: 10.79%, P = 0.01) partly mediated this relationship. No causal links were found between other lipid traits and EMS (P > 0.05 & PFDR > 0.05). In EAS ancestry, no causal relationships with EMS were detected (P > 0.05 & PFDR > 0.05). Drug-target MR indicated suggestive evidence for the influence of ANGPTL3 on EMS mediated through TG (OR = 0.798, 95% CI 0.670-0.951, P = 0.01, PFDR = 0.04, PP.H4 = 0.85%).
    Conclusions: This MR study in EUR ancestry indicated an increased EMS risk with higher serum TG levels.
    MeSH term(s) Humans ; Female ; Mendelian Randomization Analysis ; Endometriosis/genetics ; Endometriosis/blood ; Genome-Wide Association Study ; Polymorphism, Single Nucleotide ; Triglycerides/blood ; Lipids/blood ; Mediation Analysis ; Cholesterol, HDL/blood ; Cholesterol, LDL/blood ; Dyslipidemias/genetics ; Dyslipidemias/blood ; Risk Factors ; White People/genetics
    Chemical Substances Triglycerides ; Lipids ; Cholesterol, HDL ; Cholesterol, LDL
    Language English
    Publishing date 2024-05-31
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0301752
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  4. Article ; Online: Genetic and Pharmacologic Inactivation of ANGPTL3 and Cardiovascular Disease.

    Dewey, Frederick E / Gusarova, Viktoria / Dunbar, Richard L / O'Dushlaine, Colm / Schurmann, Claudia / Gottesman, Omri / McCarthy, Shane / Van Hout, Cristopher V / Bruse, Shannon / Dansky, Hayes M / Leader, Joseph B / Murray, Michael F / Ritchie, Marylyn D / Kirchner, H Lester / Habegger, Lukas / Lopez, Alex / Penn, John / Zhao, An / Shao, Weiping /
    Stahl, Neil / Murphy, Andrew J / Hamon, Sara / Bouzelmat, Aurelie / Zhang, Rick / Shumel, Brad / Pordy, Robert / Gipe, Daniel / Herman, Gary A / Sheu, Wayne H H / Lee, I-Te / Liang, Kae-Woei / Guo, Xiuqing / Rotter, Jerome I / Chen, Yii-Der I / Kraus, William E / Shah, Svati H / Damrauer, Scott / Small, Aeron / Rader, Daniel J / Wulff, Anders Berg / Nordestgaard, Børge G / Tybjærg-Hansen, Anne / van den Hoek, Anita M / Princen, Hans M G / Ledbetter, David H / Carey, David J / Overton, John D / Reid, Jeffrey G / Sasiela, William J / Banerjee, Poulabi / Shuldiner, Alan R / Borecki, Ingrid B / Teslovich, Tanya M / Yancopoulos, George D / Mellis, Scott J / Gromada, Jesper / Baras, Aris

    The New England journal of medicine

    2017  Volume 377, Issue 3, Page(s) 211–221

    Abstract: ... serum levels of triglycerides, HDL cholesterol, and LDL cholesterol than participants ... associated with decreased plasma levels of triglycerides, low-density lipoprotein (LDL) cholesterol, and high ... levels of up to 76% and LDL cholesterol levels of up to 23%.: Conclusions: Genetic and therapeutic ...

    Abstract Background: Loss-of-function variants in the angiopoietin-like 3 gene (ANGPTL3) have been associated with decreased plasma levels of triglycerides, low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein (HDL) cholesterol. It is not known whether such variants or therapeutic antagonism of ANGPTL3 are associated with a reduced risk of atherosclerotic cardiovascular disease.
    Methods: We sequenced the exons of ANGPTL3 in 58,335 participants in the DiscovEHR human genetics study. We performed tests of association for loss-of-function variants in ANGPTL3 with lipid levels and with coronary artery disease in 13,102 case patients and 40,430 controls from the DiscovEHR study, with follow-up studies involving 23,317 case patients and 107,166 controls from four population studies. We also tested the effects of a human monoclonal antibody, evinacumab, against Angptl3 in dyslipidemic mice and against ANGPTL3 in healthy human volunteers with elevated levels of triglycerides or LDL cholesterol.
    Results: In the DiscovEHR study, participants with heterozygous loss-of-function variants in ANGPTL3 had significantly lower serum levels of triglycerides, HDL cholesterol, and LDL cholesterol than participants without these variants. Loss-of-function variants were found in 0.33% of case patients with coronary artery disease and in 0.45% of controls (adjusted odds ratio, 0.59; 95% confidence interval, 0.41 to 0.85; P=0.004). These results were confirmed in the follow-up studies. In dyslipidemic mice, inhibition of Angptl3 with evinacumab resulted in a greater decrease in atherosclerotic lesion area and necrotic content than a control antibody. In humans, evinacumab caused a dose-dependent placebo-adjusted reduction in fasting triglyceride levels of up to 76% and LDL cholesterol levels of up to 23%.
    Conclusions: Genetic and therapeutic antagonism of ANGPTL3 in humans and of Angptl3 in mice was associated with decreased levels of all three major lipid fractions and decreased odds of atherosclerotic cardiovascular disease. (Funded by Regeneron Pharmaceuticals and others; ClinicalTrials.gov number, NCT01749878 .).
    MeSH term(s) Aged ; Angiopoietin-like Proteins ; Angiopoietins/antagonists & inhibitors ; Angiopoietins/genetics ; Animals ; Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/adverse effects ; Antibodies, Monoclonal/pharmacology ; Atherosclerosis/drug therapy ; Atherosclerosis/metabolism ; Cardiovascular Diseases/prevention & control ; Coronary Artery Disease/genetics ; Coronary Artery Disease/metabolism ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Double-Blind Method ; Dyslipidemias/blood ; Dyslipidemias/drug therapy ; Female ; Humans ; Lipid Metabolism/drug effects ; Lipids/blood ; Male ; Mice ; Mice, Inbred Strains ; Middle Aged ; Mutation
    Chemical Substances ANGPTL3 protein, human ; Angiopoietin-like Proteins ; Angiopoietins ; Angptl3 protein, mouse ; Antibodies, Monoclonal ; Lipids ; evinacumab
    Language English
    Publishing date 2017-05-24
    Publishing country United States
    Document type Clinical Trial, Phase I ; Journal Article ; Randomized Controlled Trial
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMoa1612790
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  5. Article ; Online: ANGPTL3 serum concentration and rare genetic variants in Finnish population.

    Tikka, Anna / Metso, Jari / Jauhiainen, Matti

    Scandinavian journal of clinical and laboratory investigation

    2017  Volume 77, Issue 8, Page(s) 601–609

    Abstract: ... TG) and low-density lipoprotein cholesterol (LDL-C) concentration in GWASs. ANGPTL3 deficiency causes ... declined TG, total cholesterol (TC), LDL-C, high-density lipoprotein cholesterol (HDL-C), apolipoprotein B ... apoB) and apolipoprotein A-I (apoA-I) serum concentration, a phenotype defined as familial combined ...

    Abstract Genetic variants of angiopoietin-like protein 3 (ANGPTL3) are associated with serum triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) concentration in GWASs. ANGPTL3 deficiency causes declined TG, total cholesterol (TC), LDL-C, high-density lipoprotein cholesterol (HDL-C), apolipoprotein B (apoB) and apolipoprotein A-I (apoA-I) serum concentration, a phenotype defined as familial combined hypolipidaemia (FHBL2). Our aim is to establish whether ANGPTL3 serum protein concentration correlates with lipoproteins and lipids in hyper- or hypolipidaemic subjects, and whether ANGPTL3 sequence variants are associated with untypical lipid profiles. Additionally, 10 subjects with very low lipoprotein concentrations were sequenced for ANGPTL3 for possible loss-of-function (LOF) variants. Study subjects were selected from Finnish FINRISK and Health 2000 surveys. ANGPTL protein concentrations were measured by ELISA method. As a result, ANGPTL3 serum concentration correlated positively with age, phospholipid transfer protein (PLTP) and cholesteryl ester transfer protein (CETP) activities, but not with any of the lipid or lifestyle attributes. No ANGPTL3 variants were found among sequenced samples. Subjects who carried ANGPTL3 sequence variants rs12563308 (n = 4) and rs199772471 (n = 1) had abnormally high TC and LDL-C concentrations. Whole exome sequencing data of these five subjects were further analyzed for rare and deleterious missense variants in genes associated with cholesterol metabolism. In conclusion, ANGPTL3 serum protein concentration did not predict lipid concentrations, unlike apolipoprotein C-III (apoC-III) which positively correlated with most of the lipid attributes. ANGPTL3 variant screen yielded five carriers with abnormally high TC concentration; the actual genetic causality, however, could not be verified.
    MeSH term(s) Adult ; Aged ; Angiopoietin-like Proteins/blood ; Angiopoietin-like Proteins/genetics ; Cholesterol, HDL/blood ; Cholesterol, LDL/blood ; Cross-Sectional Studies ; DNA Mutational Analysis ; Female ; Finland ; Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; Hypercholesterolemia/blood ; Hypercholesterolemia/genetics ; Male ; Middle Aged ; Mutation ; Polymorphism, Single Nucleotide ; Risk Factors
    Chemical Substances ANGPTL3 protein, human ; Angiopoietin-like Proteins ; Cholesterol, HDL ; Cholesterol, LDL
    Language English
    Publishing date 2017-12
    Publishing country England
    Document type Journal Article
    ZDB-ID 3150-1
    ISSN 1502-7686 ; 0036-5513
    ISSN (online) 1502-7686
    ISSN 0036-5513
    DOI 10.1080/00365513.2017.1379608
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  6. Article ; Online: HDL cholesterol and bone mineral density: is there a genetic link?

    Ackert-Bicknell, Cheryl L

    Bone

    2011  Volume 50, Issue 2, Page(s) 525–533

    Abstract: ... of these two diseases of the elderly remains unknown. Low levels of high density lipoprotein cholesterol (HDL ... serum HDL and BMD but these studies are confounded by a number of variables including age, diet, genetic ... that a single gene can affect both serum HDL and BMD. Work completed to date has demonstrated that HDL ...

    Abstract Overwhelming evidence has linked cardiovascular disease and osteoporosis, but the shared root cause of these two diseases of the elderly remains unknown. Low levels of high density lipoprotein cholesterol (HDL) and bone mineral density (BMD) are risk factors for cardiovascular disease and osteoporosis respectively. A number of correlation studies have attempted to determine if there is a relationship between serum HDL and BMD but these studies are confounded by a number of variables including age, diet, genetic background, gender and hormonal status. Collectively, these data suggest that there is a relationship between these two phenotypes, but that the nature of this relationship is context specific. Studies in mice plainly demonstrate that genetic loci for BMD and HDL co-map and transgenic mouse models have been used to show that a single gene can affect both serum HDL and BMD. Work completed to date has demonstrated that HDL can interact directly with both osteoblasts and osteoclasts, but no direct evidence links bone back to the regulation of HDL levels. Understanding the genetic relationship between BMD and HDL has huge implications for understanding the clinical relationship between CVD and osteoporosis and for the development of safe treatment options for both diseases.
    MeSH term(s) Animals ; Bone Density/genetics ; Cholesterol, HDL/genetics ; Estrogens/metabolism ; Gene-Environment Interaction ; Genetic Pleiotropy ; Humans ; Osteoblasts/metabolism
    Chemical Substances Cholesterol, HDL ; Estrogens
    Language English
    Publishing date 2011-07-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 632515-4
    ISSN 1873-2763 ; 8756-3282
    ISSN (online) 1873-2763
    ISSN 8756-3282
    DOI 10.1016/j.bone.2011.07.002
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  7. Article: Genetic but not diet-induced hypercholesterolemia causes low apolipoprotein A-IV level in rabbit sera.

    Mezdour, H / Yamamura, T / Nomura, S / Yamamoto, A

    Atherosclerosis

    1995  Volume 113, Issue 2, Page(s) 171–178

    Abstract: ... fold increase in serum cholesterol, did not significantly alter apo A-IV concentration (6.65 +/- 1.52 ... In each of the groups studied, apo A-IV was distributed in two distinct pools; a high-density lipoprotein-(HDL ... A-IV). This assay was applied to the determination of its concentration and distribution in sera ...

    Abstract The present report describes a competitive enzyme immunoassay for rabbit apolipoprotein A-IV (apo A-IV). This assay was applied to the determination of its concentration and distribution in sera from normolipidemic and hyperlipidemic rabbits. The assay was sufficiently sensitive to study this 42-kDa protein in lipoproteins fractionated from 200 microliters of serum by FPLC gel filtration. In normolipidemic sera (n = 8), apo A-IV concentration was 5.32 +/- 0.76 mg/dl. A diet rich in cholesterol (0.5%), which induced an 18-fold increase in serum cholesterol, did not significantly alter apo A-IV concentration (6.65 +/- 1.52 mg/dl, n = 8). By contrast, genetically induced hypercholesterolemia (Watanabe heritable hyperlipidemia, WHHL mutation) caused a significantly reduced level of apo A-IV (3.8 +/- 1.14 mg/dl, n = 7). In each of the groups studied, apo A-IV was distributed in two distinct pools; a high-density lipoprotein-(HDL) associated pool and a lipoprotein-free pool. However, compared to normal, the distribution of apo A-IV in WHHL rabbit sera was shifted towards the lipoprotein-free pool. Consistent with previously reported observations on apo A-I, these results are compatible with the hypothesis of an impaired reverse transport of cholesterol in WHHL rabbits, an animal model for familial hypercholesterolemia.
    MeSH term(s) Amino Acid Sequence ; Animals ; Apolipoproteins A/blood ; Apolipoproteins A/genetics ; Apolipoproteins A/isolation & purification ; Chromatography, Gel ; Diet, Atherogenic ; Disease Models, Animal ; Hypercholesterolemia/blood ; Hypercholesterolemia/genetics ; Immune Sera ; Immunoenzyme Techniques ; Molecular Sequence Data ; Mutation ; Rabbits ; Species Specificity
    Chemical Substances Apolipoproteins A ; Immune Sera ; apolipoprotein A-IV
    Language English
    Publishing date 1995-03
    Publishing country Ireland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80061-2
    ISSN 1879-1484 ; 0021-9150
    ISSN (online) 1879-1484
    ISSN 0021-9150
    DOI 10.1016/0021-9150(94)05444-n
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  8. Article: Molecular genetic study of Finns with hypoalphalipoproteinemia and hyperalphalipoproteinemia: a novel Gly230 Arg mutation (LCAT[Fin]) of lecithin:cholesterol acyltransferase (LCAT) accounts for 5% of cases with very low serum HDL cholesterol levels.

    Miettinen, H E / Gylling, H / Tenhunen, J / Virtamo, J / Jauhiainen, M / Huttunen, J K / Kantola, I / Miettinen, T A / Kontula, K

    Arteriosclerosis, thrombosis, and vascular biology

    1998  Volume 18, Issue 4, Page(s) 591–598

    Abstract: In an attempt to identify genetic factors underlying extreme alterations of serum HDL cholesterol ... enzyme activity. In the low-HDL-C group of men (n=156), 8 carriers of LCAT(Fin) and 1 carrier of the LCAT ... significantly (P<.05) higher in the low-HDL-C group (4.8%) than in the high-HDL-C group (1.6%). In addition ...

    Abstract In an attempt to identify genetic factors underlying extreme alterations of serum HDL cholesterol (HDL-C) concentrations, we examined two probands with HDL-C levels <0.2 mmol/L and subsequently screened two large cohorts of smoking men, one with very low (0.2 to 0.7 mmol/L, n=156) and the other with elevated (1.9 to 3.6 mmol/L, n=160) HDL-C levels, for the newly detected mutations as well as some other mutations proposed to affect HDL-C levels. One of the probands had corneal opacities, microalbuminuria, hypertriglyceridemia, and reduced LDL apoprotein B concentration; the other had anemia and presented with stomatocytosis in his peripheral blood. The first proband was found to be homozygous for a novel LCAT Gly230Arg (LCAT[Fin]) mutation, and the second was homozygous for an Arg399Cys mutation we described previously. Transient expression of the mutant LCAT(Fin) cDNA in COS cells disclosed markedly diminished LCAT enzyme activity. In the low-HDL-C group of men (n=156), 8 carriers of LCAT(Fin) and 1 carrier of the LCAT Arg399Cys were identified. In addition, the frequency of the lipoprotein lipase (LPL) Asn291Ser mutation was significantly (P<.05) higher in the low-HDL-C group (4.8%) than in the high-HDL-C group (1.6%). In addition, we identified 1 carrier of the intron 14G-->A mutation of cholesterol ester transfer protein (CETP) in the high-HDL-C group and subsequently demonstrated cosegregation of the mutant allele with elevated HDL-C levels in the proband's family. In conclusion, we have identified a novel LCAT gene Gly230Arg mutation (LCAT[Fin]), which, together with the LPL Asn291Ser mutation, represents a relatively common genetic cause of diminishing HDL-C levels, at least among Finns. This article also reports occurrence of a CETP mutation in subjects having non-Japanese roots.
    MeSH term(s) Adult ; Arginine/genetics ; Carrier Proteins/genetics ; Cholesterol Ester Transfer Proteins ; Cholesterol Esters/blood ; Cholesterol, HDL/blood ; Cholesterol, LDL/blood ; Finland ; Glycine/genetics ; Glycoproteins ; Humans ; Hyperlipoproteinemias/enzymology ; Hyperlipoproteinemias/genetics ; Male ; Mutation ; Pedigree ; Phosphatidylcholine-Sterol O-Acyltransferase/genetics ; Phosphatidylcholine-Sterol O-Acyltransferase/metabolism ; Polymerase Chain Reaction ; Tangier Disease/diagnosis ; Tangier Disease/enzymology ; Tangier Disease/genetics
    Chemical Substances CETP protein, human ; Carrier Proteins ; Cholesterol Ester Transfer Proteins ; Cholesterol Esters ; Cholesterol, HDL ; Cholesterol, LDL ; Glycoproteins ; Arginine (94ZLA3W45F) ; Phosphatidylcholine-Sterol O-Acyltransferase (EC 2.3.1.43) ; Glycine (TE7660XO1C)
    Language English
    Publishing date 1998-04-16
    Publishing country United States
    Document type Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/01.atv.18.4.591
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  9. Article ; Online: Bile acid improves growth, lipid utilization and antioxidative status of genetically improved farmed tilapia (Oreochromis niloticus) fed with varying protein-lipid diets reared in inland saline water

    Bhusare, Saiprasad / Sardar, Parimal / Sahu, Narottam Prasad / Shamna, Nazeemashahul / Kumar, Pankaj / Paul, Mritunjoy / Jana, Prasanta / Raghuvaran, N. / Bhavatharaniya, U.

    Animal Feed Science and Technology. 2023 Sept., v. 303 p.115677-

    2023  

    Abstract: ... activity and high density lipoprotein cholesterol (HDL-CHO) were significantly (p < 0.05) decreased ... triacylglycerol (TAG), total cholesterol (T-CHO), and low density lipoprotein cholesterol (LDL-CHO) were ... liver superoxide dismutase (SOD) and catalase (CAT) activities and serum glucose (GLU), total protein ...

    Abstract A 60-day feeding trial was conducted to find out the effect of bile acid supplemented diets with varying protein and lipid levels on growth performance, body composition, antioxidant status and physio-biochemical responses of genetically improved farmed tilapia (GIFT) juveniles reared in inland saline water (ISW) of 10 ppt. Three hetero-nitrogenous (38–32% crude protein, CP), hetero-lipidic (8–14% lipid) and hetero-caloric (409–439 Kcal digestible energy/100 g) diets were supplemented with three levels (0%, 0.05% and 0.1%) of bile acid to prepare nine experimental diets viz. P₃₈L₈B₀ (38% CP, 8% lipid and 0% bile acid), P₃₈L₈B₀.₀₅ (38% CP, 8% lipid and 0.05% bile acid), P₃₈L₈B₀.₁ (38% CP, 8% lipid and 0.1% bile acid), P₃₅L₁₁B₀ (35% CP, 11% lipid and 0% bile acid), P₃₅L₁₁B₀.₀₅ (35% CP, 11% lipid and 0.05% bile acid), P₃₅L₁₁B₀.₁ (35% CP, 11% lipid and 0.1% bile acid), P₃₂L₁₄B₀ (32% CP, 14% lipid and 0% bile acid), P₃₂L₁₄B₀.₀₅ (32% CP, 14% lipid and 0.05% bile acid) and P₃₂L₁₄B₀.₁ (32% CP, 14% lipid and 0.1% bile acid). Four hundred and five acclimated GIFT juveniles (2.51 ± 0.01 g) were randomly distributed in nine treatment groups in triplicate (stocking density 15 fish/tank, 300 L) following 3 × 3 factorial design. Results indicated that body lipid, feed conversation ratio (FCR), amylase and lipase activities, gill and liver superoxide dismutase (SOD) and catalase (CAT) activities and serum glucose (GLU), total protein, triacylglycerol (TAG), total cholesterol (T-CHO), and low density lipoprotein cholesterol (LDL-CHO) were significantly (p < 0.05) increased and weight gain percentage (WG%), specific growth rate (SGR), protease activity and high density lipoprotein cholesterol (HDL-CHO) were significantly (p < 0.05) decreased with increasing dietary lipid levels and more pronounced effect was found in fish fed 32% protein and 14% lipid. Dietary bile acid significantly (p < 0.05) increased WG%, SGR, protein efficiency ratio, lipase activity and HDL-CHO and significantly (p < 0.05) decreased FCR, gill and liver SOD and CAT activities and serum GLU, TAG, T-CHO, and LDL-CHO with more pronounced effect by 0.05% dietary bile acid. In conclusion, feeding of 35% crude protein, 11% lipid and 0.05% bile acid can cause better growth performance, antioxidant status and physio-biochemical responses of GIFT juveniles reared in ISW of 10 ppt. This information will be useful in formulating the bile acid supplemented eco-friendly low protein high lipid (LPHL) feed for profitable culture of GIFT in ISW.
    Keywords Oreochromis niloticus ; amylases ; antioxidants ; bile acids ; blood glucose ; blood serum ; body fat ; carboxylic ester hydrolases ; catalase ; crude protein ; dietary fat ; enzyme activity ; feeds ; fish ; growth performance ; high density lipoprotein cholesterol ; liver ; low density lipoprotein cholesterol ; protein efficiency ratio ; saline water ; specific growth rate ; superoxide dismutase ; technology ; triacylglycerols ; weight gain ; GIFT ; Inland saline water ; Low protein high lipid ; Digestive and oxidative stress enzymes ; Serum biochemical indices
    Language English
    Dates of publication 2023-09
    Publishing place Elsevier B.V.
    Document type Article ; Online
    Note Pre-press version
    ZDB-ID 196563-3
    ISSN 0377-8401
    ISSN 0377-8401
    DOI 10.1016/j.anifeedsci.2023.115677
    Database NAL-Catalogue (AGRICOLA)

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  10. Article: Hyperlipidemia in patients on maintenance hemo- and peritoneal dialysis: the relative pathogenetic roles of triglyceride production and triglyceride removal.

    Chan, M K / Varghese, Z / Persaud, J W / Baillod, R A / Moorhead, J F

    Clinical nephrology

    1982  Volume 17, Issue 4, Page(s) 183–190

    Abstract: ... of hypertriglyceridemia and low concentrations of high density lipoprotein cholesterol was found. Hemodialysis patients ... had low or normal total cholesterol concentrations which were significantly lower ... patients and were correlated inversely with serum triglyceride concentrations. However, when compared ...

    Abstract A study was undertaken in 76 patients on maintenance hemodialysis and 26 patients on maintenance peritoneal dialysis to elucidate the pathogenesis of hyperlipidemia in these patients. A high prevalence of hypertriglyceridemia and low concentrations of high density lipoprotein cholesterol was found. Hemodialysis patients had low or normal total cholesterol concentrations which were significantly lower than those on peritoneal dialysis. The length of treatment did not affect the prevalence of the lipid abnormalities. Both pre- and post-heparin fractional clearance rates of Intralipid were markedly reduced in both groups of dialysis patients and were correlated inversely with serum triglyceride concentrations. However, when compared with normal subjects with similar fractional clearance rates of Intralipid, both groups of dialysis patients had higher serum triglyceride concentrations, probably reflecting increased triglyceride production. Serum triglyceride concentrations in both groups of dialysis patients were positively correlated with plasma immunoreactive insulin levels. Furthermore, a significant inverse correlation was observed between plasma immunoreactive insulin levels and post-heparin fractional clearance rates of intralipid. It was concluded that insulin resistance probably caused the defective triglyceride removal, and that both decreased removal and increased production of triglycerides contributed to the hyperlipidemia in dialysis patients.
    MeSH term(s) Adult ; Cholesterol/blood ; Cholesterol, HDL ; Female ; Humans ; Hyperlipidemias/etiology ; Lipoproteins, HDL/blood ; Male ; Middle Aged ; Peritoneal Dialysis/adverse effects ; Renal Dialysis/adverse effects ; Triglycerides/blood
    Chemical Substances Cholesterol, HDL ; Lipoproteins, HDL ; Triglycerides ; Cholesterol (97C5T2UQ7J)
    Language English
    Publishing date 1982-04
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 185101-9
    ISSN 0301-0430
    ISSN 0301-0430
    Database MEDical Literature Analysis and Retrieval System OnLINE

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