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[PMID]: 28634189
[Au] Autor:Minuz P; Meneguzzi A; Femia EA; Fava C; Calabria S; Scavone M; Benati D; Poli G; Zancanaro C; Calandra S; Lucchi T; Cattaneo M
[Ad] Address:Department of Medicine, Section of Internal Medicine, University Laboratory for Medical Research (LURM) and Regional Centre for the Study of Platelets, University of Verona, Verona, Italy pietro.minuz@univr.it.
[Ti] Title:Reduced platelet count, but no major platelet function abnormalities, are associated with loss-of-function ATP-binding cassette-1 gene mutations.
[So] Source:Clin Sci (Lond);131(16):2095-2107, 2017 Aug 15.
[Is] ISSN:1470-8736
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Loss-of-function mutations of the the ATP-binding cassette-1 ( ) gene are the cause of Tangier disease (TD) in homozygous subjects and familial HDL deficiency (FHD) in heterozygous subjects. These disorders are characterized by reduced plasma HDL-cholesterol (HDL-C) and altered efflux of cholesterol from cells. Previous studies in TD patients and murine models reported defects in platelet count, morphology, and function, but the issue is still controversial. We analyzed three subjects with low to very low HDL-C levels due to the loss-of-function mutations of the gene. Two related patients with FHD were heterozygous carriers of two mutations on the same allele; one, with TD, was homozygous for a different mutation. Mild to moderate thrombocytopenia was observed in all the patients. No morphological platelet abnormalities were detected under optical or EM. History of moderate bleeding tendency was recorded only in one of the FHD patients. Only limited alterations in platelet aggregation and activation of the integrin αIIbß3 were observed in one FHD patient. While α-granule secretion (P-selectin), content, and secretion of platelet δ-granules (serotonin, ATP, and ADP) and thromboxane (TX) A synthesis were normal in all the patients, the expression of lysosomal CD63, in response to some agonists, was reduced in TD patients. In conclusion, three patients carrying genetic variants had low platelet count, with the lowest values observed in TD, not associated with major alterations in platelet morphology and response to agonists or bleeding.
[Mh] MeSH terms primary: ATP Binding Cassette Transporter 1/genetics
Blood Platelets/physiology
Mutation
Thrombocytopenia/genetics
[Mh] MeSH terms secundary: Aged
Blood Platelets/ultrastructure
Blood Specimen Collection/methods
Female
Humans
Hypoalphalipoproteinemias/blood
Hypoalphalipoproteinemias/genetics
Male
Microscopy, Electron
Middle Aged
Platelet Aggregation/physiology
Platelet Count
Platelet Function Tests/methods
Tangier Disease/blood
Tangier Disease/genetics
Thrombocytopenia/blood
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (ABCA1 protein, human); 0 (ATP Binding Cassette Transporter 1)
[Em] Entry month:1709
[Cu] Class update date: 170906
[Lr] Last revision date:170906
[Js] Journal subset:IM
[Da] Date of entry for processing:170622
[St] Status:MEDLINE
[do] DOI:10.1042/CS20170195

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[PMID]: 28614534
[Au] Autor:Nienov OH; Matte L; Dias LS; Schmid H
[Ad] Address:Health Sciences Graduate Program, Obstetrics and Gynecology, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
[Ti] Title:Peripheral polyneuropathy in severely obese patients with metabolic syndrome but without diabetes: Association with low HDL-cholesterol.
[So] Source:Rev Assoc Med Bras (1992);63(4):324-331, 2017 Apr.
[Is] ISSN:1806-9282
[Cp] Country of publication:Brazil
[La] Language:eng
[Ab] Abstract:Introduction:: The purpose of this study was to evaluate the prevalence of peripheral polyneuropathy (PPN) in subjects with grade II and III obesity (Ob-II,III) and metabolic syndrome (MetS) but without diabetes and to investigate possible associated factors. Method:: A cross-sectional study was performed in non-diabetic Ob-II,III,MetS patients using the Michigan Neuropathy Screening Instrument (MNSI) to assess the presence of PPN. Results:: A total of 24 of 218 non-diabetic Ob-II,III,MetS patients had PPN. Based on univariate analysis, serum levels of LDL-cholesterol (p=0.046) were significantly associated with PPN, while serum triglycerides (p=0.118) and low HDL-cholesterol (p=0.057) showed a tendency toward this association. On a Poisson regression analysis, when the three possible associations were included, low HDL-cholesterol (p=0.047) remained independently associated. Conclusion:: In non-diabetic Ob-II,III,MetS patients, PPN defined by the MNSI showed a high prevalence and was associated with low levels of HDL-cholesterol. In order to diagnose that complication, neurological evaluation should be performed in these patients.
[Mh] MeSH terms primary: Hypoalphalipoproteinemias/complications
Metabolic Syndrome/complications
Obesity, Morbid/complications
Polyneuropathies/epidemiology
Polyneuropathies/etiology
[Mh] MeSH terms secundary: Adult
Anthropometry
Blood Glucose/analysis
Brazil/epidemiology
Cross-Sectional Studies
Female
Humans
Hypoalphalipoproteinemias/metabolism
Hypoalphalipoproteinemias/physiopathology
Male
Metabolic Syndrome/physiopathology
Obesity, Morbid/metabolism
Obesity, Morbid/physiopathology
Poisson Distribution
Polyneuropathies/metabolism
Polyneuropathies/physiopathology
Prevalence
Prospective Studies
Risk Factors
Statistics, Nonparametric
Surveys and Questionnaires
Triglycerides/blood
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Blood Glucose); 0 (Triglycerides)
[Em] Entry month:1709
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[Js] Journal subset:IM
[Da] Date of entry for processing:170615
[St] Status:MEDLINE

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[PMID]: 27815221
[Au] Autor:Gomez Rosso L; Lhomme M; Meroño T; Dellepiane A; Sorroche P; Hedjazi L; Zakiev E; Sukhorukov V; Orekhov A; Gasparri J; Chapman MJ; Brites F; Kontush A
[Ad] Address:INSERM UMR_S 1166, Faculte de Medecine Pitie-Salpetriere, 91 Bld de l'Hopital, 75013 Paris, France; University of Pierre and Marie Curie - Paris 6, Paris, France; Laboratory of Lipids and Atherosclerosis, Department of Clinical Biochemistry, INFIBIOC, University of Buenos Aires, CONICET, Buenos Aire
[Ti] Title:Poor glycemic control in type 2 diabetes enhances functional and compositional alterations of small, dense HDL3c.
[So] Source:Biochim Biophys Acta;1862(2):188-195, 2017 02.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:High-density lipoprotein (HDL) possesses multiple biological activities; small, dense HDL3c particles displaying distinct lipidomic composition exert potent antiatherogenic activities which can be compromised in dyslipidemic, hyperglycemic insulin-resistant states. However, it remains indeterminate (i) whether such functional HDL deficiency is related to altered HDL composition, and (ii) whether it originates from atherogenic dyslipidemia, dysglycemia, or both. In the present work we analyzed compositional characteristics of HDL subpopulations and functional activity of small, dense HDL3c particles in treatment-naïve patients with well-controlled (n=10) and poorly-controlled (n=8) type 2 diabetes (T2D) and in normolipidemic age- and sex-matched controls (n=11). Our data reveal that patients with both well- and poorly-controlled T2D displayed dyslipidemia and low-grade inflammation associated with altered HDL composition. Such compositional alterations in small, dense HDL subfractions were specifically correlated with plasma HbA1c levels. Further analysis using a lipidomic approach revealed that small, dense HDL3c particles from T2D patients with poor glycemic control displayed additional modifications of their chemical composition. In parallel, antioxidative activity of HDL3c towards oxidation of low-density lipoprotein was diminished. These findings indicate that defective functionality of small, dense HDL particles in patients with T2D is not only affected by the presence of atherogenic dyslipidemia, but also by the level of glycemic control, reflecting compositional alterations of HDL.
[Mh] MeSH terms primary: Cholesterol, HDL/blood
Cholesterol, HDL/metabolism
Diabetes Mellitus, Type 2/blood
Diabetes Mellitus, Type 2/metabolism
[Mh] MeSH terms secundary: Antioxidants/metabolism
Blood Glucose/metabolism
Dyslipidemias/blood
Dyslipidemias/metabolism
Female
Glycated Hemoglobin A/metabolism
Glycemic Index/physiology
Humans
Hypoalphalipoproteinemias/blood
Hypoalphalipoproteinemias/metabolism
Lipoproteins, LDL/blood
Male
Middle Aged
Oxidation-Reduction
Oxidative Stress/physiology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Antioxidants); 0 (Blood Glucose); 0 (Cholesterol, HDL); 0 (Glycated Hemoglobin A); 0 (Lipoproteins, LDL); 0 (hemoglobin A1c protein, human)
[Em] Entry month:1710
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[Js] Journal subset:IM
[Da] Date of entry for processing:161106
[St] Status:MEDLINE

  4 / 91 MEDLINE  
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[PMID]: 27567897
[Au] Autor:Kashyap S; Kheniser K; Li L; Bena J; Kasumov T
[Ad] Address:Departemnt of Endocrinology and Metabolism, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH, 44195, USA. Kashyas@ccf.org.
[Ti] Title:The therapeutic efficacy of intensive medical therapy in ameliorating high-density lipoprotein dysfunction in subjects with type two diabetes.
[So] Source:Lipids Health Dis;15(1):141, 2016 Aug 27.
[Is] ISSN:1476-511X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: To determine whether 12 months of intensive medical therapy (IMT) improves HDL functionality parameters in subjects with type II diabetes (T2D). METHODS: Retrospective, randomized, and controlled 12-month IMT intervention trial that enrolled 13-subjects with T2D (age 51- years, fasting glucose 147 mg/dL, body mass index [BMI] 36.5 kg/m(2)) and nine healthy control (46-years, fasting glucose 90 mg/dL, BMI 26.5 kg/m2). Subjects with T2D underwent IMT and HDL functionality measures (pro-inflammatory index of high-density lipoprotein (pHDL)), paraoxonase one (PON1), ceruloplasmin (Cp), and myeloperoxidase (MPO) activity were performed on samples at baseline and at 12-months following IMT. RESULTS: At baseline, pHDL index was significantly higher in subjects with T2D (p < 0.001) and apolipoprotein A-1 levels were significantly lower (p = 0.013) vs. CONTROLS: After 12-months, there was a trend for improved pHDL activity (p = 0.083), as indicated by intent-to-treat analysis, but when the non-adherent subject was omitted (per-protocol), significant attenuations in pHDL activity (p = 0.040) were noted; Δ pHDL activity at 12-months was associated with Δ weight (r = 0.62, p = 0.032) and Δ fasting glucose (r = 0.65, p = 0.022). Moreover, PON1 activity significantly improved (p < 0.001). The aforementioned occurred in association with improvements in inflammatory markers (i.e., C-reactive protein & tumor necrosis factor), hemoglobin A1C, fasting glucose, triglycerides, high-density lipoprotein levels and adipokines. CONCLUSION: IMT ameliorates pHDL index and significantly improves anti-oxidative function, as measured by PON1. Improvements in weight and fasting glucose mediated the decrease in pHDL index. Pharmacological aids and lifestyle modification are required to improve cardiovascular risk factors, subsequent mortality risk, and promote T2D remission. Application of either form of therapy alone may only have relatively miniscule effects on the aforementioned factors, in relation to the aggregate.
[Mh] MeSH terms primary: Diabetes Mellitus, Type 2/therapy
Diet, Diabetic
Exercise Therapy
Hypoglycemic Agents/pharmacology
Lipoproteins, HDL/drug effects
[Mh] MeSH terms secundary: Adult
Apolipoprotein A-I/blood
Apolipoprotein A-I/drug effects
Biguanides/pharmacology
Biguanides/therapeutic use
Combined Modality Therapy
Diabetes Mellitus, Type 2/blood
Diabetes Mellitus, Type 2/complications
Female
Humans
Hypoalphalipoproteinemias/complications
Hypoalphalipoproteinemias/diet therapy
Hypoalphalipoproteinemias/drug therapy
Hypoalphalipoproteinemias/therapy
Hypoglycemic Agents/therapeutic use
Insulin/analogs & derivatives
Insulin/pharmacology
Insulin/therapeutic use
Lipoproteins, HDL/blood
Male
Middle Aged
Retrospective Studies
Treatment Outcome
[Pt] Publication type:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Name of substance:0 (Apolipoprotein A-I); 0 (Biguanides); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Lipoproteins, HDL)
[Em] Entry month:1704
[Cu] Class update date: 170407
[Lr] Last revision date:170407
[Js] Journal subset:IM
[Da] Date of entry for processing:160829
[St] Status:MEDLINE
[do] DOI:10.1186/s12944-016-0314-4

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[PMID]: 27565770
[Au] Autor:Schaefer EJ; Anthanont P; Diffenderfer MR; Polisecki E; Asztalos BF
[Ad] Address:Cardiovascular Nutrition Laboratory, Human Nutrition Research Center on Aging at Tufts University and Tufts University School of Medicine, Boston, MA; Boston Heart Diagnostics, Framingham, MA. Electronic address: ernst.schaefer@tufts.edu.
[Ti] Title:Diagnosis and treatment of high density lipoprotein deficiency.
[So] Source:Prog Cardiovasc Dis;59(2):97-106, 2016 Sep - Oct.
[Is] ISSN:1873-1740
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Low serum high density lipoprotein cholesterol level (HDL-C) <40 mg/dL in men and <50 mg/dL in women is a significant independent risk factor for cardiovascular disease (CVD), and is often observed in patients with hypertriglyceridemia, obesity, insulin resistance, and diabetes. Patients with marked deficiency of HDL-C (<20 mg/dL) in the absence of secondary causes are much less common (<1% of the population). These patients may have homozygous, compound heterozygous, or heterozygous defects involving the apolipoprotein (APO)AI, ABCA1, or lecithin:cholesterol acyl transferase genes, associated with apo A-I deficiency, apoA-I variants, Tangier disease , familial lecithin:cholesteryl ester acyltransferase deficiency, and fish eye disease. There is marked variability in laboratory and clinical presentation, and DNA analysis is necessary for diagnosis. These patients can develop premature CVD, neuropathy, kidney failure, neuropathy, hepatosplenomegaly and anemia. Treatment should be directed at optimizing all non-HDL risk factors.
[Mh] MeSH terms primary: Hypoalphalipoproteinemias
[Mh] MeSH terms secundary: Disease Management
Humans
Hypoalphalipoproteinemias/diagnosis
Hypoalphalipoproteinemias/etiology
Hypoalphalipoproteinemias/therapy
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1705
[Cu] Class update date: 170902
[Lr] Last revision date:170902
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:160828
[St] Status:MEDLINE

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[PMID]: 27543092
[Au] Autor:Tsay YC; Chen CH; Pan WH
[Ti] Title:Ages at Onset of 5 Cardiometabolic Diseases Adjusting for Nonsusceptibility: Implications for the Pathogenesis of Metabolic Syndrome.
[So] Source:Am J Epidemiol;184(5):366-77, 2016 Sep 01.
[Is] ISSN:1476-6256
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:To shed light on the etiology of metabolic syndrome development, it is important to understand whether its 5 component disorders follow certain onset sequences. To explore disease progression of the syndrome, we studied the ages at onset of 5 cardiometabolic diseases: abdominal obesity, diabetes, hypertension, hypertriglyceridemia, and hypo-α-lipoproteinemia. In analyzing longitudinal data from the Cardiovascular Disease Risk Factors Two-Township Study (1989-2002) in Taiwan, we adjusted for nonsusceptibility, utilizing the logistic-accelerated failure time location-scale mixture regression models for left-truncated and interval-censored data to simultaneously estimate the associations of township and sex with the susceptibility probability and the age-at-onset distribution of susceptible individuals for each disease. We then validated the onset sequences of 5 cardiometabolic diseases by comparing the overall probability density curves across township-sex strata. Visualization of these curves indicates that women tended to have onsets of abdominal obesity and hypo-α-lipoproteinemia in young adulthood, hypertension and hypertriglyceridemia in middle age, and diabetes later; men tended to have onsets of abdominal obesity, hypo-α-lipoproteinemia, and hypertriglyceridemia in young adulthood, hypertension in middle age, and diabetes later. Different onset patterns of abdominal obesity, hypo-α-lipoproteinemia, and male hypertension were identified between townships. Our proposed method provides a novel strategy for investigating both pathogenesis and preventive measures of complex syndromes.
[Mh] MeSH terms primary: Age of Onset
Disease Progression
Disease Susceptibility
Metabolic Syndrome/etiology
[Mh] MeSH terms secundary: Adult
Aged
Cardiovascular Diseases/complications
Cardiovascular Diseases/epidemiology
Cardiovascular Diseases/etiology
Diabetes Complications/epidemiology
Diabetes Complications/etiology
Diabetes Mellitus/epidemiology
Diabetes Mellitus/etiology
Female
Humans
Hypertension/complications
Hypertension/epidemiology
Hypertension/etiology
Hypertriglyceridemia/complications
Hypertriglyceridemia/epidemiology
Hypertriglyceridemia/etiology
Hypoalphalipoproteinemias/complications
Hypoalphalipoproteinemias/epidemiology
Hypoalphalipoproteinemias/etiology
Logistic Models
Longitudinal Studies
Male
Metabolic Syndrome/epidemiology
Middle Aged
Obesity, Abdominal/complications
Obesity, Abdominal/epidemiology
Obesity, Abdominal/etiology
Risk Factors
Taiwan/epidemiology
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1706
[Cu] Class update date: 171116
[Lr] Last revision date:171116
[Js] Journal subset:IM
[Da] Date of entry for processing:160821
[St] Status:MEDLINE
[do] DOI:10.1093/aje/kwv449

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[PMID]: 26828509
[Au] Autor:Yao MH; Guo H; He J; Yan YZ; Ma RL; Ding YS; Zhang JY; Liu JM; Zhang M; Li SG; Xu SZ; Niu Q; Ma JL; Guo SX
[Ad] Address:Department of Public Health and Key Laboratory of Xinjiang Endemic and Ethnic Diseases of the Ministry of Education, Shihezi University School of Medicine, Shihezi 832002, China. ymhldjxa@sina.com.
[Ti] Title:Interactions of Six SNPs in ABCA1gene and Obesity in Low HDL-C Disease in Kazakh of China.
[So] Source:Int J Environ Res Public Health;13(2):176, 2016 Jan 28.
[Is] ISSN:1660-4601
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To detect the interactions between six functional polymorphisms in ABCA1 and obesity in Kazakhs with low HDL-C levels. METHODS: A total of 204 patients with low HDL-C and 207 health control subjects, which were randomly selected from among 5692 adult Kazakhs, were matched for age and sex. We genotyped ABCA1 single nucleotide polymorphisms of rs2515602, rs3890182, rs2275542, rs2230806, rs1800976, and rs4149313. RESULTS: (1) The genotypic and allelic frequencies of rs2515602, rs2230806 and rs4149313 were different between normal HDL-C and low HDL-C subjects, the genotypic frequency of rs2275542 was also different between normal HDL-C and low HDL-C subjects (p < 0.05); (2) the level of HDL-C (rs2515602 and rs2275542) in normal HDL-C subjects were different among the genotypes (p < 0.05); the levels of TC, LDL-C (rs2515602, rs4149313); TG (rs2515602, rs1800976, rs4149313) in low HDL-C patients were different among the genotypes (p < 0.05); (3) interactions between the rs3890182, rs2275542, rs180096, and rs4149313 polymorphisms in ABCA1 gene and obesity may be associated with low HDL-C disease; (4) the C-C-C-A-A-G, T-C-C-A-A-A, T-C-C-A-A-G, C-C-C-A-A-A, C-T-G-G-A-A, and T-T-C-G-A-A haplotypes were significant between the subjects with normal HDL-C and low HDL-C level (p < 0.05). CONCLUSIONS: The differences in serum lipid levels between normal HDL-C and low HDL-C subjects among Kazakhs might partly result from ABCA1 gene polymorphisms; ABCA1 gene polymorphisms may be associated with low HDL-C disease; the low HDL-C disease might partly result from interactions between ABCA1 gene polymorphisms and obesity; the C-C-C-A-A-G, T-C-C-A-A-A, and T-C-C-A-A-G haplotypes may serve as risk factors of low HDL-C disease among Kazakhs, the C-C-C-A-A-A, C-T-G-G-A-A, and T-T-C-G-A-A haplotypes may serve as protective factor of low HDL-C disease among Kazakhs.
[Mh] MeSH terms primary: ATP Binding Cassette Transporter 1/genetics
Hypoalphalipoproteinemias/genetics
Obesity/genetics
Polymorphism, Single Nucleotide
[Mh] MeSH terms secundary: Adult
Biomarkers/blood
Case-Control Studies
China
Cholesterol, HDL/blood
Cholesterol, HDL/deficiency
Female
Genetic Markers
Genotype
Humans
Hypoalphalipoproteinemias/blood
Hypoalphalipoproteinemias/complications
Male
Middle Aged
Obesity/blood
Obesity/complications
Risk Factors
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (ABCA1 protein, human); 0 (ATP Binding Cassette Transporter 1); 0 (Biomarkers); 0 (Cholesterol, HDL); 0 (Genetic Markers)
[Em] Entry month:1609
[Cu] Class update date: 170220
[Lr] Last revision date:170220
[Js] Journal subset:IM
[Da] Date of entry for processing:160202
[St] Status:MEDLINE

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[PMID]: 26667175
[Au] Autor:Ronsein GE; Reyes-Soffer G; He Y; Oda M; Ginsberg H; Heinecke JW
[Ad] Address:From the ‡Department of Medicine, University of Washington, Seattle, WA, 98109; ronsein@iq.usp.br.
[Ti] Title:Targeted Proteomics Identifies Paraoxonase/Arylesterase 1 (PON1) and Apolipoprotein Cs as Potential Risk Factors for Hypoalphalipoproteinemia in Diabetic Subjects Treated with Fenofibrate and Rosiglitazone.
[So] Source:Mol Cell Proteomics;15(3):1083-93, 2016 Mar.
[Is] ISSN:1535-9484
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Low levels of high-density lipoprotein cholesterol (HDL-C) and high triglyceride levels contribute to the excess rate of cardiovascular events seen in subjects with type 2 diabetes. Fenofibrate treatment partially reverses dyslipidemia in these subjects. However, a paradoxical marked reduction in HDL-C and HDL's major protein, apolipoprotein A-I, is a complication of fenofibrate in combination with rosiglitazone, an insulin-sensitizing agent. Risk factors for this condition, termed hypoalphalipoproteinemia, have yet to be identified. Using a case-control study design with subjects enrolled in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial, we tested the hypothesis that alterations in HDL's protein cargo predispose diabetic subjects to fenofibrate/rosiglitazone-induced hypoalphalipoproteinemia. HDL was isolated from blood obtained from controls (no decreases or increase in HDL-C while receiving fenofibrate/rosiglitazone therapy) and cases (developed hypoalphalipoproteinemia after fenofibrate/rosiglitazone treatment) participating in the ACCORD study before they began fenofibrate/rosiglitazone treatment. HDL proteins were quantified by targeted parallel reaction monitoring (PRM) and selected reaction monitoring (SRM) with isotope dilution. This approach demonstrated marked increases in the relative concentrations of paraoxonase/arylesterase 1 (PON1), apolipoprotein C-II (APOC2), apolipoprotein C-I, and apolipoprotein H in the HDL of subjects who developed hypoalphalipoproteinemia. The case and control subjects did not differ significantly in baseline HDL-C levels or other traditional lipid risk factors. We used orthogonal biochemical techniques to confirm increased levels of PON1 and APOC2. Our observations suggest that an imbalance in HDL proteins predisposes diabetic subjects to develop hypoalphalipoproteinemia on fenofibrate/rosiglitazone therapy.
[Mh] MeSH terms primary: Apolipoprotein C-II/metabolism
Aryldialkylphosphatase/metabolism
Cardiovascular Diseases/prevention & control
Diabetes Mellitus, Type 2/drug therapy
Drug Therapy, Combination/adverse effects
Hypoalphalipoproteinemias/chemically induced
Proteomics/methods
[Mh] MeSH terms secundary: Aged
Cardiovascular Diseases/blood
Case-Control Studies
Diabetes Mellitus, Type 2/metabolism
Female
Fenofibrate/administration & dosage
Fenofibrate/adverse effects
Humans
Hypoglycemic Agents/administration & dosage
Hypoglycemic Agents/adverse effects
Hypolipidemic Agents/administration & dosage
Hypolipidemic Agents/adverse effects
Lipoproteins, HDL/blood
Male
Middle Aged
Risk Factors
Thiazolidinediones/administration & dosage
Thiazolidinediones/adverse effects
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Apolipoprotein C-II); 0 (Hypoglycemic Agents); 0 (Hypolipidemic Agents); 0 (Lipoproteins, HDL); 0 (Thiazolidinediones); 05V02F2KDG (rosiglitazone); EC 3.1.8.1 (Aryldialkylphosphatase); EC 3.1.8.1 (PON1 protein, human); U202363UOS (Fenofibrate)
[Em] Entry month:1612
[Cu] Class update date: 170301
[Lr] Last revision date:170301
[Js] Journal subset:IM
[Da] Date of entry for processing:151216
[St] Status:MEDLINE
[do] DOI:10.1074/mcp.M115.054528

  9 / 91 MEDLINE  
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[PMID]: 26687706
[Au] Autor:Pisciotta L; Vitali C; Favari E; Fossa P; Adorni MP; Leone D; Artom N; Fresa R; Calabresi L; Calandra S; Bertolini S
[Ad] Address:Department of Internal Medicine, University of Genoa, Genoa, Italy.
[Ti] Title:A complex phenotype in a child with familial HDL deficiency due to a novel frameshift mutation in APOA1 gene (apoA-IGuastalla).
[So] Source:J Clin Lipidol;9(6):837-846, 2015 Nov-Dec.
[Is] ISSN:1933-2874
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: We describe a kindred with high-density lipoprotein (HDL) deficiency due to APOA1 gene mutation in which comorbidities affected the phenotypic expression of the disorder. METHODS: An overweight boy with hypertriglyceridemia (HTG) and HDL deficiency (HDL cholesterol 0.39 mmol/L, apoA-I 40 mg/dL) was investigated. We sequenced the candidate genes for HTG (LPL, APOC2, APOA5, GPIHBP1, LMF1) and HDL deficiency (LCAT, ABCA1 and APOA1), analyzed HDL subpopulations, measured cholesterol efflux capacity (CEC) of sera and constructed a model of the mutant apoA-I. RESULTS: No mutations in HTG-related genes, ABCA1 and LCAT were found. APOA1 sequence showed that the proband, his mother and maternal grandfather were heterozygous of a novel frameshift mutation (c.546_547delGC), which generated a truncated protein (p.[L159Afs*20]) containing 177 amino acids with an abnormal C-terminal tail of 19 amino acids. Trace amounts of this protein were detectable in plasma. Mutation carriers had reduced levels of LpA-I, preß-HDL and large HDL and no detectable HDL-2 in their plasma; their sera had a reduced CEC specifically the ABCA1-mediated CEC. Metabolic syndrome in the proband explains the extremely low HDL cholesterol level (0.31 mmol/L), which was half of that found in the other carriers. The proband's mother and grandfather, both presenting low plasma low-density lipoprotein cholesterol, were carriers of the ß-thalassemic trait, a condition known to be associated with a reduced low-density lipoprotein cholesterol and a reduced prevalence of cardiovascular disease. This trait might have delayed the development of atherosclerosis related to HDL deficiency. CONCLUSIONS: In these heterozygotes for apoA-I truncation, the metabolic syndrome has deleterious effect on HDL system, whereas ß-thalassemia trait may delay the onset of cardiovascular disease.
[Mh] MeSH terms primary: Apolipoproteins A/genetics
Frameshift Mutation
Hypoalphalipoproteinemias/genetics
Phenotype
[Mh] MeSH terms secundary: Adolescent
Aged
Aged, 80 and over
Apolipoproteins A/blood
Biological Transport
Cholesterol/blood
Cholesterol/metabolism
Female
Humans
Hypoalphalipoproteinemias/blood
Hypoalphalipoproteinemias/metabolism
Macrophages/metabolism
Male
Middle Aged
Pedigree
Triglycerides/blood
Triglycerides/genetics
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Apolipoproteins A); 0 (Triglycerides); 97C5T2UQ7J (Cholesterol)
[Em] Entry month:1609
[Cu] Class update date: 170729
[Lr] Last revision date:170729
[Js] Journal subset:IM
[Da] Date of entry for processing:151222
[St] Status:MEDLINE

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[PMID]: 26530191
[Au] Autor:Figueroa C; Droppelmann K; Quiñones V; Amigo L; Mendoza C; Serrano V; Véjar M; Maiz A; Rigotti A
[Ti] Title:El ácido nicotínico aumenta el transporte celular de colesterol de las lipoproteínas de alta densidad en pacientes con hipoalfalipoproteinemia. [Nicotinic acid increases cellular transport of high density lipoprotein cholesterol in patients with hypoalphalipoproteinemia].
[So] Source:Rev Med Chil;143(9):1097-104, 2015 Sep.
[Is] ISSN:0717-6163
[Cp] Country of publication:Chile
[La] Language:spa
[Ab] Abstract:BACKGROUND: Plasma high density lipoproteins (HDL) are involved in reverse cholesterol transport mediated by the scavenger receptor class B type I (SR-BI). Nicotinic acid increases HDL cholesterol levels, even though its specific impact on SR-BI dependent-cellular cholesterol transport remains unknown. AIM: To determine the effect of nicotinic acid on HDL particle functionality in cholesterol efflux and uptake mediated by SR-BI in cultured cells in hypoalphalipoproteinemic patients. MATERIAL AND METHODS: In a pilot study, eight patients with low HDL (≤ 40 mg/dL) were treated with extended release nicotinic acid. HDL cholesterol and phospholipid levels, HDL2 and HDL3 fractions and HDL particle sizes were measured at baseline and post-therapy. Before and after nicotinic acid treatment, HDL particles were used for cholesterol transport studies in cells transfected with SR-BI. RESULTS: Nicotinic acid treatment raised total HDL cholesterol and phospholipids, HDL2 levels as well as HDL particle size. Nicotinic acid significantly increased HDL cholesterol efflux and uptake capacity mediated by SR-BI in cultured cells. CONCLUSIONS: Nicotinic acid therapy increases SR-BI-dependent HDL cholesterol transport in cultured cells, establishing a new cellular mechanism by which this lipid-lowering drug appears to modulate HDL metabolism in patients with hypoalphalipoproteinemia.
[Mh] MeSH terms primary: Cholesterol, HDL/metabolism
Hypoalphalipoproteinemias/metabolism
Hypolipidemic Agents/pharmacology
Lipoproteins, HDL/metabolism
Niacin/pharmacology
[Mh] MeSH terms secundary: Aged
Biological Transport
Cholesterol, HDL/drug effects
Female
Humans
Male
Middle Aged
Phospholipids/blood
Pilot Projects
Scavenger Receptors, Class B/metabolism
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Cholesterol, HDL); 0 (Hypolipidemic Agents); 0 (Lipoproteins, HDL); 0 (Phospholipids); 0 (SCARB1 protein, human); 0 (Scavenger Receptors, Class B); 2679MF687A (Niacin)
[Em] Entry month:1603
[Cu] Class update date: 151104
[Lr] Last revision date:151104
[Js] Journal subset:IM
[Da] Date of entry for processing:151105
[St] Status:MEDLINE


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