Role of ApoCs in Lipoprotein Metabolism

Jong, M.C.; Hofker, Marten H.; Havekes, Louis M.

doi:10.1161/01.atv.19.3.472

Cited by 470 publications

(242 citation statements)

References 176 publications

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“…APOA1, the major structural protein of HDL-cholesterol plays a key role in reverse cholesterol transport [4]. APOC3 is a critical factor in VLDL-triglyceride metabolism [5]. The physiological role of APOA4 is still largely unknown, except for its postulated function as a satiety factor or as a co-factor for intestinal fat absorption [6].…”

Section: Introductionmentioning

confidence: 99%

Plasma apolipoprotein A5 and triglycerides in type 2 diabetes

et al. 2006

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Aims/hypothesis: Variation in the human apolipoprotein (APO) A5 gene (APOA5) is associated with elevated plasma triglycerides. However, data on the exact role of plasma concentrations of APOA5 in human triglyceride homeostasis are lacking. In the present study, we estimated plasma APOA5 levels in patients with type 2 diabetes at baseline and during atorvastatin treatment, a lipid-lowering treatment that results in a reduction in plasma triglycerides and APOC3. Subjects, materials and methods: Plasma APOA5 concentration was measured by ELISA in 215 subjects with type 2 diabetes, who were taken from the Diabetes Atorvastatin Lipid-lowering Intervention (DALI) study, a 30-week randomised, double-blind, placebo-controlled study, and given atorvastatin 10 mg or 80 mg daily. Results: At baseline, average plasma APOA5 concentration was 25.7±15.6 μg/100 ml. Plasma APOA5 (R s =0.40), APOC3 (R s =0.72) and APOE (R s =0.45) were positively correlated with plasma triglyceride levels (all p<0.001). In multiple linear regression analysis, adjusted for age and sex, the variation in plasma triglycerides was explained mostly by APOC3 (52%) and only to a small extent by APOA5 (6%) and APOE (1%). Atorvastatin treatment decreased plasma triglycerides, APOA5, APOC3 and APOE (all p<0.0001). After treatment, APOC3 remained the major determinant of plasma triglyceride levels (59%), while the contributions of APOA5 and APOE were insignificant (2 and 3%). Conclusions/interpretation: Our findings reveal a positive association between plasma APOA5 and triglycerides in patients with type 2 diabetes. Treatment with atorvastatin decreased plasma APOA5, APOC3, APOE and triglycerides. In contrast to APOC3, APOA5 is not a major determinant of triglyceride metabolism in these patients.

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Section: Introductionmentioning

confidence: 99%

Plasma apolipoprotein A5 and triglycerides in type 2 diabetes

et al. 2006

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“…ApoCIII protein is a monomer of 79 amino acids, synthesized primarily in liver and to a lesser extent in small intestine (1). It circulates in plasma in association with TG dch lipoproteins and HDLs.…”

Section: Introductionmentioning

confidence: 99%

“…ApoCIII inhibitsthe lipoprotein Upase and hampers the TG clearance. Overexpression of the human APOC3 gene causes hypertriglyceridemia in transgenic mice, whereas the absence of APOC3 in knockout mice reduces plasma TG to 70% of normal (1). An Sstl polymorphism resulting from a C->G base transversion in 3' untranslated region of APOC3 gene had been studied extensively in relation to hypertriglyceridemia .…”

Section: Introductionmentioning

confidence: 99%

Study of apolipoproteinc3 Sstl polymorphism in healthy volunteers from Northern India

Chhabra

Agarwal²,

Vasisht

et al. 2003

Indian J Clin Biochem

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Several studies including a small case-control (hypertriglyceridemic / normotriglyceridemic individuals) study by us revealed close association between rare $2 allele of APOC3 Sstl polymorphism and hypertriglyceddemia. With the understanding that Asian Indians are highly vulnerable to the adverse effects of hypertdglyceridemia, we extended the investigation and studied the frequency distribution of this polymorphism in 216 healthy volunteers from Northern plains of India. We found that more than 50% of the study population had one ortwo $2 allele. This may suggest that a larger fraction of this population is genetically predisposed to hypertdglyceddemia.

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“…n-3 Fatty acid intake is also associated with a reduction in plasma biomarkers of inflammation such as C-reactive protein (CRP) (5) . The physiological effects of DHA and EPA include lowering plasma TAG concentrations, inhibiting plaque formation, decreasing platelet aggregation and reducing arrhythmias (8)(9)(10) .…”

mentioning

confidence: 99%

Relationship between fish intake, n-3 fatty acids, mercury and risk markers of CHD (National Health and Nutrition Examination Survey 1999–2002)

Smith

Barraj²,

Kantor

et al. 2009

Public Health Nutr.

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Background: Fish consumption has been shown to be inversely associated with CHD, which may be due to n-3 fatty acids. The n-3 fatty acids, EPA and DHA, are naturally found only in marine sources. Dietary intakes of methylmercury from certain fish have been hypothesized to increase the risk of CHD. Conclusions: The levels of DHA 1 EPA and other nutrients in fish may be adequate to offset the hypothesized risks of heart disease related to ingesting Hg from fish.

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Role of ApoCs in Lipoprotein Metabolism

Cited by 470 publications

References 176 publications

Plasma apolipoprotein A5 and triglycerides in type 2 diabetes

Plasma apolipoprotein A5 and triglycerides in type 2 diabetes

Study of apolipoproteinc3 Sstl polymorphism in healthy volunteers from Northern India

Relationship between fish intake, n-3 fatty acids, mercury and risk markers of CHD (National Health and Nutrition Examination Survey 1999–2002)

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