The Role of Hypertriglyceridemia in the Development of Atherosclerosis and Endothelial Dysfunction

Matsumoto, S.; Gotoh, Nozomi; Hishinuma, Saori; Abe, Yohei; Shimizu, Yoshimi; Katano, Yumi; Ishihata, Akira

doi:10.3390/nu6031236

Cited by 35 publications

(33 citation statements)

References 26 publications

(36 reference statements)

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“…A number of HDL constituents may interact with the vascular endothelium (41,42). Various of studies have reported that elevated TG, TC, LDL and VLDL levels and decreased HDL levels may serve a role in the development of endothelial damage and vascular dysfunction (43,44). Obesity, which is primarily caused by intake and storage of nutritional substrates, is an important public health issue (45).…”

Section: Discussionmentioning

confidence: 99%

Maternal lipids, BMI and IL‑17/IL‑35 imbalance in concurrent gestational diabetes mellitus and preeclampsia

Cao¹,

Wang

Ting-mei³

et al. 2018

Exp Ther Med

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The objective of the present study was to investigate the role of blood glucose, lipid metabolism, body mass index (BMI), C-reactive protein (CRP) as well as an interleukin (IL)-17/IL-35 imbalance in the pathogenesis of concurrent gestational diabetes mellitus (GDM) and preeclampsia (PE) (DPE). The mRNA expression of forkhead box protein 3 (FoxP3), IL-35 [including Epstein-Barr virus-induced gene 3 (EBI3) and P35 subunits] and IL-17 in the peripheral blood mononuclear cells of patients with DPE (n=30), GDM (n=33), PE (n=33) and normal pregnancy (n=33) were determined by reverse transcription-quantitative polymerase chain reaction. The serum levels of IL-35, IL-17 and CRP were analyzed using ELISA. Serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL) and fasting blood glucose (FBG) were also detected. The levels of low-density lipoprotein (LDL) were calculated using the Friedewald formula. Body weight and height were determined in order to calculate the BMI. It was observed that the levels of FBG were markedly elevated in patients with GDM, PE and DPE. In addition, significantly higher serum TG, TC, LDL and very LDL were detected in patients with GDM, PE and DPE compared with those in subjects with normal pregnancies. By contrast, the concentration of HDL was lower in the patient groups. In addition, higher BMI values were identified in patients with GDM, PE and DPE. A decreased expression of FoxP3, P35 and EBI3 mRNA, and an elevated expression of IL-17 in PBMCs was detected in patients with GDM, PE and DPE. In addition, higher serum levels of IL-17 and CRP, as well as lower levels of IL-35, were observed. Furthermore, in patients with DPE, positive correlations of diastolic blood pressure with IL-17 levels, BMI and TG, as well as IL-17 levels with BMI and proteinuria were identified. In conclusion, the present study indicated that abnormal maternal lipids, hyperglycemia, high BMI, high CRP and IL-17/IL-35 imbalance may have a role in the pathophysiology of DPE. Therefore, pregnant women and clinicians should be made aware that maternal hyperlipidaemia, hyperglycemia, high BMI, high CRP levels and IL-17/IL-35 imbalance may lead to DPE.

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Section: Discussionmentioning

confidence: 99%

Maternal lipids, BMI and IL‑17/IL‑35 imbalance in concurrent gestational diabetes mellitus and preeclampsia

Cao¹,

Wang

Ting-mei³

et al. 2018

Exp Ther Med

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“…Postprandial lipemia is hypothesized to be a risk factor for cardiovascular disease by inducing endothelial dysfunction [20]. The vascular endothelial lining functions to maintain adequate blood flow and regulate coagulation and inflammation.…”

Section: Role Of Postprandial Lipemia In Endothelial Inflammation Andmentioning

confidence: 99%

Postprandial Lipemia as Cardiovascular Disease Risk Factor

Amba¹,

Mercado-Asis²

2019

Dyslipidemia

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Postprandial lipemia (PPL) is characterized by prolonged and increased levels of lipids especially triglycerides (TG) and triglyceride-rich lipoprotein levels after a meal. There are an increasing number of evidence that postprandial lipemia is a significant risk factor for cardiovascular disease because of its causative role in atherosclerosis and endothelial dysfunction. This has serious implications because common dietary patterns are characterized by high fat content and meal consumption; hence, most will be in a postprandial state resulting to frequent and prolonged exposure to high lipid levels. The review will present the current evidences for the role of postprandial lipemia as a risk factor for cardiovascular disease and its association with other cardiovascular risk factors, namely, diabetes and obesity. We will also present recommendations on the diagnosis and management of postprandial lipemia.

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“…Postprandial hyperlipidemia is characterized by triglyceride-rich lipoproteins (TRL) such as chylomicrons, very low-density lipoproteins and their remnants. Both endothelial dysfunction and elevated plasma triglycerides are thought to play important roles in atherosclerosis [26; 27; 28; 29; 30; 31; 32; 33; 34; 35], but the influence the lens effect may have on NO bioavailability, however, does not appear to have been fully considered. At a constant rate of endothelial NO production, increased NO consumption within TRL could decrease the amount of NO available for direct vasodilation and proper endothelial function.…”

Section: Introductionmentioning

confidence: 99%

Postprandial lipids accelerate and redirect nitric oxide consumption in plasma

et al. 2016

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Nitric oxide (NO) and O2 are both three- to four-fold more soluble in biological lipids than in aqueous solutions. Their higher concentration within plasma lipids accelerates NO autoxidation to an extent that may be of importance to overall NO bioactivity. This study was undertaken to test the hypothesis that increased plasma lipids after a high-fat meal appreciably accelerate NO metabolism and alter the byproducts formed. We found that plasma collected from subjects after consumption of a single high-fat meal had a higher capacity for NO consumption and consumed NO more rapidly compared to fasting plasma. This increased NO consumption showed a direct correlation with plasma triglyceride concentrations (p=0.006). The accelerated NO consumption in postprandial plasma was reversed by removal of the lipids from the plasma, was mimicked by the addition of hydrophobic micelles to aqueous buffer, and could not be explained by the presence of either free hemoglobin or ceruloplasmin. The products of NO consumption were shifted in postprandial plasma, with 55% more nitrite (n=12, p=0.002) but 50% less SNO (n=12, p=0.03) production compared to matched fasted plasma. Modeling calculations indicated that NO autoxidation was accelerated by about 48-fold in the presence of plasma lipids. We conclude that postprandial triglyceride-rich lipoproteins exert a significant influence on NO metabolism in plasma.

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The Role of Hypertriglyceridemia in the Development of Atherosclerosis and Endothelial Dysfunction

Cited by 35 publications

References 26 publications

Maternal lipids, BMI and IL‑17/IL‑35 imbalance in concurrent gestational diabetes mellitus and preeclampsia

Maternal lipids, BMI and IL‑17/IL‑35 imbalance in concurrent gestational diabetes mellitus and preeclampsia

Postprandial Lipemia as Cardiovascular Disease Risk Factor

Postprandial lipids accelerate and redirect nitric oxide consumption in plasma

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