What Is The Role Of Triglycerides In The Human Body – Decreased efficiency of very-low-density lipoprotein lipolysis is linked to both hypertriglyceridemia and hypercholesterolemia, but can be counteracted by high-density lipoprotein.

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What Is The Role Of Triglycerides In The Human Body

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The Dangers Of High Triglycerides

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Triglyceride-rich lipoproteins and their residues as silent promoters of atherosclerotic cardiovascular disease and other metabolic disorders: a review

Lipoproteins, Cholesterol, And Diet Explained

By Radu Sascău Radu Sascău Scilit Preprints.org Google Scholar 1, 2 , Alexandra Clement Alexandra Clement Scilit Preprints.org Google Scholar 2, * , Rodica Radu Rodica Radu Scilit Preprints.org Google Scholar 1, 2 , Cristina Pristari Pristari Pristari org Google Scholar 1, 2 and Cristian Stătescu Cristian Stătescu Scilit Preprints.org Google Scholar 1, 2

Received: 30 April 2021 / Revised: 18 May 2021 / Accepted: 20 May 2021 / Published: 22 May 2021

While targeting elevated serum levels of low-density lipoprotein cholesterol has been a mainstay of atherosclerosis prevention and treatment for decades, evidence regarding the atherogenic role of hypertriglyceridemia is still controversial. Triglycerides, triglyceride-rich lipoproteins (ie, chylomicrons and very-low-density lipoprotein particles) and their remnants are major determinants of significant residual cardiovascular risk in various epidemiological population-based studies of statin-treated subjects. As the triglyceride-glucose index and the triglyceride to high-density lipoprotein ratio are emerging as surrogate indicators of peripheral artery disease and atherosclerotic cerebrovascular disease, further research addressing the complex relationship between triglycerides and atherosclerosis may conclude. Therefore, this review aims to provide insight into the current clinical and epidemiological state of knowledge on the relationship between triglycerides and atherosclerotic cardiovascular disease. It also aims to highlight the relationship between triglycerides and other metabolic disorders, including diabetes mellitus, and the potential benefits of triglyceride-lowering agents on cardiovascular outcomes and all-cause mortality.

Coronary artery disease (CHD), peripheral artery disease (PAD), and atherosclerotic cerebrovascular disease represent major consequences of atherosclerosis, with atherosclerosis-induced cardiovascular disease responsible for a significant clinical and economic burden [1, 2]. Although targeting elevated serum levels of low-density lipoprotein cholesterol (LDL) has been a mainstay of atherosclerosis prevention and treatment for decades, evidence regarding the atherogenic role of hypertriglyceridemia is still controversial [3].

What Are Triglycerides And Their Role In The Body?

Hypertriglyceridemia is a common metabolic disorder characterized by plasma concentrations of triglycerides (TGs) greater than 150 mg/dL. Regarding its prevalence, a decreasing trend has been observed for US adults aged 20 and older, from 33.3% during 2001–2004 to 25.1% in 2009–2012 [ 4 ].

Nevertheless, it should be acknowledged that the average of multiple TGs measurements has an increased predictive power for cardiovascular events. Aberra et al. This information was validated by, who analyzed 15,792 individuals with no evidence of cardiovascular disease (CVD), from the Atherosclerosis Risk in Communities and Framingham Offspring studies, and followed up for 10 years. Interestingly, in this research, a “normal” or “optimal” concentration of TGs (less than 150 mg/dL) was associated with cardiovascular risk, especially in women and in individuals with high levels of high-density lipoprotein (HDL) [5] .

Various epidemiological population-based studies in statin-treated subjects have identified TGs, triglyceride-rich lipoproteins (ie, chylomicrons and very-low-density lipoprotein particles (VLDL)), and their residues as major determinants of significant residual cardiovasculature. . This residual risk appears to be exceptionally high in subjects with type 2 diabetes mellitus (T2DM), metabolic syndrome, and obesity [7].

In 4988 statin-treated Japanese diabetic patients included in a post hoc analysis of intensive statin therapy for hypercholesterolemic patients with diabetic retinopathy (EMPATHY) study, both fasting and non-fasting triglycerides (TGs) levels were positively associated with cardiovascular events. emphasizing the significant residual cardiovascular risk attributable to TGs [8].

Triglyceride Rich Lipoproteins: Their Role In Atherosclerosis

Regarding the effects of hypertriglyceridemia in the primary prevention of cardiovascular disease (CVD), a large Korean nationwide study involving 5,688,055 statin-naive young subjects aged 20–39 years showed that from all four major lipid components (total cholesterol, LDL, HDL, and TGs), TGs concentration exhibited the strongest association with the occurrence of death, myocardial infarction, and stroke (adjusted hazard ratio, 1.20; p < 0.001) [9].

Complementarily, the importance of preserving a normal lipid profile as a keystone of primary prevention of CVD is confirmed by the results of a large retrospective observational study of 1,451,997 young adults aged 20 to 49 years from Japan Medical Data. Central Health Database. In this analysis, LDL ≥ 140 mg/dL, HDL < 40 mg/dL, and TGs ≥ 150 mg/dL were independently associated with a higher incidence of myocardial infarction, angina pectoris, and heart failure during a median follow-up of 1148 years. ± 893 days [10].

In light of the above-mentioned data, this review aims to provide insight into the current clinical and epidemiological state of knowledge on the relationship between triglycerides and atherosclerotic cardiovascular disease. It is intended to highlight the relationship between triglycerides and other metabolic disorders, including diabetes mellitus, and the potential benefits of triglyceride-lowering agents on cardiovascular outcomes and all-cause mortality.

Triglyceride-containing lipoproteins (TRLs) is a general term used for chylomicrons (CMs) and VLDL. Intermediate-density lipoprotein (IDL) particles have also been implicated as TRLs, but their role has been less evaluated [11].

Quantitative Determination Of The Tg In Serum Or Plasma

Exogenous TGs are absorbed by intestinal cells and incorporated into nascent CM transported by the lymphatic system, where these particles are enriched with apolipoprotein C-II, apolipoprotein C-III, and apolipoprotein E. Increased cardiometabolic risk. ApoB48 is due to residual lipoproteins CM lipolysis, and according to the results of a cross-sectional study involving 1045 young women and men (aged 17 years), increased fasting plasma apoB48 has been linked to higher cardiometabolic risk in adolescence [12].

Endogenous TGs are mainly produced in the liver and secreted into the plasma by VLDL [ 13 ]. In hypertriglyceridemia, plasmatic levels of VLDL-VLDL are significantly increased.

(containing about 30% TGs) shows a moderate increase [14]. ApoB-100 is found only in VLD and IDL, is absent in CMs and plays an important role in atherogenesis, according to the most recent data that re-prioritized the role of TGs and TRLs in atherosclerotic cardiovascular disease (ASCVD) risk [11]. .

TGs located in the core of TRLs (CMs and VLDL) are hydrolyzed by lipoprotein lipase (to liberate fatty acids and glycerol), a metabolic process giving rise to so-called “remnant” lipoproteins, which are highly atherogenic. Residual concentration of cholesterol, containing 40 times more cholesterol per particle than LDL (Figure 1) [15].

Role Of Brown Fat In Lipoprotein Metabolism And Atherosclerosis

Although extensive epidemiological evidence links TGs, TRLs and remnants to atherosclerotic cardiovascular disease, the underlying mechanistic relationships are still ambiguous and not fully understood. In addition to the large amount of cholesterol in the residue, several other mechanisms have been hypothesized. Importantly, TRL residues (also known as residual cholesterol), due to their smaller size, are directly produced by macrophages in foam cells compared to LDL, which becomes atherogenic after being oxidized [ 16 , 17 , 18 , 19 ].

Residues in apoB, apoE and apoCII and interactions between matrix proteoglycans favor the accumulation of these particles in arterial walls [20, 21, 22]. Oxidized free fatty acids resulting from TRL lipolysis trigger a significant inflammatory response and alter endothelial function [6, 23]. Concomitantly, TRL residues increase endothelial expression of proatherothrombogenic molecules (eg, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and tissue factor), as emphasized in previous experimental studies, thus optimizing their [6] Creating a setting. , 24]. In addition to endothelial dysfunction and increased production of proinflammatory molecules, residues of TRL are responsible for activation of the coagulation cascade and inhibition of fibrinolysis [ 25 , 26 ].

On these bases, the relationship between residual TRLs and increased cardiovascular risk has been additionally validated by a Danish study of 109,574 patients with a previous diagnosis of myocardial infarction or ischemic stroke, where a low residual cholesterol of 0.8 m.

It is believed that TGs increase the risk of ASCVD through the process of VLDL-LDL breakdown. This metabolic event results in increased levels of LDL and remnant lipoproteins that exert severe atherogenic effects on the arterial wall [14]. For this reason,

Lipolysis (triglyceride Breakdown)

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