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Macronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Intermediate density lipoproteins (IDL): The removal of triglycerides from VLDL by muscle and adipose tissue results in the formation of IDL particles which are enriched in cholesterol. These particles contain apolipoprotein B-100 and E. These IDL particles are pro-atherogenic (112).
Atherosclerosis
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
After the absorption phase, the liver maintains the availability of lipids in circulation.128 This function regulates the production and discharge of triglyceride-rich VLDL particles. The metabolic pathway of VLDL is similar to that of chylomicrons (Figure 26), and lipoprotein lipase converts VLDL to intermediate density lipoprotein (IDL). During this process, cholesteryl esters are removed from the particles and apoB remains as the sole protein component in the lipoprotein complexes. IDL is further converted to LDL in the liver by a lipase by break down of triglycerides to fatty acids (Figure 27). Nascent HDL is rich in protein, phospholipid, and cholesterol, but deficient in cholesteryl ester. The reduction of HDL production is associated with the retention of cholesteryl ester in tissues. These findings suggest that HDL is pivotal for the removal of cholesteryl esters from peripheral tissues, including blood vessels, to the liver where they are metabolized24,63,150,224,406,466,471,532,577,619,620,622
Fat
Published in Geoffrey P. Webb, Nutrition, 2019
Chylomicrons are the form in which ingested fat is transported to the liver and tissues after its absorption from the intestine. They are normally absent from fasting blood. Levels of VLDL should also be low in fasting blood because it is rapidly converted to LDL (see section on transport of endogenously produced lipids). This means that blood lipid determinations should be measured in fasting blood samples to avoid any distortion due to variable amounts of postprandial chylomicrons and large amounts of VLDL. IDL is a transitory intermediate that normally represents only a very small fraction of total lipoproteins. The principal lipoproteins in normal fasting blood are LDL, HDL and relatively small amounts of VLDL.
Evolving concepts on the management of dyslipidaemia
Published in Acta Clinica Belgica, 2020
Olivier S. Descamps, Ann Verhaegen, Fabien Demeure, Michel Langlois, Ernst Rietzschel, Ann Mertens, Johan De Sutter, Caroline Wallemacq, Patrizio Lancellotti, Guy De Backer
LDL but also other apoB-containing lipoproteins (VLDL and IDL) causes atherosclerosis. So, the new 2019 ESC/EAS guidelines emphasizes the use of the level of apolipoprotein B or, if not available, the ‘non-HDL-C level’ as secondary targets. The ‘non-HDL-C’ level takes into account the cholesterol of all of the atherogenic apoB-containing lipoproteins: LDL, small dense LDL, IDL and VLDL and lipoprotein(a) (Figure 1). It appears to be more stable over time than triglyceride levels in practice and is well correlated with the incidence of ASCVD. It is thus used as secondary target (or even primary target if triglycerides exceed 400 mg/dL rendering the LDL-C countless by the Friedewald formula) especially in patients with elevated triglycerides, with metabolic syndrome or with diabetes [27].
An in-depth analysis shows a hidden atherogenic lipoprotein profile in non-diabetic chronic kidney disease patients
Published in Expert Opinion on Therapeutic Targets, 2019
Marcelino Bermudez-Lopez, Carles Forne, Nuria Amigo, Milica Bozic, David Arroyo, Teresa Bretones, Nuria Alonso, Serafi Cambray, Maria Dolores Del Pino, Didac Mauricio, Jose Luis Gorriz, Elvira Fernandez, Jose Manuel Valdivielso
Cholesterol content in LDL particles was assessed by traditional methods and by NMR (referred as LDL-C and LDLNMR-C, respectively). Both techniques revealed the same pattern with a strong correlation (.82, p < .001). NMR analysis revealed that LDL particles lost cholesterol but gained triglycerides (referred as LDL-TG) in CKD patients compared to controls. Similarly, CKD patients showed a lower LDLNMR-C/LDL-P ratio, indicating that although their cholesterol content decreased, there were more circulating LDL particles. Finally, there was a reduction of the average LDL size in CKD 3 compared to controls due to an accumulation of small particles (higher small/total LDL particles ratio) and a reduction of large particles (lower large/total LDL particles ratio). Intermediate-density lipoproteins (IDL) accumulated cholesterol (referred as IDL-C) and triglycerides (referred as IDL-TG) in CKD patients. However, the IDL-C/IDL-TG ratio also increased, indicating a higher cholesterol gain (Table 2).
Experimental therapies targeting apolipoprotein C-III for the treatment of hyperlipidemia – spotlight on volanesorsen
Published in Expert Opinion on Investigational Drugs, 2019
Dimitrios Milonas, Konstantinos Tziomalos
In the circulation, APOC3 is mainly present in TRLs (chylomicrons and VLDL) and, to a lesser extent, in LDL and HDL particles [8]. Notably, the amount of APOC3 on HDL is high in the postabsorptive phase and low postprandially [8]. APOC3 is a key regulator of lipoprotein metabolism and plasma triglyceride levels. More specifically, it is known to inhibit LPL-mediated hydrolysis of TRLs and attenuate the uptake of TG-rich remnant lipoproteins by the liver [8,9]. At higher concentrations, APOC3 also inhibits the activity of hepatic lipase, an enzyme that plays an important role in the conversion of VLDL to intermediate-density lipoprotein (IDL) and LDL [10]. Thus, elevated levels of APOC3 in the plasma have been associated with impaired clearance of TRLs from the circulation resulting in the accumulation of atherogenic VLDL and chylomicron remnants in the circulation [11]. On the other hand, inhibition of LPL and hepatic lipase results in a decrease in LDL levels [8–11]. Besides its effect on lipoprotein metabolism, APOC3 has not only direct atherogenic properties by stimulating the adhesion of blood monocytes to endothelial cells and inducing the production of inflammatory mediators in these cells but also increases the binding of LDL to vascular proteoglycan, thereby enhancing LDL retention in the arterial wall [12].