Journal articles: 'Remnant cholesterol'

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Sultan, F., D. Lagrange, X. Le Liepvre, and S. Griglio. "Chylomicron-remnant uptake by freshly isolated hepatocytes. Effect of heparin and of hepatic triacylglycerol lipase." Biochemical Journal 258, no. 2 (March 1, 1989): 587–94. http://dx.doi.org/10.1042/bj2580587.

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Chylomicron remnants labelled biologically with [3H]cholesterol were efficiently taken up by freshly isolated hepatocytes during a 3 h incubation in Krebs bicarbonate medium. Their [3H]cholesteryl ester was hydrolysed (74% net hydrolysis), and 0.1 mM-chloroquine could partially inhibit this hydrolysis, provided that hepatocytes were first preincubated for 2 h 30 min at 37 degrees C. This hydrolysis was also measured in preincubated cells with remnants double-labelled (3H and 14C) on their free cholesterol moiety; [3H]cholesterol arising from [3H]cholesteryl ester hydrolysis was recovered in the free [3H]cholesterol pool. A dose-response study showed saturation of remnant uptake at 180 micrograms of remnant protein/10(7) cells. Heparin (10 units/ml) increased remnant uptake by 63% (P less than 0.01), [3H]cholesteryl ester accumulation in the cell pellet by 110% (P less than 0.025) and hepatic lipase activity secreted in the medium by 2.4-fold (P less than 0.01) and by 3.3-fold (P less than 0.01) at the end of the preincubation and incubation periods respectively. Addition of 100 munits of semi-purified hepatic lipase preparation/flask stimulated remnant uptake by 44-69%, and [3H]cholesteryl ester accumulation in the presence of chloroquine by 2.1-fold (P less than 0.025). When hepatic lipase was incubated solely with the remnants, it decreased their triacylglycerol and phospholipid contents by 24% and 26% respectively. Thus freshly isolated hepatocytes may be used to study chylomicron-remnant uptake. Hepatic lipase, which seems to underly the stimulating effect of heparin, facilitates remnant uptake in vitro, and this could be mediated by at least one (or both) of its hydrolytic properties.

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Redgrave, T. G., C. L. Elsegood, J. C. L. Mamo, and M. J. Callow. "Effects of hypothyroidism on the metabolism of lipid emulsion models of triacylglycerol-rich lipoproteins in rats." Biochemical Journal 273, no. 2 (January 15, 1991): 375–81. http://dx.doi.org/10.1042/bj2730375.

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Methimazole-treated hypothyroid rats were injected intravenously with triacylglycerol/cholesteryl oleate/cholesterol/phospholipid emulsions designed to model the composition of chylomicrons. Compared with controls, hypothyroidism decreased the clearance rates of emulsion cholesteryl oleate. Clearance of emulsion triolein was affected much less and could be accounted for by residual triolein in remnants, suggesting that triacylglycerol lipolysis by lipoprotein lipase was unaffected by hypothyroidism but that clearance of remnants from plasma was decreased. Assays in vitro showed increased activities of lipoprotein lipase and hepatic lipase in hypothyroid rats. Emulsions were incubated with post-heparin plasma lipoprotein lipase to prepare remnants in vitro. The clearance from plasma of pre-formed remnants was slower after injection into hypothyroid rats than in control rats. Uptake of remnant cholesteryl oleate by the liver was significantly decreased in the hypothyroid rats. Treatment of hypothyroid rats for 7 days with 3,3′,5′-tri-iodo-L-thyronine (T3) reversed the inhibition of hepatic remnant uptake and normalized plasma cholesterol. A thyroid hormone analogue with decreased hypermetabolic side-effects, L-94901, attenuated plasma cholesterol and improved but did not normalize remnant clearance. Emulsions incubated with plasma from hypothyroid rats had a decreased ratio of apolipoprotein E/apolipoprotein C compared with control rats or hypothyroid rats treated with T3. The change in the apolipoprotein E/apolipoprotein C ratio probably accounts for the defect in remnant clearance in hypothyroidism.

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WATTS, G. F., D. C. F. CHAN, P. H. R. BARRETT, I. J. MARTINS, and T. G. REDGRAVE. "Preliminary experience with a new stable isotope breath test for chylomicron remnant metabolism: a study in central obesity." Clinical Science 101, no. 6 (November 20, 2001): 683–90. http://dx.doi.org/10.1042/cs1010683.

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We aimed to investigate the metabolism of chylomicron remnants in the postabsorptive state employing a new stable isotope breath test in centrally obese men without overt hyperlipidaemia. Groups of 12 centrally obese and 12 non-obese men of similar age and with similar plasma cholesterol and triacylglycerol (triglyceride) levels were studied. The catabolism of chylomicron remnants was measured using an intravenous injection of a remnant-like emulsion containing cholesteryl [13C]oleate. Isotopic enrichment of 13CO2 in breath was determined using isotope-ratio mass spectrometry, and a multi-compartmental model (SAAM II program) was used to estimate the fractional catabolic rate (FCR) of the chylomicron remnant-like particles. The plasma concentrations of low-density lipoprotein (LDL)-cholesterol, non-high-density lipoprotein (HDL)-cholesterol and insulin were significantly higher (P < 0.05) in the obese than the control subjects. The obese subjects had significantly lower HDL-cholesterol (P < 0.05) and, in particular, a decreased FCR of the remnant-like particles compared with lean subjects (0.061±0.014 and 0.201±0.048pools/h respectively; P = 0.016). In the obese group, the FCR of remnant-like particles was inversely associated with the waist/hip ratio, and with plasma triacylglycerol, cholesterol, LDL-cholesterol and non-HDL-cholesterol levels. In multiple regression analysis, the waist/hip ratio was the best predictor of the FCR of the emulsion. In conclusion, this new test suggests that postabsorptive chylomicron remnant catabolism is impaired in centrally obese subjects without overt hyperlipidaemia. This defect may be due to the degree of adiposity.

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Chan, Dick C., Gerald F. Watts, P. Hugh Barrett, John CL Mamo, and Trevor G. Redgrave. "Markers of Triglyceride-rich Lipoprotein Remnant Metabolism in Visceral Obesity." Clinical Chemistry 48, no. 2 (February 1, 2002): 278–83. http://dx.doi.org/10.1093/clinchem/48.2.278.

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Abstract Background: Triglyceride-rich lipoprotein remnants are atherogenic, and this may be particularly important in visceral obesity. We investigated remnant metabolism in obese men by measuring remnant-like particle-cholesterol (RLP-C), apolipoprotein (apo) B-48, apoC-III, and the clearance of a labeled remnant-like emulsion. Methods: Fasting RLP-C, apoB-48, and apoC-III concentrations were measured in 48 viscerally obese men and 10 lean controls. RLP-C was determined by immunoseparation assay, apoB-48 by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and enhanced chemiluminescence, and apoC-III by immunoturbidimetric assay. The catabolism of chylomicron remnants was measured by intravenous injection of a remnant-like emulsion containing cholesteryl [13C]oleate, with isotopic enrichment of 13CO2 in breath determined by isotope-ratio mass spectrometry and a multicompartmental model to estimate fractional catabolic rate (FCR) of the emulsion. Results: Compared with controls, obese men had significantly increased plasma concentrations of RLP-C, apoB-48, and apoC-III (P <0.001 for all). Plasma total apoB-100, non-HDL-cholesterol, LDL-cholesterol, triglycerides, and insulin resistance (HOMA score) were also significantly higher in the obese group (P <0.001 for all). Obese men had a significantly lower FCR of the remnant-like emulsion compared with controls (P = 0.020). Conclusions: Viscerally obese individuals have insulin resistance and increased plasma concentrations of triglyceride-rich lipoprotein remnants, which may be attributable to decreased catabolism of these particles.

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McPherson, Ruth. "Remnant Cholesterol." Journal of the American College of Cardiology 61, no. 4 (January 2013): 437–39. http://dx.doi.org/10.1016/j.jacc.2012.11.009.

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Bowler, A., T. G. Redgrave, and J. C. L. Mamo. "Chylomicron-remnant clearance in homozygote and heterozygote Watanabe-heritable-hyperlipidaemic rabbits is defective. Lack of evidence for an independent chylomicron-remnant receptor." Biochemical Journal 276, no. 2 (June 1, 1991): 381–86. http://dx.doi.org/10.1042/bj2760381.

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Lymph chylomicrons radiolabelled in triacylglycerol and cholesteryl ester were injected into control and Watanabe heritable-hyperlipidaemic (WHHL) rabbits. Clearance of chylomicrons was slower in heterozygote and homozygote WHHL rabbits. Slower remnant clearance in WHHL rabbits was confirmed by monitoring the clearance from plasma of preformed chylomicron remnants. Use of chylomicron-like lipid emulsions injected into control and WHHL rabbits also confirmed the defect in remnant clearance in heterozygote WHHL and homozygote WHHL groups. Clearance from plasma of emulsion triolein was delayed in both WHHL groups compared with controls, owing to slower remnant clearance. The clearance from plasma of radioiodinated rabbit low-density lipoproteins (LDL) in heterozygote WHHL rabbits was the same as control rabbits. Defective chylomicron-remnant removal but normal LDL clearance in the heterozygote WHHL corresponded to elevated concentrations of plasma triacylglycerol and normal concentrations of plasma cholesterol. Receptor versus non-receptor clearances of chylomicron remnants were studied by comparing the clearance of emulsions with and without unesterified cholesterol respectively. Unlike control rabbits, there were no significant differences in the clearances of the two emulsion types in either the homozygote or heterozygote WHHL rabbits, indicating that the apolipoprotein-B100/E receptor is the primary route for clearance of chylomicron remnants from plasma.

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Langsted, Anne, Anne Marie Reimer Jensen, Anette Varbo, and Børge G. Nordestgaard. "Low High-Density Lipoprotein Cholesterol to Monitor Long-Term Average Increased Triglycerides." Journal of Clinical Endocrinology & Metabolism 105, no. 4 (December 11, 2019): e1657-e1666. http://dx.doi.org/10.1210/clinem/dgz265.

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Abstract Context Increased triglyceride-rich remnants represent a causal risk factor for ischemic cardiovascular disease. Objective We tested the hypothesis that low high-density lipoprotein (HDL) cholesterol can be used to monitor long-term high triglycerides/remnant cholesterol, just as high hemoglobin A1c (HbA1c) can be used to monitor long-term high glucose levels. Design, Setting, Participants, and Interventions We studied cross-sectionally 108 731 individuals, dynamically 1313 individuals with lipid measurement at 10 repeated visits, short-term 305 individuals during a fat load, and long-term 10 479 individuals with 2 lipid measurements 10 years apart. Main Outcome Measures Levels of HDL cholesterol and triglycerides. Results Cross-sectionally, HDL cholesterol was inversely associated with triglycerides (R2 = 0.26) and remnant cholesterol (R2 = 0.26). Dynamically, major changes in triglyceride levels from measurement to measurement were mimicked by corresponding modest changes in HDL cholesterol. In the short-term after a fat load, median triglycerides increased 96% while HDL cholesterol decreased only 1%. Long-term, in individuals with measurements 10 years apart, those who initially had the highest triglycerides and corresponding lowest HDL cholesterol, still had highest triglycerides and lowest HDL cholesterol 10 years later. Prospectively, individuals with increased triglycerides/remnant cholesterol had increased risk of myocardial infarction; however, when the HDL cholesterol monitoring was removed, increased triglycerides/remnant cholesterol were largely no longer associated with increased risk of myocardial infarction. Conclusions Low HDL cholesterol is a stable marker of average high triglycerides/remnant cholesterol. This suggests that low HDL cholesterol can be used to monitor long-term average high triglycerides and remnant cholesterol, analogous to high HbA1c as a long-term monitor of average high glucose levels.

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Lambert, M. S., K. M. Botham, and P. A. Mayes. "Variations in composition of dietary fats affect hepatic uptake and metabolism of chylomicron remnants." Biochemical Journal 310, no. 3 (September 15, 1995): 845–52. http://dx.doi.org/10.1042/bj3100845.

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The hepatic metabolism of [1-14C]oleate- and [1,2-3H]cholesterol-dual-labelled chylomicron remnants derived from olive, corn, palm and fish oil and butter fat was compared by adding each lipoprotein separately to the perfusate of isolated livers from rats fed on a normal diet. Labelled remnants from butter fat and fish oil were removed more rapidly from the perfusate than remnants derived from olive, corn and palm oil. The oxidation of labelled remnant fatty acid from olive oil, fish oil or butter fat was four to seven times greater than that from corn and palm oil. Labelled fatty acid in fish oil remnants was incorporated into phospholipid significantly more efficiently than the labelled fatty acid in olive, corn or palm oil remnants, with butter fat giving an intermediate value. For all the remnants, there was a significant amount of hydrolysis of labelled esterified cholesterol by the liver which was dependent on the magnitude of hepatic uptake of each type of remnant. The recovery of remnant [3H]cholesterol label in the bile was 50% less with palm oil remnants than with all the other remnants studied. The results indicate that the fatty acid composition of chylomicron remnants has a major impact on their uptake and metabolism by the liver.

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Miyauchi, Kazuhito, Norihiko Kayahara, Masato Ishigami, Hideyuki Kuwata, Hideharu Mori, Hiroyuki Sugiuchi, Tetsumi Irie, Akira Tanaka, Shizuya Yamashita, and Taku Yamamura. "Development of a Homogeneous Assay to Measure Remnant Lipoprotein Cholesterol." Clinical Chemistry 53, no. 12 (December 1, 2007): 2128–35. http://dx.doi.org/10.1373/clinchem.2007.092296.

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Abstract Background: Quantification of triglyceride-rich lipoprotein (TRL) remnants is useful for risk assessment of coronary artery disease and the diagnosis of type III hyperlipoproteinemia. Although an immunoseparation procedure for remnant-like particle cholesterol has been evaluated extensively in recent years, available methods for measuring TRL remnants have not achieved wide use in routine laboratory practice, suggesting a need for a homogeneous assay that can measure TRL remnant cholesterol in serum or plasma without pretreatment. Methods: We screened for suitable surfactants that exhibited favorable selectivity toward the VLDL remnant (VLDLR) fraction, including intermediate-density lipoproteins (IDLs). We investigated the principal characteristics of this assay by gel filtration of lipoproteins and their particle size distribution. We developed a simple assay and evaluated its performance with the Hitachi-7170 analyzer. Results: Polyoxyethylene-polyoxybutylene block copolymer (POE-POB) exhibited favorable selectivity toward VLDLR and IDL fractions. POE-POB removed apolipoprotein (apo) E and apo C-III from IDL particles in the presence of cholesterol esterase (CHER), and the particle size distribution of IDLs became smaller after the reaction. These results revealed that IDL particles are specifically modified in the presence of CHER and POE-POB, making their component cholesterol available for enzymatic assay. Addition of phospholipase D improved the reactivity toward chylomicron remnants (CMRs). We found a high correlation [y = 1.018x− 0.01 mmol/L, r = 0.962 (n = 160)] between the proposed assay and the immunoseparation assay in serum from healthy individuals. Conclusion: The homogeneous assay described in this report can measure TRL remnant cholesterol, including CMRs, VLDLRs, and IDLs, with high sensitivity and specificity.

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CHAN, Dick C., Gerald F. WATTS, P. Hugh R. BARRETT, Frans H. O'NEILL, Trevor G. REDGRAVE, and Gilbert R. THOMPSON. "Relationships between cholesterol homoeostasis and triacylglycerol-rich lipoprotein remnant metabolism in the metabolic syndrome." Clinical Science 104, no. 4 (March 14, 2003): 383–88. http://dx.doi.org/10.1042/cs1040383.

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The dysmetabolic syndrome of insulin resistance and visceral obesity is characterized by elevated plasma concentration of triacylglycerol-rich lipoprotein (TRL) remnants that may be related to increased cardiovascular risk. Perturbed hepato-intestinal cholesterol metabolism may play a contributory role in this abnormality. We therefore investigated the association between plasma markers of cholesterol absorption and synthesis with TRL remnant metabolism in 35 men with the metabolic syndrome (MS). Plasma campesterol:cholesterol and lathosterol:cholesterol ratios were measured as estimates of cholesterol absorption and synthesis respectively. Remnant metabolism was assessed by measuring remnant-like particle-cholesterol (RLP-C), apolipoprotein (apo)B-48 and the fractional catabolic rate (FCR) of a labelled remnant-like emulsion. Compared with controls, subjects with the MS had significantly lower plasma campesterol:cholesterol ratio, but higher lathosterol:cholesterol ratio (P<0.05). Plasma RLP-C and apoB-48 concentrations were also higher (P<0.01) and the remnant-like emulsion FCR was lower (P<0.05). The plasma campesterol:cholesterol ratio was inversely correlated (P<0.05) with plasma triacylglycerols (r =-0.346), RLP-C (r =-0.443), apoB-48 (r =-0.427) and plasma lathosterol:cholesterol ratio (r =-0.366); the campesterol:cholesterol ratio was also positively correlated with the remnant-like emulsion FCR (r = 0.398, P<0.05). In multiple regression analysis, the significant correlations between plasma campesterol:cholesterol ratio and plasma triacylglycerols, RLP-C, apoB-48 and FCR of the remnant-like emulsion were independent of age, dietary energy and plasma lathosterol. Our findings suggest that in subjects with the MS alterations in cholesterol absorption and synthesis may be closely linked with the kinetic defects in TRL metabolism.

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Bravo, E., and M. Napolitano. "Mechanisms involved in chylomicron remnant lipid uptake by macrophages." Biochemical Society Transactions 35, no. 3 (May 22, 2007): 459–63. http://dx.doi.org/10.1042/bst0350459.

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Although it is clear that chylomicron remnants are atherogenic, events leading to their internalization by macrophages are still debated. The lack of apoE (apolipoprotein E) in CRLPs (chylomicron remnant-like particles) reduces macrophage TAG (triacylglycerol) content by approx. 50%, suggesting that, as well as apoE-mediated endocytic uptake, apoE receptor-independent mechanisms are involved in the induction of foam cells by chylomicron remnants. Evaluation of the radioactivity associated with macrophages after incubation with CRLPs containing radiolabelled lipids suggests that the TAG and cholesterol carried by the particles have different kinetics of internalization. In addition, inhibition-based experiments indicate that cholesteryl ester-selective uptake and the extracellular lipoprotein lipase hydrolysis of TAG contribute to cholesterol and TAG accumulation respectively. Thus plasma TAG and cholesterol carried by remnant particles have to be considered two independent and non-interchangeable risk factors for athero-related diseases. In addition, the interaction between CRLPs and macrophages is modulated by dietary oxidized lipids and other lipophilic components. The presence of oxidized lipids, such as 7β-hydroxycholesterol and 7-oxocholesterol, the major cholesterol oxidation products found in atherosclerotic lesions, in CRLPs interferes with the mechanisms of their internalization, but does not cause quantitative changes of accumulated lipids, while the presence of the plant carotenoid, lycopene, or the antioxidant drug, probucol, enhances lipid accumulation in macrophages by increasing the rate of uptake of the particles and raising the intracellular synthesis of TAG. In conclusion, several mechanisms contribute to the macrophage uptake of postprandial lipoproteins, however, little is known of the balance and modulation between the different pathways.

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Yang, Na, Miao Wang, Jing Liu, Jun Liu, Yongchen Hao, and Dong Zhao. "The Level of Remnant Cholesterol and Implications for Lipid-Lowering Strategy in Hospitalized Patients with Acute Coronary Syndrome in China: Findings from the Improving Care for Cardiovascular Disease in China—Acute Coronary Syndrome Project." Metabolites 12, no. 10 (September 24, 2022): 898. http://dx.doi.org/10.3390/metabo12100898.

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Elevated remnant cholesterol is associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD). We aimed to evaluate the concentrations and general distribution of remnant cholesterol at admission in patients hospitalized for acute coronary syndrome (ACS), and those in patients who reached the low-density lipoprotein cholesterol (LDL-C) target or non-high-density lipoprotein cholesterol (non-HDL-C) target. Patients with ACS who were enrolled in the Improving Care for Cardiovascular Disease in China—ACS project from 2014 to 2019 were included. Elevated remnant cholesterol concentrations were defined as ≥1.0 mmol/L. Among 94,869 patients, the median (interquartile range) remnant cholesterol concentration at admission was 0.6 mmol/L (0.4–0.9 mmol/L) and 19.2% had elevated remnant cholesterol concentrations. Among patients with LDL-C concentrations < 1.4 mmol/L, 24.4% had elevated remnant cholesterol concentrations, while the proportion was 13.3% among patients with LDL-C concentrations between 1.4 and 1.7 mmol/L. Among patients with non-HDL-C concentrations < 2.6 mmol/L, 2.9% had elevated remnant cholesterol concentrations but 79.6% had LDL-C concentrations ≥ 1.4 mmol/L. Even among patients with LDL-C < 1.4 mmol/L and non-HDL-C < 2.6 mmol/L, 10.9% had elevated remnant cholesterol. In conclusion, one fifth of patients with ACS have elevated remnant cholesterol concentrations at admission. Elevated remnant cholesterol concentrations are present in patients with LDL-C or/and non-HDL-C concentrations within the target, which represents an unmet need to add remnant cholesterol as a target for the secondary prevention of ASCVD.

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Elshazly, Mohamed B., Preethi Mani, Steven Nissen, Danielle M. Brennan, Donald Clark, Seth Martin, Steven R. Jones, et al. "Remnant cholesterol, coronary atheroma progression and clinical events in statin-treated patients with coronary artery disease." European Journal of Preventive Cardiology 27, no. 10 (November 19, 2019): 1091–100. http://dx.doi.org/10.1177/2047487319887578.

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Aim Remnant cholesterol has been proposed to promote atherosclerotic cardiovascular disease independent of low-density lipoprotein cholesterol, yet the underlying mechanisms are not well understood. We aimed to study the association of remnant cholesterol with coronary atheroma progression and clinical events. Methods We analyzed data from 5754 patients with coronary artery disease undergoing serial intravascular ultrasonography who were enrolled in 10 trials examining various medical therapies. Remnant cholesterol was calculated as (non-high-density lipoprotein cholesterol – low-density lipoprotein cholesterol (estimated using the Hopkins–Martin equation)). Changes in percentage atheroma volume and 2-year major adverse cardiovascular events were compared across various levels of remnant cholesterol, and multivariable models were used to assess the independent relationship of remnant cholesterol with changes in percentage atheroma volume. Results The mean age was 58.1 ± 9.2 years, 28% were women and 96% received a statin. Percentage atheroma volume progression (changes in percentage atheroma volume > 0) occurred in a linear fashion at on-treatment remnant cholesterol levels of 25 mg/dL or greater. The highest on-treatment remnant cholesterol quartile demonstrated greater percentage atheroma volume progression (+0.53 ± 0.26 vs. –0.15 ± 0.25%, P < 0.001) and 2-year major adverse cardiovascular events (23% vs. 14%, log–rank P < 0.001) compared with the lowest. In multivariable analyses, changes in percentage atheroma volume significantly correlated with on-treatment remnant cholesterol ( P < 0.001] independent of low-density lipoprotein cholesterol, apolipoprotein B, C-reactive protein, high-density lipoprotein cholesterol levels and clinical risk factors. Changes in percentage atheroma volume also significantly correlated with changes in remnant cholesterol following multivariable adjustment. Conclusions In statin-treated patients with atherosclerotic cardiovascular disease, remnant cholesterol was associated with coronary atheroma progression regardless of conventional lipid parameters, C-reactive protein or clinical risk factors. Higher remnant cholesterol levels also correlated with higher major adverse cardiovascular events. These data support further investigations into remnant cholesterol-lowering interventions in statin-treated patients harboring residual atherosclerotic cardiovascular disease risk.

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Kaysen, G. A., L. Mehendru, X. M. Pan, and I. Staprans. "Both peripheral chylomicron catabolism and hepatic uptake of remnants are defective in nephrosis." American Journal of Physiology-Renal Physiology 263, no. 2 (August 1, 1992): F335—F341. http://dx.doi.org/10.1152/ajprenal.1992.263.2.f335.

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We showed previously that proteinuria caused delayed chylomicron (CM) clearance in the rat and postulated the existence of a primary defect in CM hydrolysis. It was possible that reduced CM clearance resulted from increased lipogenesis causing saturation of catabolic sites and not from a primary defect in CM catabolism. To clarify this point we measured kinetically the absolute rate of triglyceride (TG) uptake from CM in rats with Heymann nephritis (HN) and normal Sprague-Dawley rats (SD) and determined TG uptake in individual tissues using [3H]TG- and [14C]cholesterol-labeled CM. Hepatic [14C]cholesterol uptake was reduced in HN (69.3 +/- 6 vs. 7.2 +/- 2% of dose, P less than 0.001). TG uptake was reduced in HN measured kinetically (1.01 +/- 0.09 vs. 0.213 +/- 0.028 mg TG.min-1.100 g body wt-1, P less than 0.001) and reduced in all tissues (heart, skeletal muscle, fat, and liver). CM are catabolized on the vascular endothelium to atherogenic, cholesterol-rich remnant (CM remnant) particles, which are then rapidly taken up by the liver. We measured hepatic CM remnant uptake in SD and in HN using [14C]cholesterol-labeled CM remnant. CM remnant uptake was significantly reduced in HN (58 +/- 1.2 vs. 20 +/- 0.86% uptake, P less than 0.01). CM remnants were increased significantly in plasma of HN. Thus the nephrotic syndrome causes a primary defect in the uptake of TG from CM that is expressed in all tissues and a separate defect in hepatic CM remnant uptake. Although CM remnant generation is impaired because of defective CM hydrolysis, the defect in hepatic CM remnant uptake is so severe that these particles accumulate in blood, posing a potential risk for atherogenesis.

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Lippiello, P. M., P. J. Sisson, and M. Waite. "The uptake and metabolism of chylomicron-remnant lipids by rat liver parenchymal and non-parenchymal cells in vitro." Biochemical Journal 232, no. 2 (December 1, 1985): 395–401. http://dx.doi.org/10.1042/bj2320395.

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The uptake and metabolism of chylomicron-remnant lipids by individual liver cell types was examined by incubating remnants with monolayer cultures of hepatocytes, Kupffer cells, and endothelial cells from rat liver. Remnants were prepared in vitro from radiolabelled mesenteric-lymph chylomicra, utilizing either purified lipoprotein lipase from bovine milk, or plasma isolated from heparinized rats. The resulting particles contained [3H]phosphatidylcholine and cholesterol, and [14C]oleate in the acylglycerol, phospholipid, fatty-acid and cholesterol-ester fractions. The capacities of the three cell types for uptake of both [3H]lipids and [14C]lipids were determined to be, on a per-cell basis, in the order: Kupffer greater than hepatocytes greater than endothelial. The relative proportions of [3H]phospholipid and total [3H]cholesterol taken up by hepatocytes and non-parenchymal cells remained constant with time. The uptake of [14C]oleoyl lipids by all three cell types was slightly greater than that of the total [3H]cholesterol and [3H]phospholipid components. There was evidence of cholesterol-ester hydrolysis and turnover of [14C]oleate in the phospholipid fraction in hepatocytes and Kupffer cells, but not endothelial cells, over the first 2 h. With both remnant preparations, these observations indicate that significant differences exist between the three major liver cell types with respect to the uptake and metabolism of remnant lipid components.

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Morise, Anthony P., Jennifer Tennant, Sari D. Holmes, and Danyel H. Tacker. "The Effect of Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors on Nonfasting Remnant Cholesterol in a Real World Population." Journal of Lipids 2018 (July 19, 2018): 1–8. http://dx.doi.org/10.1155/2018/9194736.

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Background. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors have demonstrated significant effects on low-density lipoprotein (LDL) cholesterol and nonhigh density lipoprotein (HDL) cholesterol. To date, there have been limited reports on the effect of PCSK9 inhibitors on remnant cholesterol. Objectives. Assess the effect of PCSK9 inhibitors on nonfasting remnant cholesterol in a real world population. Identify whether pretreatment triglyceride levels are associated with PCSK9 inhibition success as indicated by changes in remnant cholesterol levels. Methods. Patients in our adult lipid clinic (n = 109) receiving PCSK9 inhibition for atherosclerotic cardiovascular disease or familial hypercholesterolemia who had available pre- and post-PCSK9 inhibition standard nonfasting lipid data were, retrospectively, selected for data analysis. Remnant cholesterol was the difference between non-HDL and LDL cholesterol. LDL cholesterol was measured directly and calculated from Friedewald and Martin/Hopkins methods. Data were analyzed using repeated measures ANOVA and multivariable linear regression for differential effects on remnant and LDL cholesterol based upon pretreatment nonfasting triglyceride levels. Results. Remnant cholesterol as well as total, LDL, non-HDL cholesterol, and triglycerides decreased significantly (P<0.001) after PCSK9 inhibition. Patients with higher pretreatment triglyceride levels showed greater decrease in remnant cholesterol after PCSK9 inhibition (P<0.001) than those with lower pretreatment triglycerides. Conclusions. In patients receiving PCSK9 inhibitors, remnant cholesterol as determined from nonfasting blood was reduced in proportion to pretreatment triglycerides.

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Jepsen, Anne-Marie K., Anne Langsted, Anette Varbo, Lia E. Bang, Pia R. Kamstrup, and Børge G. Nordestgaard. "Increased Remnant Cholesterol Explains Part of Residual Risk of All-Cause Mortality in 5414 Patients with Ischemic Heart Disease." Clinical Chemistry 62, no. 4 (April 1, 2016): 593–604. http://dx.doi.org/10.1373/clinchem.2015.253757.

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Abstract BACKGROUND Increased concentrations of remnant cholesterol are causally associated with increased risk of ischemic heart disease. We tested the hypothesis that increased remnant cholesterol is a risk factor for all-cause mortality in patients with ischemic heart disease. METHODS We included 5414 Danish patients diagnosed with ischemic heart disease. Patients on statins were not excluded. Calculated remnant cholesterol was nonfasting total cholesterol minus LDL and HDL cholesterol. During 35836 person-years of follow-up, 1319 patients died. RESULTS We examined both calculated and directly measured remnant cholesterol; importantly, however, measured remnant cholesterol made up only 9% of calculated remnant cholesterol at nonfasting triglyceride concentrations <1 mmol/L (89 mg/dL) and only 43% at triglycerides >5 mmol/L (443 mg/dL). Multivariable-adjusted hazard ratios for all-cause mortality compared with patients with calculated remnant cholesterol concentrations in the 0 to 60th percentiles were 1.2 (95% CI, 1.1–1.4) for patients in the 61st to 80th percentiles, 1.3 (1.1–1.5) for the 81st to 90th percentiles, 1.5 (1.1–1.8) for the 91st to 95th percentiles, and 1.6 (1.2–2.0) for patients in the 96th to 100th percentiles (trend, P < 0.001). Corresponding values for measured remnant cholesterol were 1.0 (0.8–1.1), 1.2 (1.0–1.4), 1.1 (0.9–1.5), and 1.3 (1.1–1.7) (trend, P = 0.006), and for measured LDL cholesterol 1.0 (0.9–1.1), 1.0 (0.8–1.2), 1.0 (0.8–1.3), and 1.1 (0.8–1.4) (trend, P = 0.88). Cumulative survival was reduced in patients with calculated remnant cholesterol ≥1 mmol/L (39 mg/dL) vs <1 mmol/L [log-rank, P = 9 × 10−6; hazard ratio 1.3 (1.2–1.5)], but not in patients with measured LDL cholesterol ≥3 mmol/L (116 mg/dL) vs <3 mmol/L [P = 0.76; hazard ratio 1.0 (0.9–1.1)]. CONCLUSIONS Increased concentrations of both calculated and measured remnant cholesterol were associated with increased all-cause mortality in patients with ischemic heart disease, which was not the case for increased concentrations of measured LDL cholesterol. This suggests that increased concentrations of remnant cholesterol explain part of the residual risk of all-cause mortality in patients with ischemic heart disease.

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Varbo, Anette, Jacob J. Freiberg, and Børge G. Nordestgaard. "Extreme Nonfasting Remnant Cholesterol vs Extreme LDL Cholesterol as Contributors to Cardiovascular Disease and All-Cause Mortality in 90000 Individuals from the General Population." Clinical Chemistry 61, no. 3 (March 1, 2015): 533–43. http://dx.doi.org/10.1373/clinchem.2014.234146.

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Abstract BACKGROUND Increased nonfasting remnant cholesterol, like increased LDL cholesterol, is causally associated with increased risk for ischemic heart disease (IHD). We tested the hypothesis that extreme concentrations of nonfasting remnant and LDL cholesterol are equal contributors to the risk of IHD, myocardial infarction (MI), and all-cause mortality. METHODS We compared stepwise increasing concentrations of nonfasting remnant and LDL cholesterol for association with risk of IHD, MI, and all-cause mortality in approximately 90 000 individuals from the Danish general population. During up to 22 years of complete follow-up, 4435 participants developed IHD, 1722 developed MI, and 8121 died. RESULTS Compared with participants with nonfasting remnant cholesterol <0.5 mmol/L (19.3 mg/dL), hazard ratios for IHD ranged from 1.3 (95% CI 1.1–1.5) for remnant cholesterol of 0.5–0.99 mmol/L (19.3–38.2 mg/dL) to 2.4 (1.9–2.9) for remnant cholesterol of ≥1.5 mmol/L (58 mg/dL) (P for trend <0.001). Compared with participants with LDL cholesterol <3.0 mmol/L (115.8 mg/dL), hazard ratios for IHD ranged from 1.3 (1.1–1.5) for LDL cholesterol of 3–3.99 mmol/L (115.8–154 mg/dL) to 2.3 (1.9–2.8) for LDL cholesterol of ≥5 mmol/L (193 mg/dL) (P < 0.001). Corresponding hazard ratios for MI ranged from 1.8 (1.4–2.3) to 3.4 (2.5–4.8) for remnant cholesterol (P < 0.001), and from 1.7 (1.4–2.2) to 4.7 (3.5–6.3) for LDL cholesterol (P < 0.001). Nonfasting remnant cholesterol concentrations were associated stepwise with all-cause mortality ranging from hazard ratio 1.0 (0.9–1.1) to 1.6 (1.4–1.9) (P < 0.001), whereas LDL cholesterol concentrations were associated with decreased all-cause mortality risk in a U-shaped pattern, with hazard ratios from 0.8 (0.7–0.8) to 0.9 (0.8–1.0) (P = 0.002). After mutual adjustment, LDL cholesterol best predicted MI, and remnant cholesterol best predicted all-cause mortality. CONCLUSIONS Both lipoproteins were associated equally with risk of IHD and MI; however, only nonfasting remnant cholesterol concentrations were associated stepwise with increased all-cause mortality risk.

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Rowsathien, Sathienwit, Krisada Sastravaha, Prajongjit Chamsaard, and Prin Vathesatogkit. "Correlation between Levels of Remnant Cholesterol versus LDL, A Cross-Sectional study." International Journal of Scientific Research and Management 10, no. 12 (December 17, 2022): 740–63. http://dx.doi.org/10.18535/ijsrm/v10i12.mp02.

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Background: High levels of LDL cholesterol were directly related to the risk of atherosclerosis, metabolic diseases, and cardiovascular complications. However, in some groups of patients with low levels, they were also found. Lead to the risk of other lipid components, including Remnant cholesterol. A recent study found related to cardiovascular risk as well. Currently, no direct comparison between Remnant cholesterol and LDL cholesterol level. Objective: To study the correlation between Remnant cholesterol and LDL levels both in fasting and non-fasting states with the medical conditions that increase the risk of cardiovascular disease. Materials and methods: To determine the association between remnant cholesterol and LDL. 200 cases of Thai begins at the age of 18 years old were tested for total cholesterol, LDL, HDL, and TG level both in the fasting and non-fasting states. The obtained values were calculated for Remnant cholesterol levels and analysed for a direct correlation between the two levels, which also includes a comparative analysis. The AUC was used to assess the prognostic accuracy of lipid levels to diagnose the condition that poses cardiovascular risks. Results: In the sample of 200 patients tested for lipid. At a mean age of 64.5 years, 42 percent were female and 76.5 percent received statins. We found that remnant cholesterol had a poor correlation with LDL levels when compared among the fasting conditions (r=0.164, 0.119), as well as among the statin used or not (r=0.118, 0.293). The analysis found that remnant cholesterol does well correlate with TG levels (r=0.770). Also, the predictive value of Remnant cholesterol over LDL levels for detect diabetes mellitus, coronary artery disease, and overweight (AUC=0.610, 0.588, 0.593). Conclusion: In this study. We found that remnant cholesterol does correlate poorly with LDL in any fasting state. Prediction of the incidence of diabetes mellitus, coronary heart disease, and overweight has seemed better with remnant cholesterol. More studies may need for decreasing the knowledge gap and provide a better guide for disease prevention.

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Varbo, Anette, Jacob J. Freiberg, and Børge G. Nordestgaard. "Remnant Cholesterol and Myocardial Infarction in Normal Weight, Overweight, and Obese Individuals from the Copenhagen General Population Study." Clinical Chemistry 64, no. 1 (January 1, 2018): 219–30. http://dx.doi.org/10.1373/clinchem.2017.279463.

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Abstract BACKGROUND We tested whether high remnant cholesterol is associated with high myocardial infarction risk, independent of whether an individual is normal weight, overweight, or obese. METHODS A total of 106216 individuals from the Copenhagen General Population Study were followed for up to 11 years, during which 1565 experienced a myocardial infarction. Individuals were grouped by clinically meaningful remnant cholesterol concentrations of <0.5 mmol/L (19 mg/dL), 0.5 to 0.99 mmol/L (19–38 mg/dL), 1.0 to 1.49 mmol/L (39–58 mg/dL), and ≥1.5 mmol/L (58 mg/dL), and by body mass index (BMI) of <18.5 kg/m2 (underweight), 18.5 to 24.9 kg/m2 (normal weight), 25 to 29.9 kg/m2 (overweight), and ≥30 kg/m2 (obese). RESULTS Median calculated remnant cholesterol was 0.40 mmol/L [interquartile range (IQR), 0.30–0.55 mmol/L] [15 mg/dL (12–21 mg/dL)] for underweight, 0.50 mmol/L (IQR, 0.37–0.71 mmol/L) [19 mg/dL (14–27 mg/dL)] for normal weight, 0.70 mmol/L (IQR, 0.49–1.00 mmol/L) [27 mg/dL (19–39 mg/dL)] for overweight, and 0.85 mmol/L (IQR, 0.61–1.20 mmol/L) [(33 mg/dL (24–46 mg/dL)] for obese individuals. On continuous scales, remnant cholesterol was positively correlated with BMI until reaching a plateau of approximately 1 mmol/L (39 mg/dL) at BMI >35 kg/m2. R2 from an unadjusted linear regression for the correlation between calculated remnant cholesterol and BMI was 12%. Stepwise higher remnant cholesterol was associated with stepwise higher myocardial infarction risk in a similar pattern for normal weight, overweight, and obese individuals. When compared with individuals with remnant cholesterol <0.5 mmol/L (19 mg/dL), individuals with remnant cholesterol ≥1.5 mmol/L (58 mg/dL) had hazard ratios for myocardial infarction of 2.0 (95% CI, 1.3–3.2) for normal weight, 1.9 (95% CI, 1.4–2.6) for overweight, and 2.3 (95% CI, 1.4–3.5) for obese individuals. Directly measured remnant cholesterol increased 0.91 mmol/L (95% CI, 0.89–0.94 mmol/L) [35 mg/dL (34–36 mg/dL)] per 1 mmol/L (39 mg/dL) increase in calculated remnant cholesterol. CONCLUSIONS Remnant cholesterol and BMI were positively correlated; however, high remnant cholesterol was associated with higher myocardial infarction risk across the examined BMI subcategories, indicating that remnant cholesterol is a risk factor for myocardial infarction independent of overweight and obesity.

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Mansbach, C. M., and R. F. Dowell. "Role of the intestine in chylomicron remnant clearance." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 1 (July 1, 1995): G144—G152. http://dx.doi.org/10.1152/ajpgi.1995.269.1.g144.

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When 810 mumol of [3H]glyceryl trioleate (TO) were infused intraduodenally over 6 h into rats, 29% of the triacylglycerol (TG) acyl groups in the mucosa were not from the infusate. We tested the hypothesis that chylomicron remnants contribute to the mucosal pool of nondietary TG acyl groups, since the acyl group composition of the chylomicron remnants was 58% oleate, compared with 90% in their parent chylomicrons. Purified 3H-labeled remnants were generated from chylomicrons formed in rats receiving TO intraduodenally, with 95% of the remnant disintegrations per minute (dpm) being in TG. The 3H-remnants were infused intravenously into rats receiving either saline or 135 mumol/h TO intraduodenally. In the saline-infused rats, 32% of the infused 3H dpm were in the proximal and 19% in the distal intestine and 32% were in the liver. In the fat-infused rats, 12% of the infused 3H dpm were in the proximal and 5% were in the distal gut and 29% were in the liver. When [3H]cholesterol-labeled remnants were infused intravenously and saline was infused intraduodenally, the percentage uptake into the mucosa was nearly the same as with the TG label, but comparable uptake by the liver increased. We conclude that the intestine competes with the liver for chylomicron remnant TG and cholesterol.

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NAPOLITANO, Mariarosaria, Kelly V. BATT, Michael AVELLA, Elena BRAVO, and Kathleen M. BOTHAM. "Lipid synthesis in macrophages derived from the human cell line THP-1: modulation of the effects of native and oxidized chylomicron-remnant-like particles by oestrogen." Clinical Science 101, no. 4 (September 14, 2001): 403–13. http://dx.doi.org/10.1042/cs1010403.

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The effects of native and oxidized chylomicron remnants on the synthesis of cholesteryl ester and triacylglycerol in macrophages, and the way that this is influenced by exposure of the cells to oestrogen, was investigated using the human monocyte cell line THP-1 and chylomicron-remnant-like particles containing human apolipoprotein E (CRLPs). Synthesis of the lipids was measured by the incorporation of [3H]oleate into cholesteryl ester and triacylglycerol. CRLPs (5-40μg of cholesterol/ml) containing either trilinolein or triolein as the triacylglycerol component caused a dose-dependent decrease in cholesteryl ester formation, while triacylglycerol production was unchanged. After oxidation of the CRLPs, the level of thiobarbituric acid-reactive substances was increased by 6.3-fold and 2.2-fold in particles containing trilinolein and triolein respectively. Furthermore, CRLPs containing oxidized trilinolein lost their ability to down-regulate cholesterol esterification, while CRLPs containing oxidized triolein did not. Both types of oxidized CRLPs decreased triacylglycerol synthesis. Treatment of the macrophages with 17β-oestradiol caused increases of approx. 94% and 34% in the synthesis of cholesteryl ester and triacylglycerol respectively in the absence of CRLPs. The differences between control and oestrogen-treated cells were abolished, however, when CRLPs (40μg of cholesterol/ml) were added to the incubations. In addition, in contrast with their lack of effect in control cells, CRLPs containing oxidized trilinolein decreased cholesterol esterification in oestrogen-treated cells by approx. 48%. These findings with CRLPs suggest that chylomicron remnants have significant effects on cholesteryl ester and triacylglycerol synthesis in macrophages, which may be modulated both by the oxidation state of the particles and by oestrogen.

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Baratta, Francesco, Nicholas Cocomello, Mattia Coronati, Domenico Ferro, Daniele Pastori, Francesco Angelico, and Maria Del Ben. "Cholesterol Remnants, Triglyceride-Rich Lipoproteins and Cardiovascular Risk." International Journal of Molecular Sciences 24, no. 5 (February 21, 2023): 4268. http://dx.doi.org/10.3390/ijms24054268.

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Randomized clinical trials with statins and other lipid-lowering drugs have shown the presence of a “residual cardiovascular risk” in those treated to “target” for LDL-cholesterol. This risk is mainly associated to lipid components other than LDL and in particular to remnant cholesterol (RC) and to lipoproteins rich in triglycerides in fasting and non-fasting conditions. During fasting, RCs correspond to the cholesterol content of the VLDL and their partially depleted triglyceride remnant containing apoB-100. Conversely, in non-fasting conditions, RCs include also cholesterol present in chylomicrons containing apoB-48. Therefore, RCs refer to total plasma cholesterol minus HDL-cholesterol and LDL-cholesterol, that is, all the cholesterol present in the VLDL, chylomicrons and in their remnants. A large body of experimental and clinical data suggests a major role of RCs in the development of atherosclerosis. In fact, RCs easily pass the arterial wall and bind to the connective matrix stimulating the progression of smooth muscle cells and the proliferation of resident macrophages. RCs are a causal risk factor for cardiovascular events. Fasting and non-fasting RCs are equivalent for predicting vascular events. Further studies on drugs effect on RC levels and clinical trials to evaluate the efficacy of RC reduction on cardiovascular events are needed.

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Nnamdi, Chinonso, Amah Ubuo, Anaelechi Onuegbu, Madu Olisekodiaka, Chima Okpara, Ekenedirichukwu Okwara, Adamma Analike, and Chidiadi Njoku. "Remnant Cholesterol and Leptin: Any Association in Normal Weight, Over Weight and Obese Individuals in South East Nigeria." ULUTAS MEDICAL JOURNAL 8, no. 4 (2022): 135. http://dx.doi.org/10.5455/umj.20220616022839.

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Introduction: Leptin circulating levels increase with weight gain and decrease with weight loss. The amount of leptin circulating in the body is proportional to an individual's fat. We investigated the association of leptin and remnant cholesterol in normal-weight, overweight and obese participants in southeast Nigeria. Materials and Methods: This is a cross-sectional random study. A total of 90 healthy obese, overweight, and normal-weight participants who met the inclusion criteria were randomly enrolled in the study. They were grouped using their body mass index of 18.5 to 24.9 kg/m2 (average weight), 25 to 29.9 kg/m2 (overweight), and ≥30 kg/m2 (obese). The measured parameters were analyzed using standard methods. Results: Our results showed that there was a progressive increase of remnant cholesterol among the group, but there was no statistical difference (p>0.05) in the mean calculated remnant cholesterol (mmol/l) between the obese (0.72±0.4mmol/l), overweight (0.68±0.46), and average weight (0.50±0.28mmol/l) participants. There was a significant difference in the mean level of Leptin (ug/l) of the obese participants compared to regular weight participants (0.63±0.29 vs. 0.25±0.26, 0.001) and overweight when compared to average weight (0.51±0.27 vs. 0.25±0.26, 0.003). Remnant cholesterol did not correlate with body mass index (BMI) in those that are obese, overweight, or normal weight. Leptin correlated positively with BMI but inversely with Remnant cholesterol. Conclusion: The result obtained from this study suggests that leptin has a positive relationship with BMI, and calculated Remnant cholesterol does not appear to have a direct relationship with obesity. There was no association between leptin and remnant cholesterol among the groups.

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Twickler, T. B., G. M. Dallinga-Thie, J. S. Cohn, and M. J. Chapman. "Elevated Remnant-Like Particle Cholesterol Concentration." Circulation 109, no. 16 (April 27, 2004): 1918–25. http://dx.doi.org/10.1161/01.cir.0000125278.58527.f3.

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Varbo, Anette, and Børge G. Nordestgaard. "Remnant cholesterol and ischemic heart disease." Current Opinion in Lipidology 25, no. 4 (August 2014): 266–73. http://dx.doi.org/10.1097/mol.0000000000000093.

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Mearns, Bryony M. "Role of remnant cholesterol in IHD." Nature Reviews Cardiology 10, no. 10 (August 27, 2013): 553. http://dx.doi.org/10.1038/nrcardio.2013.132.

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Öörni, Katariina, Satu Lehti, Peter Sjövall, and Petri T. Kovanen. "Triglyceride-Rich Lipoproteins as a Source of Proinflammatory Lipids in the Arterial Wall." Current Medicinal Chemistry 26, no. 9 (May 21, 2019): 1701–10. http://dx.doi.org/10.2174/0929867325666180530094819.

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Apolipoprotein B –containing lipoproteins include triglyceride-rich lipoproteins (chylomicrons and their remnants, and very low-density lipoproteins and their remnants) and cholesterol-rich low-density lipoprotein particles. Of these, lipoproteins having sizes below 70-80 nm may enter the arterial wall, where they accumulate and induce the formation of atherosclerotic lesions. The processes that lead to accumulation of lipoprotein-derived lipids in the arterial wall have been largely studied with a focus on the low-density lipoprotein particles. However, recent observational and genetic studies have discovered that the triglyceriderich lipoproteins and their remnants are linked with cardiovascular disease risk. In this review, we describe the potential mechanisms by which the triglyceride-rich remnant lipoproteins can contribute to the development of atherosclerotic lesions, and highlight the differences in the atherogenicity between low-density lipoproteins and the remnant lipoproteins.

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Kuznetsova, A. S. "Interrelationship of dyslipidemia with indicators of regional hemodynamics in patients with atherosclerosis of the visceral branches of the abdominal aorta." Regional blood circulation and microcirculation 15, no. 3 (September 30, 2016): 44–49. http://dx.doi.org/10.24884/1682-6655-2016-15-3-44-49.

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Introduction and aim - to determine the relationship of dyslipidemia and endothelial shear rate in the unpaired visceral arteries in patients with atherosclerosis in the abdominal aorta pool. Mathereals and methods. The study included 50 people. All patients were examined by a single protocol. Conduct a full clinical-laboratory and instrumental examination, supplemented by the following laboratory parameters: total cholesterol (TC), triglycerides, HDL, LDL, apolipoprotein A1, apolipoprotein B, Remnant cholesterol calculated using the formula: total cholesterol - (HDL+LDL). All patients underwent Doppler ultrasound unpaired branches of the abdominal aorta ultrasound scanner Voluson E6 (General Electric) was performed, Toshiba Aplio 500. Measurement of the shear rate (shear rate) is determined by the formula: SR=4xVpeak/Vd, Vpeak - peak flow rate visceral branches of the abdominal aorta, Vd - end-diastolic diameter of the visceral branches of the abdominal aorta. Results and discussion. The analysis of the various characteristics of the regional blood flow showed lower values of shear rate in the celiac trunk in patients with atherosclerosis of the visceral branches of the aorta. In the group of patients with abdominal aortic atherosclerosis pool demonstrated significantly lower levels of HDL, higher levels of VLDL, atherogenic factor, apolipoprotein B, triglycerides and Remnant cholesterol. Correlation analysis revealed an inverse association between the level of Remnant cholesterol and shear rate in the celiac trunk (r = -0.284, p = 0.04). Conclusions. The development of atherosclerosis in the celiac trunk and/or the superior mesenteric artery is associated with higher triglycerides, VLDL, Remnant cholesterol, apoliporoteinom B. In patients with atherosclerosis of visceral arteries decrease in endothelial shear rate in the celiac trunk was correlated with increased levels of Remnant cholesterol.

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Langsted, A., C. M. Madsen, and B. G. Nordestgaard. "Contribution of remnant cholesterol to cardiovascular risk." Journal of Internal Medicine 288, no. 1 (April 7, 2020): 116–27. http://dx.doi.org/10.1111/joim.13059.

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Burnett, John R., Amanda J. Hooper, and Robert A. Hegele. "Remnant Cholesterol and Atherosclerotic Cardiovascular Disease Risk." Journal of the American College of Cardiology 76, no. 23 (December 2020): 2736–39. http://dx.doi.org/10.1016/j.jacc.2020.10.029.

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Castañer, Olga, Xavier Pintó, Isaac Subirana, Antonio J. Amor, Emilio Ros, Álvaro Hernáez, Miguel Ángel Martínez-González, et al. "Remnant Cholesterol, Not LDL Cholesterol, Is Associated With Incident Cardiovascular Disease." Journal of the American College of Cardiology 76, no. 23 (December 2020): 2712–24. http://dx.doi.org/10.1016/j.jacc.2020.10.008.

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Chinonso, Nnamdi J., Ubuo K. Amah, Onuegbu J. Anaelechi, Okeke C. Stellarmaris, Oti D. Chukwudi, Iwuagwu G. Obioma, Ikechukwu S. Nwaisaac, and Ahams E. Chika. "Comparative Study of Remnant Cholesterol, Some Lipid Fractions and FBS Level in Overweight and Obese Participants in South East Nigeria." Asian Journal of Research in Biochemistry 12, no. 3 (May 5, 2023): 11–19. http://dx.doi.org/10.9734/ajrb/2023/v12i3235.

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Background: Obesity is one of the characteristics of metabolic disorders, it has been linked to cardiovascular diseases. Remnant cholesterol has been proposed to be a link between obesity and coronary heart disease, thus a risk factor for the development of cardiovascular disease in obese people. We compared the level of calculated non-fasting remnant cholesterol, fasting and non-fasting lipid profile and fasting blood sugar in overweight, obese and normal weight participants in Nnewi, a town in South East Nigeria. Methods: In this cross-sectional study, a total of 90 apparently healthy obese, overweight and normal weight participants who met the inclusion criteria were randomly enrolled. They were grouped using their body mass index of 18.5 to 24.9 kg/m2 (normal weight), 25 to 29.9 kg/m2 (overweight) and ≥30 kg/m2 (obese). The parameters were analyzed using standard methods. Results: Our results shows that there was progressive increase of remnant cholesterol among the group, this increase has no statistical difference (p>0.05) in the mean calculated remnant cholesterol (mmol/l) between the obese (0.72±0.4), overweight (0.68±0.46), and normal weight (0.50±0.28) participants. The mean fasting Very Low Density Lipoprotein (VLDL) and Triglyceride (TG) (mmol/l) were significantly higher (p<0.05) in overweight compared to normal weight participants (0.76±0.31 vs. 0.47±0.22) and (1.72±0.60 vs. 1.09±0.51) and obese participants (0.82±0.23 vs. 0.47±0.22) and (1.85±0.59 vs. 1.09±0.51) when compared to normal weight participants respectively. FBS levels (mmol/l) were significantly lower in normal weight participants when compared to overweight participants (3.45±0.79 vs. 4.46±1.82) and obese participants (3.46± 0.79 vs. 4.94±1.26). Conclusion: The results obtained from this study demonstrated a progressive increase in the level of remnant cholesterol which was not statistically significant among apparently healthy individuals across the group. Furthermore we did not observed Remnant cholesterol as a sole predictor to obesity which will lead to cardiovascular diseases, with the rising prevalence of obesity in developing country as well as its associated complications and risks.

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Packard, Chris J. "Remnants, LDL, and the Quantification of Lipoprotein-Associated Risk in Atherosclerotic Cardiovascular Disease." Current Atherosclerosis Reports 24, no. 3 (February 17, 2022): 133–42. http://dx.doi.org/10.1007/s11883-022-00994-z.

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Abstract Purpose of Review Implementation of intensive LDL cholesterol (LDL-C) lowering strategies and recognition of the role of triglyceride-rich lipoproteins (TRL) in atherosclerosis has prompted re-evaluation of the suitability of current lipid profile measurements for future clinical practice. Recent Findings At low concentrations of LDL-C (< 1.8 mmol/l/70 mg/dl), the Friedewald equation yields estimates with substantial negative bias. New equations provide a more accurate means of calculating LDL-C. Recent reports indicate that the increase in risk per unit increment in TRL/remnant cholesterol may be greater than that of LDL-C. Hence, specific measurement of TRL/remnant cholesterol may be of importance in determining risk. Non-HDL cholesterol and plasma apolipoprotein B have been shown in discordancy analyses to identify individuals at high risk even when LDL-C is low. Summary There is a need to adopt updated methods for determining LDL-C and to develop better biomarkers that more accurately reflect the abundance of TRL remnant particles.

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Carrella, Massimino, Annalisa Csillaghy, Renato de Mercato, and Agesilao D'Arienzo. "Biliary Excretion of Chylomicron Remnant Cholesterol in the Rat: Responses to the Expansion of Their Plasma Pool and Promoting Role of Stimulated Bile-Acid Synthesis." Clinical Science 89, no. 2 (August 1, 1995): 121–28. http://dx.doi.org/10.1042/cs0890121.

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1. Chylomicron remnants, the intermediate intestinal lipoproteins carrying the bulk of dietary cholesterol, are actively taken up and degraded in the hepatocytes, releasing cholesterol which can be excreted in bile. To study this pathway, a mass of remnants, leading to a consistent rise in hepatic cholesterol, was administered as an intravenous bolus in rats with chronic bile fistula equilibrated by water, electrolyte and taurocholate infusions, and changes in biliary lipids and bile acids were evaluated for up to 24 h in comparison with baseline. 2. A mean 16% increase in the net output of bile acids was observed at each time interval after lipoprotein injection, accounting for a 24 h cumulative excretion of approximately one-third of the administered cholesterol mass. These changes did not reach statistical significance however. The cholesterol output and concentrations of all biliary lipids did not vary either. Without taurocholate replacement, remnants injection was followed by a 15–20% decrease in bile acid and bile lipid secretion, presumably due to an insufficient hepatic bile-acid flux. 3. When [3H]cholesterol-labelled remnants were administered at the same mass in the chronic equilibrated bile fistula model, 21% of injected radioactivity was excreted in 24 h, distributing mostly in acidic rather than neutral sterols (20.02 ± 1.85 compared with 1.07 ± 0.04), with an acidic to neutral sterol mean ratio of 16. 4. To exclude interfering effects from the administered cholesterol mass and chronic bile fistula, 3H-labelled remnants were also studied as a cholesterol trace injected in rats with acute bile fistula. In this case, however, 24 h total sterol radioactivity only reached approximately 10% of that injected, and partitioned relatively less in acidic (6.84 ± 0.59) than in neutral (3.15 ± 0.39) sterols, with an acidic to neutral sterol mean ratio of 2. 5. The study suggests that remnant cholesterol reaches bile mainly in the form of bile acids, by a steady slow-rate process which is magnified under conditions of stimulated bile-acid synthesis.

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Wieczorek, Ewa, Agnieszka Ćwiklińska, Agnieszka Kuchta, Barbara Kortas-Stempak, Anna Gliwińska, and Maciej Jankowski. "The Differential Effects of HDL Subpopulations on Lipoprotein Lipase (LPL)-Mediated VLDL Catabolism." Biomedicines 9, no. 12 (December 5, 2021): 1839. http://dx.doi.org/10.3390/biomedicines9121839.

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High-density lipoprotein (HDL) subpopulations functional assessment is more relevant for HDL anti-atherogenic activity than cholesterol level. The aim of the study was to assess the impact of HDL-2 and HDL-3 on lipoprotein lipase (LPL)-mediated very-low-density lipoprotein (VLDL) catabolism related to hypertriglyceridemia development. VLDL and HDLs were isolated from serum by ultracentrifugation. VLDL was incubated with LPL in the absence and presence of total HDL or HDL subpopulations. Next, VLDL remnants were separated, and their composition and electrophoretic mobility was assessed. Both HDL subpopulations increased the efficiency of triglyceride lipolysis and apolipoprotein CII and CIII removal from VLDL up to ~90%. HDL-3 exerted significantly greater impact than HDL-2 on apolipoprotein E (43% vs. 18%, p < 0.001), free cholesterol (26% vs. 18%, p < 0.05) and phospholipids (53% vs. 43%, p < 0.05) removal from VLDL and VLDL remnant electrophoretic mobility (0.18 vs. 0.20, p < 0.01). A greater release of these components was also observed in the presence of total HDL with a low HDL-2/HDL-3 cholesterol ratio. Both HDL subpopulations affect VLDL composition during lipolysis, but HDL-3 exhibited a greater effect on this process. Altered composition of HDL related to significant changes in the distribution between HDL-2 and HDL-3 can influence the VLDL remnant features, affecting atherosclerosis progression.

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Wilson, Peter W. F., and Alan T. Remaley. "Ischemic Heart Disease Risk and Remnant Cholesterol Levels." Journal of the American College of Cardiology 79, no. 24 (June 2022): 2398–400. http://dx.doi.org/10.1016/j.jacc.2022.04.016.

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Toth, Peter P., Harold Bays, William Brown, Joanne Tomassini, Colin Wang, Adam Polis, and Andrew Tershakovec. "CHOLESTEROL IN REMNANT-LIPOPROTEINS AS MEASURED BY DIFFERENT." Journal of the American College of Cardiology 65, no. 10 (March 2015): A1569. http://dx.doi.org/10.1016/s0735-1097(15)61569-8.

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Cully, Megan. "Remnant cholesterol is associated with ischaemic heart disease." Nature Reviews Cardiology 10, no. 3 (January 22, 2013): 119. http://dx.doi.org/10.1038/nrcardio.2013.3.

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Kaltoft, Morten, Anne Langsted, and Børge G. Nordestgaard. "Triglycerides and remnant cholesterol associated with risk of aortic valve stenosis: Mendelian randomization in the Copenhagen General Population Study." European Heart Journal 41, no. 24 (April 8, 2020): 2288–99. http://dx.doi.org/10.1093/eurheartj/ehaa172.

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Abstract Aims We tested the hypothesis that higher levels of plasma triglycerides and remnant cholesterol are observationally and genetically associated with increased risk of aortic valve stenosis. Methods and results We included 108 559 individuals from the Copenhagen General Population Study. Plasma triglycerides, remnant cholesterol (total cholesterol minus low-density lipoprotein and high-density lipoprotein cholesterol), and 16 genetic variants causing such increased or decreased levels were determined. Incident aortic valve stenosis occurred in 1593 individuals. Observationally compared to individuals with triglycerides <1 mmol/L (<89 mg/dL), the multifactorially adjusted hazard ratio for aortic valve stenosis was 1.02 [95% confidence interval (CI) 0.87–1.19] for individuals with triglycerides of 1.0–1.9 mmol/L (89–176 mg/dL), 1.22 (1.02–1.46) for 2.0–2.9 mmol/L (177–265 mg/dL), 1.40 (1.11–1.77) for 3.0–3.9 mmol/L (266–353 mg/dL), 1.29 (0.88–1.90) for 4.0–4.9 mmol/L (354–442 mg/dL), and 1.52 (1.02–2.27) for individuals with triglycerides ≥5 mmol/L (≥443 mg/dL). By age 85, the cumulative incidence of aortic valve stenosis was 5.1% for individuals with plasma triglycerides <2.0 mmol/L (77 mg/dL), 6.5% at 2.0–4.9 mmol/L (177–442 mg/dL), and 8.2% for individuals with plasma triglycerides ≥5.0 mmol/L (443 mg/dL). The corresponding values for remnant cholesterol categories were 4.8% for <0.5 mmol/L (19 mg/dL), 5.6% for 0.5–1.4 mmol/L (19–57 mg/dL), and 7.4% for ≥1.5 mmol/L (58 mg/dL). Genetically, compared to individuals with allele score 13–16, odds ratios for aortic valve stenosis were 1.30 (95% CI 1.20–1.42; Δtriglycerides +12%; Δremnant cholesterol +11%) for allele score 17–18, 1.41 (1.31–1.52; +25%; +22%) for allele score 19–20, and 1.51 (1.22–1.86; +51%; +44%) for individuals with allele score 21–23. Conclusion Higher triglycerides and remnant cholesterol were observationally and genetically associated with increased risk of aortic valve stenosis.

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Hirao, Yuhko, Katsuyuki Nakajima, Tetsuo Machida, Masami Murakami, and Yasuki Ito. "Development of a Novel Homogeneous Assay for Remnant Lipoprotein Particle Cholesterol." Journal of Applied Laboratory Medicine 3, no. 1 (July 1, 2018): 26–36. http://dx.doi.org/10.1373/jalm.2017.024919.

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Abstract Background Quantification of remnant lipoprotein particle cholesterol (RLP-C) by automated assay is useful in routine clinical laboratories to assess coronary artery disease risk and diagnose type III hyperlipoproteinemia. Methods Enzymes and surfactants were screened to establish a homogeneous RLP-C assay using the chylomicron-VLDL, LDL, and HDL fractions isolated by ultracentrifugation, along with the RLP fraction isolated by immunoaffinity gel. All data were generated using a Hitachi analyzer. Results A specific cholesterol esterase with a polyoxyethelene styrenated phenyl ether derivative (surfactant) was used for the establishment of a homogeneous RLP-C assay. This cholesterol esterase with subunits of >40 kDa (H-CE) was found to react with lipoproteins other than RLP, whereas this enzyme with subunits of <40 kDa (L-CE) reacted with RLP. H-CE was applied for the first reaction step with the specific surfactant to decompose non-RLP lipoproteins, degrading non-RLP cholesterol into water and oxygen in the presence of cholesterol oxidase and catalase. For the second step, L-CE was applied to release cholesterol from RLP, and then the released RLP-C was determined in a standard cholesterol oxidase and peroxidase system. This new homogeneous assay exhibited good correlation with the RLP-C immunoseparation method. Conclusions We established a simple, rapid, automated homogeneous assay for RLP-C. The assay can determine RLP-C levels in 10 min in a fully automated manner, processing a large number of samples in routine clinical laboratories.

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Leary, Elizabeth Teng, Tao Wang, Daniel J. Baker, Donald D. Cilla, Jianhua Zhong, G. Russell Warnick, Katsuyuki Nakajima, and Richard J. Havel. "Evaluation of an immunoseparation method for quantitative measurement of remnant-like particle-cholesterol in serum and plasma." Clinical Chemistry 44, no. 12 (December 1, 1998): 2490–98. http://dx.doi.org/10.1093/clinchem/44.12.2490.

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Abstract Substantial evidence indicates that triglyceride-rich lipoprotein remnants are atherogenic. Additional research has, however, been limited by available methods for separation and quantification of remnants. We have evaluated an immunoseparation assay developed to measure cholesterol in remnant-like particles (RLP-C). This method uses monoclonal antibodies to human apolipoproteins B-100 and A-I to remove most of the apolipoprotein B-100-containing lipoproteins (namely LDL and nascent VLDL) and apolipoprotein A-I-containing lipoproteins (namely chylomicrons and HDL), leaving behind a fraction of triglyceride-rich lipoproteins, including chylomicron and VLDL remnants, both of which are enriched in apolipoprotein E. Cholesterol in the unbound fraction is measured with a sensitive enzymatic assay. The RLP-C concentration was highly correlated with total triglyceride-rich lipoproteins (sum of VLDL-cholesterol and IDL-cholesterol) separated by ultracentrifugation and by polyacrylamide gel electrophoresis (r = 0.86 and 0.76, respectively). The within-run and run-to-run imprecision (CV) of the assay was ∼6% and 10%, respectively. The assay was not affected by hemoglobin up to 5000 mg/L (500 mg/dL), bilirubin up to 342 mmol/L (20 mg/dL), glucose up to 67 mmol/L (1200 mg/dL), or ascorbic acid up to 170 mmol/L (3.0 mg/dL). In 726 subjects (men, n = 364; women, n = 362) in the US, the 75th percentiles of RLP-C concentration were 0.17 mmol/L (6.6 mg/dL) and 0.23 mmol/L (8.8 mg/dL) in sera obtained after overnight fasting or randomly, respectively. A group of 151 patients from nine US centers and one Canadian center with coronary artery atherosclerosis established by angiography had higher median RLP-C concentrations than 302 gender- and age-matched controls (P <0.05). We conclude that the RLP-C assay compares favorably to ultracentrifugation and electrophoresis and provides a convenient and economical approach to measure triglyceride-rich lipoprotein remnants in routine clinical laboratories.

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YU, Kenneth C. W., and John C. L. MAMO. "Chylomicron-remnant-induced foam cell formation and cytotoxicity: a possible mechanism of cell death in atherosclerosis." Clinical Science 98, no. 2 (January 11, 2000): 183–92. http://dx.doi.org/10.1042/cs0980183.

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The effects of chylomicron remnants on cytoplasmic lipid loading and cell viability were assessed in cultures of human monocyte-derived macrophages and rabbit arterial smooth muscle cells. At a cholesterol concentration of 150 μg/ml, chylomicron remnants induced substantial cytoplasmic lipid loading of macrophages, but not of smooth muscle cells, within 6 h of exposure. Chylomicron remnants were found to be cytotoxic to macrophages and smooth muscle cells, although the latter were generally more resistant. Chylomicron remnants contained no detectable oxysterols (> 1 ng) and contained less non-esterified (‘free’) fatty acids than non-lipolysed nascent chylomicrons. Chylomicron-remnant-induced cytotoxicity appeared to be time- and dose-dependent. Macrophage and smooth muscle cell viability were inversely related to the production of superoxide free radicals and were significantly improved in the combined presence of superoxide dismutase and catalase. Collectively, our data suggest that, in macrophages, cell viability is compromised as a consequence of superoxide free radical production following uptake of chylomicron remnants. We would suggest that, in arterial smooth muscle cells, chylomicron-remnant-induced cell death also occurs as a consequence of superoxide free radical production. Our observations in the present study suggest that macrophage foam cells in atherosclerotic plaques might be derived from the cellular uptake of chylomicron remnants. Furthermore, arterial accumulation of chylomicron remnants might contribute to plaque destabilization as a consequence of cell death following superoxide free radical production by macrophages and smooth muscle cells.

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杜, 柯锐. "Remnant Cholesterol and Status of Dyslipidemia in Hemodialysis Patients." Advances in Clinical Medicine 12, no. 07 (2022): 6106–12. http://dx.doi.org/10.12677/acm.2022.127880.

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Nordestgaard, Børge G. "A New Start for Triglycerides and Remnant Cholesterol—Nonfasting." Clinical Chemistry 63, no. 8 (August 1, 2017): 1418–19. http://dx.doi.org/10.1373/clinchem.2016.268938.

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Pirillo, Angela, Giuseppe D. Norata, and Alberico L. Catapano. "Beyond LDL-C levels, does remnant cholesterol estimation matter?" European Journal of Preventive Cardiology 27, no. 10 (February 3, 2020): 1088–90. http://dx.doi.org/10.1177/2047487319899622.

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Ohnishi, Hirofumi, Sigeyuki Saitoh, Satoru Takagi, Jun-ichi Ohata, Takeshi Isobe, Yuka Kikuchi, Hiroshi Takeuchi, and Kazuaki Shimamoto. "Relationship between insulin-resistance and remnant-like particle cholesterol." Atherosclerosis 164, no. 1 (September 2002): 167–70. http://dx.doi.org/10.1016/s0021-9150(02)00057-6.

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Toth, Peter P., W. Virgil Brown, Harold E. Bays, Joanne E. Tomassini, Colin Wang, Adam B. Polis, and Andrew M. Tershakovec. "Cholesterol in Remnant-Lipoproteins as Measured by Different Methods." Journal of Clinical Lipidology 9, no. 3 (May 2015): 414–15. http://dx.doi.org/10.1016/j.jacl.2015.03.017.

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Schwartz, Gregory G., Markus Abt, Michael Miller, Hardi Mundl, and Anders Olsson. "REMNANT CHOLESTEROL AND RESIDUAL RISK AFTER ACUTE CORONARY SYNDROME." Journal of the American College of Cardiology 63, no. 12 (April 2014): A257. http://dx.doi.org/10.1016/s0735-1097(14)60257-6.

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Toth, P. P., H. E. Bays, W. V. Brown, J. E. Tomassini, Y. Wang, A. B. Polis, and A. M. Tershakovec. "Cholesterol in remnant-lipoproteins as measured by different methods." Atherosclerosis 241, no. 1 (July 2015): e39. http://dx.doi.org/10.1016/j.atherosclerosis.2015.04.142.

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Journal articles on the topic 'Remnant cholesterol'

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