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Articles On The Topic: "remnant"

Our observation that subjects with MetS exhibit a 40 % higher fasting concentration of apo B-48 compared to those without suggests an impairment in chylomicron metabolism in these subjects. Our findings confirm and extend those previously reported in a Japanese population where it was reported that subjects with MetS had on average a 34 % or 42 % higher fasting apo B-48 concentration (in males and females respectively) compared to control subjects without MetS [18]. Interestingly we also observed that elevated apo B-48 concentration was only observed in subjects who exhibited three or greater MetS components (and hence exhibited MetS) suggesting that impaired chylomicron metabolism is reliant on the altered phenotype of MetS rather than simply being a consequence of its individual parameters. Chylomicron metabolism may be impaired in subjects with MetS at the level of production, lipolysis and/or clearance. Increased production of apo B-48 particles via elevated availability of substrate in enterocytes (i.e. due to increased expression of NPC1L1), increased MTP activity, decreased LPL activity and reduced LDL receptor and LDL receptor protein activity have been proposed as a possible mechanism of the altered chylomicron metabolism [34, 35]. In subjects with MetS, hepatic overproduction of VLDL has been reported [36, 37]. Alternatively, exaggerated secretion of chylomicron particles in MetS may be indicative of intestinal hypertrophy, however this cannot be determined in this cross sectional study.

Articles on the topic: "remnant"

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In subjects without MetS, there was a relatively weak correlation of triglyceride with apo B-48, contrasting the result observed in the MetS group. Since triglyceride concentration in plasma is mainly contributed by the triglyceride associated with VLDL particles, the association between apo B-48 and triglyceride concentration suggests a common metabolic defect that is more pronounced in those with MetS, leading to accumulation of these triglyceride-rich lipoproteins. In order to standardise for the magnitude of these parameters we also examined the association between the Z scores of apo B-48 and anthropometric and lipid/metabolic determinants. This allowed us to compare the slope of these relationships when standardised for one standard deviation change in each parameter, and also to correct for age and gender. However the slope of the association of Z-scores for most of these parameters was remarkably low, and although triglyceride had the highest slope for association with apo B-48 in the no MetS group, it had a low coefficient of variation suggesting that triglyceride is a poor surrogate marker of chylomicron remnant homeostasis. In subjects with MetS, the slope of the association of Z scores for apo B-48 with triglyceride and non-HDL cholesterol and the coefficient of variation were increased, nonetheless these measures were still not predictive of chylomicron remnant homeostasis.

In subjects with MetS the elevated triglyceride concentration is suggestive of a lipolytic defect. Although not directly measured in this study, subjects with MetS may have decreased expression of LPL as a consequence of insulin resistance [24]. A defect in lipolysis would be expected to promote an increased residency time for TRLs including chylomicron particles and favour increased lipid exchange promote accumulation of TRL remnants [38, 39]. In the plasma compartment, remodelling of lipoproteins involves the exchange of cholesteryl ester and triglyceride between triglyceride-rich (chylomicron and hepatic derived) lipoproteins and cholesterol-rich lipoproteins (LDL and HDL particles). Although we have observed an increased circulating concentration of chylomicron remnants in subjects with MetS this change was not associated with a decrease in HDL cholesterol concentrations. It seems that other factors independent to chylomicron metabolism such as HDL particle instability due to insulin resistance may implicate the low concentration of HDL cholesterol in MetS [40].

Clearance of chylomicron remnants post hydrolysis is a highly efficient process that occurs principally via internalization by LDL receptor and LDL receptor-related protein 1 after remnants were bound to the HSPG of the surface of hepatocytes facilitated by apo E [41]. Insulin resistance has been reported to associate with diminished remnant clearance by impairing the HSPG structure via modulation of hepatic SULF2 expression [42] and by altering LDL receptor via PCSK9 [43]. If accumulation of chylomicron remnants in MetS occurs principally as a consequence of impaired lipoprotein binding and/or depressed receptor expression, then by extension one would anticipate a strong association with LDL cholesterol. The findings show that in subjects with MetS, the association of LDL cholesterol with apo B-48 was strengthened in comparison to control subjects with presumably adequate expression of apo B/E receptor. The findings suggest that decreased expression may have contributed to an accumulation of chylomicron remnants in MetS subjects. However as only one-third of the variability in apo B-48 can be explained by LDL cholesterol, this does not support the contention that LDL cholesterol serves as a good surrogate marker of pro-atherogenic remnant homeostasis in plasma, and that MetS is not associated with a major defect in high affinity clearance pathways. The latter may be indicative of the findings that chylomicron remnants require greater clusters for apo B/E receptors on the plasma membrane for internalization, whereas LDL particles interact with singular receptors. A modest reduction in receptor expression will therefore have a greater effect on clearance of chylomicron remnants in comparison to LDL particles. By extension, LDL cholesterol would be a poor predictor of remnant homeostasis, particularly if receptor expression is attenuated.

Background: Liver resection represents the first choice of treatment for primary and secondary liver malignancies, offering the patient the best chance of long-term survival. The extensive use of major hepatectomy increases the risk of post-hepatectomy liver failure (PHLF), which is associated with a high frequency of postoperative complications, mortality and increased length of hospital stay. Aims: The aim of this review is to investigate the different risk factors related to the occurrence of PHLF and to identify the limits for a safe liver resection in patients with normal liver and injured liver (cirrhosis, cholestasis, steatosis and post-chemotherapy liver injury). Methods: A literature search was undertaken in PubMed and related search engines, looking for articles relating to hepatic failure following hepatectomy in normal liver or injured liver. Results: In spite of improvements in surgical and postoperative management, the parameters determining how much liver can be resected are still largely undefined. A number of preoperative, intraoperative and postoperative factors all contribute to the likelihood of liver failure after surgery. The safe limits for liver resection can be estimated from the data of the literature for patients with normal liver and for those with different types of liver injury. Conclusions: Preoperative assessment that includes evaluation of liver volume and function of the remnant liver is a mandatory prerequisite before major hepatectomy. The critical residual liver volume for patients able to predict PHLF is mainly related to the presence of pre-existing liver disease and liver function. Among patients with normal liver, the limit for safe resection ranges from 20 to 30% future remnant liver of total liver volume. In patients with injured liver (cirrhosis, cholestasis or steatosis), preoperative assessment of the risk of PHLF should include future remnant liver volumetry and accurate liver function evaluation, including different dynamic liver function tests.

We searched PubMed, Embase, and the Cochrane Library to identify RCTs published from the initial date to 24 December 2017 that compared the remnant preservation technique with the standard technique for primary ACL reconstruction. The title and abstract fields were searched for the following terms in each database: anterior cruciate ligament, remnant, preservation. A manual search was also performed for articles potentially missed by the electronic search. The search history of each database is supplied in Additional file 1, Additional file 2, and Additional file 3.

A summary of the study selection process is presented in Fig. 1. Our search identified 415 records. A total of 284 citations were discarded because they were duplicates or did not fit the eligibility criteria. After full-text verification of the remaining 15 articles, seven studies with a combined 412 patients (208 in the remnant preservation technique group and 204 in the standard technique group) were included in the meta-analysis [17,18,19,20,21,22,23].

Elevated LDL-C is a well-known risk factor for CAD, which is commonly considered as the primary therapy target [3, 4]. However, after reduction of LDL-C to recommended levels, there is still a considerable residual risk of MACEs [5]. A growing amount of studies supported the notion that RC might contribute to this residual risk, which is of particular interest based on the fact that burgeoning prevalence of DM is associated with increased TG levels and its potential intersection with CAD [6, 7]. Emerging evidence indicated that RC was capable of converging a variety of proatherogenic effects, including monocyte activation, upregulation of proinflammatory cytokines, and increased prothrombotic factors production [5, 8]. In-vitro and animal investigations provided the evidence that elevated RC levels could lead to atherosclerosis in the same way as elevated levels of LDL-C by penetrating the arterial wall, being taken up by macrophage and causing foam cell formation. These data may suggest that RC is more important than TG to explain the residual risk though their circulating concentrations are correlated [24,25,26]. Numerous clinical studies also indicated that high RC concentrations were related to increased risk for atherosclerosis and CAD [27]. A recent study showed that RC was associated with coronary atheroma progression independent of conventional lipid parameters [28]. In addition to observational studies, a number of genetic studies have strongly shown that higher RC is a causal risk factor for CAD [2, 9]. More recently, the latest guideline for dyslipidemia management underlined the atherogenic effect of apoB and revealed that the clinical benefit of lipid-lowering therapy might attribute to the reduction of apoB-containing particles, which mostly referred to RC [3]. Hence, the atherogenic effects of RC may explain the associations with an increased incidence of MACEs, as demonstrated in the present study. 041b061a72


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