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- Adiels, Martin, 1976, et al.
(författare)
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Diabetic dyslipidaemia
- 2006
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Ingår i: Curr Opin Lipidol. - 0957-9672 .- 1473-6535. ; 17:3, s. 238-46
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE OF REVIEW: Diabetic dyslipidaemia is a cluster of plasma lipid and lipoprotein abnormalities that are metabolically interrelated. The increase of large type 1 very low density lipoprotein particles in type 2 diabetes initiates a sequence of events that generates atherogenic remnants, small dense low-density lipoprotein and small dense high-density lipoprotein particles. Thus, it is of great importance to elucidate the mechanisms behind the overproduction of large very low density lipoprotein particles in diabetic dyslipidaemia. This review discusses the pathophysiology of very low density lipoprotein metabolism in type 2 diabetes and recent concepts of lipid management of diabetic dyslipidaemia. RECENT FINDINGS: Results indicate that triglyceride and apolipoprotein B production in types 1 and 2 very low density lipoprotein are significantly correlated, suggesting a coupling of the two processes governing the metabolism of these lipoprotein subpopulations. Insulin resistance, hyperglycaemia, and liver fat were associated with excess hepatic production of type 1 but not type 2 very low density lipoprotein particles. These data provide support for the independent regulation of types 1 and 2 very low density lipoprotein apolipoprotein B production. SUMMARY: Recent data suggest that the assembly of very low density lipoprotein is fundamentally altered in type 2 diabetes, explaining the overproduction of large type 1 very low density lipoprotein as well as the inability of insulin to suppress production of type 1 very low density lipoprotein in type 2 diabetes. Future discoveries hopefully will delineate the regulatory steps to allow more targeted treatment of diabetic dyslipidaemia.
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| 3. |
- Borén, Jan, 1963, et al.
(författare)
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The central role of arterial retention of cholesterol-rich apolipoprotein-B-containing lipoproteins in the pathogenesis of atherosclerosis: a triumph of simplicity
- 2016
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Ingår i: Current Opinion in Lipidology. - : Ovid Technologies (Wolters Kluwer Health). - 0957-9672 .- 1473-6535. ; 27:5, s. 473-483
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Tidskriftsartikel (refereegranskat)abstract
- Purpose of reviewToday, it is no longer a hypothesis, but an established fact, that increased plasma concentrations of cholesterol-rich apolipoprotein-B (apoB)-containing lipoproteins are causatively linked to atherosclerotic cardiovascular disease (ASCVD) and that lowering plasma LDL concentrations reduces cardiovascular events in humans. Here, we review evidence behind this assertion, with an emphasis on recent studies supporting the response-to-retention' model - namely, that the key initiating event in atherogenesis is the retention, or trapping, of cholesterol-rich apoB-containing lipoproteins within the arterial wall.Recent findingsNew clinical trials have shown that ezetimibe and anti-PCSK9 antibodies - both nonstatins - lower ASCVD events, and they do so to the same extent as would be expected from comparable plasma LDL lowering by a statin. These studies demonstrate beyond any doubt the causal role of apoB-containing lipoproteins in atherogenesis. In addition, recent laboratory experimentation and human Mendelian randomization studies have revealed novel information about the critical role of apoB-containing lipoproteins in atherogenesis. New information has also emerged on mechanisms for the accumulation in plasma of harmful cholesterol-rich and triglyceride-rich apoB-containing remnant lipoproteins in states of overnutrition. Like LDL, these harmful cholesterol-rich and triglyceride-rich apoB-containing remnant lipoprotein remnants become retained and modified within the arterial wall, causing atherosclerosis.SummaryLDL and other cholesterol-rich, apoB-containing lipoproteins, once they become retained and modified within the arterial wall, cause atherosclerosis. This simple, robust pathophysiologic understanding may finally allow us to eradicate ASCVD, the leading killer in the world.
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| 6. |
- Koopen, Annefleur M., et al.
(författare)
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Human microbiome as therapeutic intervention target to reduce cardiovascular disease risk
- 2016
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Ingår i: Current Opinion in Lipidology. - 0957-9672 .- 1473-6535. ; 27, s. 615-622
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Forskningsöversikt (refereegranskat)abstract
- Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved. Purpose of review: The absolute burden of cardiovascular risk remains high despite currently available preventive and therapeutic options. In search for novel therapeutic leads, mounting evidence has linked the gut microbiota as well as their metabolites to the development of cardiometabolic diseases. Recent findings: The intestinal microbiota influences the host via different metabolic pathways as inducer of endotoxemia, formation of trimethylamine-N-oxide, production of short chain fatty acids, and is a regulator in intestinal bile acid metabolism. Disruption of the gut microbiome may disturb the homeostasis of the microbial ecosystem to an alternative stable state associated with pathophysiological traits in microbiota and host. However, causality has not been shown yet. Summary: We are just beginning to understand how the gut microbiota influence our cardiometabolic health and various innovative therapeutic options are in the developing (preclinical) phase. This review focuses on the current evidence whether and to what extent the intestinal microbiota are involved in cardiovascular disease and whether this is based on merely association or causal relations.
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| 7. |
- Landberg, Rikard
(författare)
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Diet and endothelial function: from individual components to dietary patterns
- 2012
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Ingår i: Current Opinion in Lipidology. - 0957-9672 .- 1473-6535. ; 23, s. 147-155
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Tidskriftsartikel (refereegranskat)abstract
- The currently available evidence supports beneficial effects of various dietary compounds on endothelial function. However, in order to obtain strong evidence for relevant health effects that can be used for specific dietary recommendations, more long-term studies using well characterized diets/supplements in a large number of individuals are needed.
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| 8. |
- Landberg, Rikard
(författare)
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Dietary flavonoids and the development of type 2 diabetes and cardiovascular diseases: review of recent findings
- 2013
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Ingår i: Current Opinion in Lipidology. - 0957-9672 .- 1473-6535. ; 24, s. 25-33
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Forskningsöversikt (refereegranskat)abstract
- Evidence from cohort studies and randomized trials suggest beneficial effects of food sources of anthocyanidins (berries) and flavan-3-ols (green tea and cocoa) on cardiovascular health. These findings need to be confirmed in long-term randomized trials, and evaluation of pure compounds will be important to establish what specific flavonoids and doses are effective.
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| 9. |
- Larsson, Susanna C.
(författare)
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Mendelian randomization as a tool for causal inference in human nutrition and metabolism
- 2021
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Ingår i: Current Opinion in Lipidology. - : Wolters Kluwer. - 0957-9672 .- 1473-6535. ; 32:1, s. 1-8
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE OF REVIEW: The current review describes the fundamentals of the Mendelian randomization framework and its current application for causal inference in human nutrition and metabolism.RECENT FINDINGS: In the Mendelian randomization framework, genetic variants that are strongly associated with the potential risk factor are used as instrumental variables to determine whether the risk factor is a cause of the disease. Mendelian randomization studies are less susceptible to confounding and reverse causality compared with traditional observational studies. The Mendelian randomization study design has been increasingly used in recent years to appraise the causal associations of various nutritional factors, such as milk and alcohol intake, circulating levels of micronutrients and metabolites, and obesity with risk of different health outcomes. Mendelian randomization studies have confirmed some but challenged other nutrition-disease associations recognized by traditional observational studies. Yet, the causal role of many nutritional factors and intermediate metabolic changes for health and disease remains unresolved.SUMMARY: Mendelian randomization can be used as a tool to improve causal inference in observational studies assessing the role of nutritional factors and metabolites in health and disease. There is a need for more large-scale genome-wide association studies to identify more genetic variants for nutritional factors that can be utilized for Mendelian randomization analyses.
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| 10. |
- Olivecrona, Gunilla
(författare)
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Role of lipoprotein lipase in lipid metabolism
- 2016
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Ingår i: Current Opinion in Lipidology. - 0957-9672 .- 1473-6535. ; 27:3, s. 233-241
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Forskningsöversikt (refereegranskat)abstract
- Purpose of review A major step in energy metabolism is hydrolysis of triacylglycerol-rich lipoproteins (TRLs) to release fatty acids that can be used or stored. This is accomplished by lipoprotein lipase (LPL) at 'binding lipolysis sites' at the vascular endothelium. A multitude of interactions are involved in this seemingly simple reaction. Recent advances in the understanding of some of these factors will be discussed in an attempt to build a comprehensive picture.Recent findings The first event in catabolism of TRLs is that they dock at the vascular endothelium. This requires LPL and GPIHBP1, the endothelial transporter of LPL. Kinetic studies in rats with labeled chylomicrons showed that once a chylomicron has docked in the heart it stays for minutes and a large number of triacylglycerol molecules are split. The distribution of binding between tissues reflects the amount of LPL, as evident from studies with mutant mice. Clearance of TRLs is often slowed down in metabolic disease, as was demonstrated both in mice and men. In mice, this was directly connected to decreased amounts of endothelial LPL.Summary The LPL system is central in energy metabolism and results from interplay between several factors. Rapid and exciting progress is being made.
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