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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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| 4. |
- Attman, Per-Ola, 1941, et al.
(författare)
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Dyslipidemia of kidney disease.
- 2009
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Ingår i: Current opinion in lipidology. - 1473-6535. ; 20:4, s. 293-9
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE OF REVIEW: Chronic kidney disease is associated with specific alterations of lipoprotein metabolism that may be linked to accelerated atherosclerosis and cardiovascular disease. This review summarizes current knowledge of the pathophysiology of renal dyslipidemia and the therapeutic options. RECENT FINDINGS: The renal dyslipidemia is characterized by accumulation of intact and partially metabolized triglyceride-rich apoB-containing and apoC-containing lipoproteins. Increased concentrations of atherogenic apoC-III rich lipoproteins, the hallmark of renal dyslipidemia, may result from disturbances of insulin metabolism and action in chronic kidney disease. Novel findings strongly suggest that apoC-III triggers a cascade of pro-inflammatory events, which ultimately can result in endothelial dysfunction and vascular damage. Disappointingly, recently reported intervention trials with statins have failed to show any benefit on cardiovascular disease in patients with advanced renal failure. SUMMARY: During recent years, our understanding of the character and biological significance of the dyslipidemia of chronic kidney disease, and its link to cardiovascular disease, has increased. However, our knowledge about its proper management is still very limited.
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| 7. |
- Berglund, Lisa, et al.
(författare)
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Nuclear factor of activated T-cells transcription factors in the vasculature: the good guys or the bad guys?
- 2008
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Ingår i: Current Opinion in Lipidology. - 1473-6535. ; 19:5, s. 483-490
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE OF REVIEW: The nuclear factor of activated T-cells (NFAT) proteins are a family of Ca/calcineurin-dependent transcription factors that were first characterized in T-lymphocytes as inducers of cytokine gene expression. Since then, NFAT proteins have been shown to play varied roles outside of the immune system, including in the cardiovascular system. Cells in the vessel wall display a diverse array of Ca signaling modalities, which are subject to change during disease. The fact that NFAT proteins are able to decode and translate these signals into changes in gene expression makes them potential regulators of vascular pathogenesis. RECENT FINDINGS: It is now clear that NFAT signaling is required for normal vascular patterning during embryogenesis and for vascular endothelial growth factor-induced angiogenesis. The overall role of NFAT signaling in the vasculature, however, is less clear during adult life. This review aims to give an update on mechanisms that regulate NFAT activation in vascular cells, with an emphasis on the role of mitochondria and of upstream activators such as lipids and glucose. It also addresses recent work implicating NFAT proteins as mediators of vascular disease. SUMMARY: A better understanding of the NFAT-signaling pathway in the vasculature may open up an unexplored area for the development of new therapeutic approaches for treating vascular disease.
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| 8. |
- Bjorkhem, I
(författare)
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Cerebrotendinous xanthomatosis
- 2013
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Ingår i: Current opinion in lipidology. - 1473-6535. ; 24:4, s. 283-287
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Tidskriftsartikel (refereegranskat)
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