ATVB In Focus Metabolic Syndrome and Atherosclerosis

By Martin Adiels, S. Olofsson, Marja-Riitta Taskinen, Jan Boren. 2008

833 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/2d596faa33b48ec57836e671e94af8ee14cb2a14

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Citations in the corpus

Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel (2020, background): “The rate of VLDL production is also influenced by metabolic factors, such as insulin resistance, and lipolysis and clearance of VLDL are markedly affected by apoC-III and angiopoietin-like 3 (ANGPTL3) content and lipase activities.(91,94) The LDL subclass profile is principally determined by the nat”
2016 ESC/EAS Guidelines for the Management of Dyslipidaemias. (2016, background): “The increase in large VLDL particles in T2DM initiates a sequence of events that generates atherogenic remnants, small dense LDL and small TG-rich dense HDL particles.(349) These components are not isolated abnormalities but are closely linked to each other.”
Sugar consumption, metabolic disease and obesity: The state of the controversy (2015, unknown): “Increased levels of intra-hepatic lipid content promote very low density lipoprotein 1 (VLDL1) production and secretion (37), which leads to increased levels of postprandial TG and dyslipidemia (38).”
ESC/EAS Guidelines for the management of dyslipidaemias: the Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS). (2011, background): “The increase in large VLDL particles in type 2 diabetes initiates a sequence of events that generates atherogenic remnants, small dense LDL and small dense HDL particles.(171) These components are not isolated abnormalities but are metabolically closely linked to each other.”
Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. (2009, background): “While we propose that increased VLDL synthesis/secretion is the main contributor (31), the significantly different postprandial postheparin LPL responses between the 2 treatment groups suggest that reduced TG clearance might also contribute to fructose-induced postprandial hypertriglyceridemia.”
Triglyceride-rich lipoproteins and their remnants: metabolic insights, role in atherosclerotic cardiovascular disease, and emerging therapeutic strategies—a consensus statement from the European Atherosclerosis Society (2021, background): “53,54 VLDL assembly and secretion are upregulated by (i) the delivery of FA released from insulin-resistant adipocytes, (ii) the increased delivery of remnant TG–FA to the liver due to reduced peripheral lipolysis of chylomicron and VLDL–TG, and (iii) the increased de novo lipogenesis 55 ( Figure 4…”