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Lipoproteins for Biomedical Applications: Medical Imaging and Drug Delivery
Published in Vladimir Torchilin, Handbook of Materials for Nanomedicine, 2020
Pratap C. Naha, Stephen E. Henrich, David P. Cormode, C. Shad Thaxton
VLDL is synthesized via a two-step process in the hepatocytes of the liver. First, microsomal triglyceride transfer protein (MTP) transfers lipids to apolipoprotein B (apoB) during its translation. Next, fusion occurs between apoB-containing precursor particles and triglyceride droplets to form mature VLDL [51]. The main role of VLDL is in the transport of endogenous lipids. VLDL is converted to intermediate density lipoprotein (IDL) after interactions with lipoprotein lipase, and then to LDL [52]. The LDLr is expressed in many tissues and causes LDL internalization via receptor mediated endocytosis. The internalized LDL degrades in lysosomes releasing cholesterol to the cell [53].
Physical activity and lipidomics in a population at high risk of type 2 diabetes mellitus
Published in Journal of Sports Sciences, 2020
Joseph Henson, Charlotte L. Edwardson, Melanie J. Davies, Jason M.R. Gill, Liam M. Heaney, Kamlesh Khunti, Leong Ng, Naveed Sattar, Francesco Zaccardi, Thomas Yates
Our findings also extend previous findings by showing that low levels of physical activity (<500 cpm), indicative of sedentary behaviour, are detrimentally associated with HDL concentrations (Healy et al., 2011; Henson et al., 2013). Interestingly, the time spent below 500 cpm was also detrimentally associated with Apo-A1 and the concentration of very large, large, medium and small VLDL particles. VLDLs are substrates for lipoprotein lipase (LPL)-mediated triglyceride removal, with larger VLDL particles carrying more triglycerides than smaller particles and correlating with insulin resistance (Garvey et al., 2003). Although the precise mechanism of sedentary behaviour and (in)activity-induced lipid changes is unclear, muscle LPL regulation is thought to be one of the most sensitive metabolic responses to sedentary behaviour and low‐intensity contractile activity and may explain why even small amounts of physical activity appear to confer cardiovascular benefits (Bey & Hamilton, 2003). The mechanistic relevance of LPL to sedentary behaviour has been demonstrated in animal models (Hamilton et al., 2007) whereas in humans moderate intensity activity was shown to increase the affinity of large VLDL particles for LPL clearance (Ghafouri et al., 2015). However, further insight is needed into the precise impact of increased sedentary time and reduced physical activity on LPL activity.