Decoding the role of angiopoietin-like protein 4/8 complex–mediated plasmin generation in the regulation of LPL activity

Chen, Yan Q.; Zhen, Eugene Y.; Russell, Anna M.; Ehsani, Mariam; Siegel, Robert W.; Qian, Yuewei; Konrad, Robert J.

doi:10.1016/j.jlr.2023.100441

Cited by 6 publications

(1 citation statement)

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“…ApoB (48 or 100) is not transported between TRL and HDL particles, whereas apoCI, apoCII, apoCIII, and apoE are, depending on the nutritional or metabolic state. LPL activity is increased by apoCII and apoAV while decreased by apoCI, apoCIII, and apoE ( 83 ). The rate-limiting element in lipolysis, which is mediated by LPL, appears to be apoCII.…”

Section: Chylomicron Intravascular Catabolismmentioning

confidence: 99%

The chylomicron saga: time to focus on postprandial metabolism

Gugliucci

2024

Front. Endocrinol.

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Since statins have had such tremendous therapeutic success over the last three decades, the field of atherosclerosis has become somewhat LDL-centric, dismissing the relevance of triglycerides (TG), particularly chylomicrons, in atherogenesis. Nonetheless, 50% of patients who take statins are at risk of developing atherosclerotic cardiovascular disease (ASCVD) and are unable to achieve their goal LDL-C levels. This residual risk is mediated, in part by triglyceride rich lipoproteins (TRL) and their remnants. Following his seminal investigation on the subject, Zilversmit proposed that atherosclerosis is a postprandial event in 1979 (1–4). In essence, the concept suggests that remnant cholesterol-rich chylomicron (CM) and very-low density lipoprotein (VLDL) particles play a role in atherogenesis. Given the foregoing, this narrative review addresses the most recent improvements in our understanding of postprandial dyslipidemia. The primary metabolic pathways of chylomicrons are discussed, emphasizing the critical physiological role of lipoprotein lipase and apoCIII, the importance of these particles’ fluxes in the postprandial period, their catabolic rate, the complexities of testing postprandial metabolism, and the role of angiopoietin-like proteins in the partition of CM during the fed cycle. The narrative is rounded out by the dysregulation of postprandial lipid metabolism in insulin resistance states and consequent CVD risk, the clinical evaluation of postprandial dyslipidemia, current research limits, and potential future study directions.

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Section: Chylomicron Intravascular Catabolismmentioning

confidence: 99%