Apolipoprotein A5, a unique modulator of fasting and postprandial triglycerides

May-Zhang, Linda S.; Liu, Min; Black, Dennis D.; Tso, Patrick

doi:10.1016/j.bbalip.2022.159185

Cited by 5 publications

(10 citation statements)

References 77 publications

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“…Since its discovery, ApoAV has been called “a potent TG reducer” and has been characterized as having a “low concentration, high impact” ( Figure 8 ). It seems that apoAV is expressed mostly in the liver [ 88 , 89 ]. The circulating, mature version of the protein is extremely hydrophobic, highly helical, and is largely bound to HDL and to a lesser extent to VLDL in rats.…”

Section: Apo Av a Unique Modulator Of Fasting And Postprandial Tgs: T...mentioning

confidence: 99%

“…The circulating, mature version of the protein is extremely hydrophobic, highly helical, and is largely bound to HDL and to a lesser extent to VLDL in rats. In human plasma, apoAV is found to be associated with HDL, VLDL, and chylomicrons, but not LDL ( Figure 8 ) Heparin, heparin sulfate proteoglycans (HSPGs), and glycosylphosphatidylinositol high-density lipoprotein binding protein 1 (GPIHBP1) are all engaged by a group of positively charged amino acids found in apoAV [ 89 ]. Its plasma concentration in humans is extremely small when compared to other apolipoproteins, ranging from 20 to 500 ng/mL, which, when calculated on a molar basis, is around 1000 times lower than apoB100 and 10,000 times lower than apoA1 [ 89 ].…”

Section: Apo Av a Unique Modulator Of Fasting And Postprandial Tgs: T...mentioning

confidence: 99%

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Triglyceride-Rich Lipoprotein Metabolism: Key Regulators of Their Flux

Gugliucci

2023

JCM

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The residual risk for arteriosclerotic cardiovascular disease after optimal statin treatment may amount to 50% and is the consequence of both immunological and lipid disturbances. Regarding the lipid disturbances, the role of triglyceride-rich lipoproteins (TRLs) and their remnants has come to the forefront in the past decade. Triglycerides (TGs) stand as markers of the remnants of the catabolism of TRLs that tend to contain twice as much cholesterol as compared to LDL. The accumulation of circulating TRLs and their partially lipolyzed derivatives, known as “remnants”, is caused mainly by ineffective triglyceride catabolism. These cholesterol-enriched remnant particles are hypothesized to contribute to atherogenesis. The aim of the present narrative review is to briefly summarize the main pathways of TRL metabolism, bringing to the forefront the newly discovered role of apolipoproteins, the key physiological function of lipoprotein lipase and its main regulators, the importance of the fluxes of these particles in the post-prandial period, their catabolic rates and the role of apo CIII and angiopoietin-like proteins in the partition of TRLs during the fast-fed cycle. Finally, we provide a succinct summary of the new and old therapeutic armamentarium and the outcomes of key current trials with a final outlook on the different methodological approaches to measuring TRL remnants, still in search of the gold standard.

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Section: Apo Av a Unique Modulator Of Fasting And Postprandial Tgs: T...mentioning

confidence: 99%

Section: Apo Av a Unique Modulator Of Fasting And Postprandial Tgs: T...mentioning

confidence: 99%

Triglyceride-Rich Lipoprotein Metabolism: Key Regulators of Their Flux

Gugliucci

2023

JCM

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“…A remarkable trait of apoAV is its ability to escape luminal proteolysis and be taken up intact by enterocytes. Numerous studies support the notion that apoAV contributes significantly to the enhancement of plasma lipoprotein clearance via enhancement of TRL lipolysis and enhancement of liver absorption of remnant particles ( 100 ). Will it develop into a drug target?…”

Section: Chylomicron Intravascular Catabolismmentioning

confidence: 89%

“…The liver is the primary site of synthesis for the unique lipid-modulating protein known as apoAV, which also affects the gut, blood flow, liver, and adipose tissue ( 74 , 100 , 101 ). The apolipoprotein gene cluster APOA1/C3/A4 on human chromosome 11q23 is known to influence lipid metabolism.…”

Section: Chylomicron Intravascular Catabolismmentioning

confidence: 99%

“…ApoAV has been referred to as “a potent TG reducer” and has been described as having a “low concentration, high impact” since its discovery. When measured on a molar basis, it has a plasma concentration in humans that is incredibly low relative to other apolipoproteins, ranging from 20 to 500 ng/ml, which is roughly 1,000 times lower than apoB and 10,000 times lower than apoAI ( 74 , 100 ).…”

Section: Chylomicron Intravascular Catabolismmentioning

confidence: 99%

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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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