Postprandial lipoprotein metabolism: VLDL vs chylomicrons

Nakajima, Katsuyuki; Nakano, Takamitsu; Tokita, Yoshiharu; Nagamine, Takahiko; Inazu, Akihiro; Kobayashi, Junji; Mabuchi, Hiroshi; Stanhope, Kimber L.; Havel, Peter J.; Okazaki, Mitsuyo; Ai, Masumi; Tanaka, Akira

doi:10.1016/j.cca.2011.04.018

Cited by 133 publications

(121 citation statements)

References 110 publications

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“…VLDLsized TG fractions may contain CM remnant, VLDL remnant, and VLDL. In humans, it has been reported that approximately 80% (or more) of the remnants observed in the postprandial state constitute VLDL-remnant (apoB-100 particles) ( 35 ). However, because rodents produce apoB48-containing lipoproteins in the liver, it was diffi cult to distinguish their origin by the size of apoB.…”

Section: Discussionmentioning

confidence: 99%

The ddY mouse: a model of postprandial hypertriglyceridemia in response to dietary fat

Yamazaki

Kishimoto

Ezaki

2012

Journal of Lipid Research

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This article is available online at http://www.jlr.org TG levels ( 10 ); however, a difference in fasting TG level only partially accounts for the interindividual variation in the magnitude of postprandial lipemia. Indeed, it is known that the postprandial TG response is infl uenced by genetic background, dietary composition, physical activity, age, gender, and obesity ( 11-13 ).To examine the factors that affect postprandial hypertriglyceridemia and their mechanisms and effects on arteries in vivo, a mouse model of hypertriglyceridemia in response to dietary fat is required ( 14 ). However, no rodent models of postprandial hypertriglyceridemia have been reported. This is possibly due to the lack of cholesteryl ester transfer protein (CETP) in rodents, a hypothesis supported by the fi nding that CETP transgenic mice have increased postprandial hypertriglyceridemia ( 15 ) and that CETP defi ciency in humans results in signifi cantly reduced fasting and postprandial hypertriglyceridemia with an increase in HDL cholesterol ( 16 ). In humans, postprandial lipemia has been evaluated after induction by an oral fatload or a high-fat (HF) diet ( 17 ). During our studies of dietary effects on fatty liver and obesity, we found that the blood TG concentration in response to changes in dietary fat differed markedly between ddY and C57BL/6J mice. When a single HF diet was given to 24 h-fasted ddY and C57BL/6J mice, ddY mice showed a 3-fold increase in blood TG concentration after 3 h feeding either a saffl ower oil-rich or a butter-rich diet ( 18, 19 ), whereas there was no signifi cant increase in TG concentration in C57BL/6J mice ( 20 ).In this study, we compared TG responses after oral ingestion of fat in several strains of mice. ddY mice displayed marked postprandial hypertriglyceridemia in response to dietary fat, representing a suitable animal model of postprandial hyperlipidemia.Abstract Postprandial hyperlipidemia (lipemia) is a risk factor for atherosclerosis. However, mouse models of postprandial hyperlipidemia have not been reported. Here, we report that ddY mice display marked postprandial hypertriglyceridemia in response to dietary fat. In ddY mice, the fasting serum total triacylglyceride (TG) concentration was 134 mg/dl, which increased to 571 mg/dl after an intragastric saffl ower oil load (0.4 ml/mouse). In C57BL/6J mice, these concentrations were 57 and 106 mg/dl, respectively. By lipoprotein analysis, ddY mice showed increases in chylomicron-and VLDL-sized TG fractions (remnants and VLDL) after fat load. In C57BL/6J mice, post-heparin plasma LPL activity after fat load was increased 4.8-fold relative to fasting. However, in ddY mice, the increase of LPL activity after fat load was very small (1.2-fold) and not signifi cant. High fat feeding for 10 weeks led to obesity in ddY mice. A difference in LPL amino acid composition between C57BL/6J and ddY mice was detected but was deemed unlikely to cause hypertriglyceridemia because hypertriglyceridemia was not evident in other strains harboring the ddY-type LPL ...

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Section: Discussionmentioning

confidence: 99%

The ddY mouse: a model of postprandial hypertriglyceridemia in response to dietary fat

Yamazaki

Kishimoto

Ezaki

2012

Journal of Lipid Research

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“…triglyceride levels as an independent cardiovascular risk factor (12)(13)(14). The goal of this study was to unravel the mechanism by which plant sterols and plant stanols lower plasma triglyceride concentrations in high-fat diet (HFD) fed wild-type mice by evaluating changes in processes that result in triglyceride appearance in the circulation.…”

Section: Methodsmentioning

confidence: 99%

Serum TG-lowering properties of plant sterols and stanols are associated with decreased hepatic VLDL secretion

Schonewille

Brufau

Shiri-Sverdlov

et al. 2014

Journal of Lipid Research

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“…Western individuals remain in a postprandial state for most of the day (7). Consequently, repeated acute dietary stressors induced by a high-fat meal (HFM) could trigger a large increase of most risk factors for cardiovascular diseases related to obesity, such as increased circulating cholesterol, TG, and glucose (8).…”

Section: Introductionmentioning

confidence: 99%

Orange juice with a high-fat meal prolongs postprandial lipemia in apparently healthy overweight/obese women

Coelho

Hermsdorff

Gomide

et al. 2017

Arch. Endocrinol. Metab.

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Objective: We investigated the postprandial response of lipid markers to a high-fat meal (HFM) with two different beverages in apparently healthy normal-weight and overweight/obese women. Subjects and methods: This crossover, randomized study enrolled 36 women, of whom 21 had normal weight (body mass index [BMI] 22 ± 1.8 kg/m 2 ) and 15 had overweight/obesity (BMI 31 ± 3.7 kg/m 2 ). In two different test days, the participants ingested a HFM (37% of energy as saturated fat) with 500 mL of water (HFM-W) or 500 mL of orange juice (HFM-OJ). Blood samples were collected at baseline (12-hour fasting), and at 2, 3, and 5 hours postprandial. The analysis included fasting and postprandial total cholesterol, HDL-c, LDL-c, triglycerides (TG), uric acid, and complement C3. Brazilian Clinical Trials Registry (ReBEC); Primary Identification Number: RBR-2h3wjn (www. ensaiosclinicos.gov.br). Results: TG levels increased at 3 hours with HFM-OJ in normal-weight women (p = 0.01) and returned to normal levels at 5h. TG increased at 3 hours with HFM-W (p = 0.01) and HFM-OJ (p = 0.02), and remained high at 5 hours (p = 0.03) in overweight/obese women. Complement C3 remained unchanged, but showed different responses between meals (p = 0.01 for positive incremental area under the curve [piAUC] HFM-OJ vs. HFM-W, respectively). Conclusions: In apparently healthy overweight/obese women compared with normal-weight ones, the concomitant intake of orange juice with a HFM prolonged postprandial lipemia but had no effect on postprandial complement C3 concentrations.

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Postprandial lipoprotein metabolism: VLDL vs chylomicrons

Cited by 133 publications

References 110 publications

The ddY mouse: a model of postprandial hypertriglyceridemia in response to dietary fat

The ddY mouse: a model of postprandial hypertriglyceridemia in response to dietary fat

Serum TG-lowering properties of plant sterols and stanols are associated with decreased hepatic VLDL secretion

Orange juice with a high-fat meal prolongs postprandial lipemia in apparently healthy overweight/obese women

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