Dietary cholesterol and apolipoprotein A-I are trafficked in endosomes and lysosomes in the live zebrafish intestine

Otis, Jessica P.; Shen, Meifen; Caldwell, Blake A.; Gaido, Oscar E. Reyes; Farber, Steven A.

doi:10.1152/ajpgi.00080.2018

Cited by 11 publications

(10 citation statements)

References 58 publications

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“…Zebrafish and mammals share considerable overlap in major organs and in key nodes of metabolic control such as insulin signalling and appetite regulation 1–3 . Transgenic zebrafish with tissue-specific fluorescence have been implemented in studies of pancreatic β-cell regeneration 4 , dietary cholesterol trafficking 5 , gluconeogenesis 6 , and iron metabolism 7 , while recent advances in targeted mutagenesis have contributed to the rise in zebrafish models of metabolic disorders 8–11 .…”

Section: Introductionmentioning

confidence: 99%

Parallel Reaction Monitoring reveals structure-specific ceramide alterations in the zebrafish

Zhang

Trauger

Vidoudez

et al. 2019

Sci Rep

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Extensive characterisations of the zebrafish genome and proteome have established a foundation for the use of the zebrafish as a model organism; however, characterisation of the zebrafish lipidome has not been as comprehensive. In an effort to expand current knowledge of the zebrafish sphingolipidome, a Parallel Reaction Monitoring (PRM)-based liquid chromatography-mass spectrometry (LC-MS) method was developed to comprehensively quantify zebrafish ceramides. Comparison between zebrafish and a human cell line demonstrated remarkable overlap in ceramide composition, but also revealed a surprising lack of most sphingadiene-containing ceramides in the zebrafish. PRM analysis of zebrafish embryogenesis identified developmental stage-specific ceramide changes based on long chain base (LCB) length. A CRISPR-Cas9-generated zebrafish model of Farber disease exhibited reduced size, early mortality, and severe ceramide accumulation where the amplitude of ceramide change depended on both acyl chain and LCB lengths. Our method adds an additional level of detail to current understanding of the zebrafish lipidome, and could aid in the elucidation of structure-function associations in the context of lipid-related diseases.

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Section: Introductionmentioning

confidence: 99%

Parallel Reaction Monitoring reveals structure-specific ceramide alterations in the zebrafish

Zhang

Trauger

Vidoudez

et al. 2019

Sci Rep

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“…Gene expression of apoab, but not apoa1a, was significantly induced by BDE-47, a response attenuated in co-exposure with high PS. The apolipoprotein genes apoa1a and apoba are comparatively well-characterized in early zebrafish development ( Otis and Farber, 2016 ; Otis et al, 2019 ; Thierer et al, 2019 ; Templehof et al, 2021 ) and have been shown to be responsive to feeding status ( Cruz-Garcia and Schlegel, 2014 ) and contaminants including BPA and PFOS as well as their replacement compounds BPS and F-53B ( Sant et al, 2017 ; Wang W et al, 2018 ; Shi et al, 2019 ; Martínez et al, 2020 ). Gene expression of apoba is, similarly to apoa1a ( Babin et al, 1997 ) , strongly induced in the yolk syncytial layer at 2 dpf ( Thierer et al, 2019 ; Templehof et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Metabolic Consequences of Developmental Exposure to Polystyrene Nanoplastics, the Flame Retardant BDE-47 and Their Combination in Zebrafish

et al. 2022

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Single-use plastic production is higher now than ever before. Much of this plastic is released into aquatic environments, where it is eventually weathered into smaller nanoscale plastics. In addition to potential direct biological effects, nanoplastics may also modulate the biological effects of hydrophobic persistent organic legacy contaminants (POPs) that absorb to their surfaces. In this study, we test the hypothesis that developmental exposure (0–7 dpf) of zebrafish to the emerging contaminant polystyrene (PS) nanoplastics (⌀100 nm; 2.5 or 25 ppb), or to environmental levels of the legacy contaminant and flame retardant 2,2′,4,4′-Tetrabromodiphenyl ether (BDE-47; 10 ppt), disrupt organismal energy metabolism. We also test the hypothesis that co-exposure leads to increased metabolic disruption. The uptake of nanoplastics in developing zebrafish was validated using fluorescence microscopy. To address metabolic consequences at the organismal and molecular level, metabolic phenotyping assays and metabolic gene expression analysis were used. Both PS and BDE-47 affected organismal metabolism alone and in combination. Individually, PS and BDE-47 exposure increased feeding and oxygen consumption rates. PS exposure also elicited complex effects on locomotor behaviour with increased long-distance and decreased short-distance movements. Co-exposure of PS and BDE-47 significantly increased feeding and oxygen consumption rates compared to control and individual compounds alone, suggesting additive or synergistic effects on energy balance, which was further supported by reduced neutral lipid reserves. Conversely, molecular gene expression data pointed to a negative interaction, as co-exposure of high PS generally abolished the induction of gene expression in response to BDE-47. Our results demonstrate that co-exposure to emerging nanoplastic contaminants and legacy contaminants results in cumulative metabolic disruption in early development in a fish model relevant to eco- and human toxicology.

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“…This is a limitation of the FPLC method we have used for the sample preparation. For the fasted experiment, we assumed that the main source of apoA-I was the liver but we cannot exclude an intestinal production as suggested in animal models 14,15 . Then, we can only estimate the production related to the meal stimulation.…”

Section: Discussionmentioning

confidence: 99%

Effect of fasting and feeding on apolipoprotein A-I kinetics in preβ1-HDL, α-HDL, and triglyceride-rich lipoproteins

Chétiveaux¹,

Croyal²,

Ouguerram³

et al. 2020

Sci Rep

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The aim of this study was to compare the kinetics of apolipoprotein (apo)A-I during fed and fasted states in humans, and to determine to what extent the intestine contributes to apoA-I production. A stable isotope study was conducted to determine the kinetics of apoA-I in preβ1 high-density lipoprotein (HDL) and α-HDL. Six healthy male subjects received a constant intravenous infusion of 2H3-leucine for 14 h. Subjects in the fed group also received small hourly meals. Blood samples were collected hourly during tracer infusion and then daily for 4 days. Tracer enrichments were measured by mass spectrometry and then fitted to a compartmental model using asymptotic plateau of very-low-density lipoprotein (VLDL) apoB100 and triglyceride-rich lipoprotein (TRL) apoB48 as estimates of hepatic and intestinal precursor pools, respectively. The clearance rate of preβ1-HDL-apoA-I was lower in fed individuals compared with fasted subjects (p < 0.05). No other differences in apoA-I production or clearance rates were observed between the groups. No significant correlation was observed between plasma apoC-III concentrations and apoA-I kinetic data. In contrast, HDL-apoC-III was inversely correlated with the conversion of α-HDL to preβ1-HDL. Total apoA-I synthesis was not significantly increased in fed subjects. Hepatic production was not significantly different between the fed group (17.17 ± 2.75 mg/kg/day) and the fasted group (18.67 ± 1.69 mg/kg/day). Increase in intestinal apoA-I secretion in fed subjects was 2.20 ± 0.61 mg/kg/day. The HDL-apoA-I kinetics were similar in the fasted and fed groups, with 13% of the total apoA-I originating from the intestine with feeding.

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Dietary cholesterol and apolipoprotein A-I are trafficked in endosomes and lysosomes in the live zebrafish intestine

Cited by 11 publications

References 58 publications

Parallel Reaction Monitoring reveals structure-specific ceramide alterations in the zebrafish

Parallel Reaction Monitoring reveals structure-specific ceramide alterations in the zebrafish

Metabolic Consequences of Developmental Exposure to Polystyrene Nanoplastics, the Flame Retardant BDE-47 and Their Combination in Zebrafish

Effect of fasting and feeding on apolipoprotein A-I kinetics in preβ1-HDL, α-HDL, and triglyceride-rich lipoproteins

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