Journal
DISEASE MODELS & MECHANISMS
Volume 7, Issue 7, Pages 915-927Publisher
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/dmm.015800
Keywords
Dyslipidemia; Lipoprotein; Yolk syncytial layer; Yolk sac; Placenta; Lecithotrophic
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Funding
- Instituto Nacional de Ciencia e Tecnologia [FAPEMIG: CBB-APQ-00075-09, CNPq 573646/2008-2]
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES) fellowship grant
- National Institutes of Health [F31DK079421, T32GM007231, R01DK093399]
- National Institutes of Health's Zebrafish Functional Genomics Consortium [R01GM63904]
- Carnegie Institution for Science endowment
- G. Harold and Leila Y. Mathers Charitable Foundation
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Dyslipidemias are a major cause of morbidity and mortality in the world, particularly in developed nations. Investigating lipid and lipoprotein metabolism in experimentally tractable animal models is a crucial step towards understanding and treating human dyslipidemias. The zebrafish, a well-established embryological model, is emerging as a notable system for studies of lipid metabolism. Here, we describe the value of the lecithotrophic, or yolk-metabolizing, stages of the zebrafish as a model for studying lipid metabolism and lipoprotein transport. We demonstrate methods to assay yolk lipid metabolism in embryonic and larval zebrafish. Injection of labeled fatty acids into the zebrafish yolk promotes efficient uptake into the circulation and rapid metabolism. Using a genetic model for abetalipoproteinemia, we show that the uptake of labeled fatty acids into the circulation is dependent on lipoprotein production. Furthermore, we examine the metabolic fate of exogenously delivered fatty acids by assaying their incorporation into complex lipids. Moreover, we demonstrate that this technique is amenable to genetic and pharmacologic studies.
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