Browsing by Subject "Triglyceride"

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    Docosahexaenoic acid supplementation during pregnancy as phospholipids or triglycerides produces different placental uptake but similar fetal brain accretion in neonatal piglets
    (CAMBRIDGE UNIVERSITY PRESS, 2017-11-23) Gázquez, Antonio; Ruíz-Palacios, María; Larqué Daza, Elvira; Fisiología
    The great variety of n-3 long chain polyunsaturated fatty acid sources raises the question of the most adequate for using as a docosahexaenoic acid (DHA) supplement during pregnancy. Placental and fetal availability of different DHA sources remains unclear. We investigated DHA availability in maternal lipoproteins, placenta and fetal tissues in pregnant sows fed DHA as phospholipid (PL) or triglyceride (TG) to identify the best DHA source during this period. Pregnant Iberian sows were fed with diets containing 0.8% DHA of total fatty acids as PL from egg yolk or TG from algae oil during the last third of gestation (40 days). Maternal tissues, placentas and fetal tissues were obtained at delivery and DHA quantified by gas-chromatography. MFSD2a carrier expression was analysed in both placenta and fetal brain by western blotting. Sows fed DHA-PL diet showed higher DHA incorporation in plasma LDL but not in plasma total lipids. No differences were found in DHA content between groups in maternal liver, adipose tissue or brain. Placental tissue incorporated more DHA in both total lipids and PL fraction in sows fed DHA-PL. However, this did not lead to an enhanced DHA accretion either in fetal plasma, fetal liver or fetal brain. MFSD2a expression was similar between both experimental groups. Maternal DHA supplementation during pregnancy in sow either as PL or TG produces similar DHA accretion in fetal tissues but not in placenta. Both fat sources are equally available for fetal brain.
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    Vitamin B12 Induces Hepatic Fatty Infiltration through Altered Fatty Acid Metabolism
    (Cell Physiol Biochem Press GmbH&Co. KG, Duesseldorf, ) Boachie, J.; Adaikalakoteswari, A.; Gazquez Garcia, A.; Zammit, V.; Larque Daza, E.; Saravanan, P.; Fisiología
    Background/Aims: Rise in global incidence of obesity impacts metabolic health. Evidence from human and animal models show association of vitamin B12 (B12) deficiency with elevated BMI and lipids. Human adipocytes demonstrated dysregulation of lipogenesis by low B12 viahypomethylation and altered microRNAs. It is known de novo hepatic lipogenesis plays a key role towards dyslipidaemia, however, whether low B12 affects hepatic metabolism of lipids is not explored. Methods: HepG2 was cultured in B12-deficient EMEM medium and seeded in different B12 media: 500nM(control), 1000pM(1nM), 100pM and 25pM(low) B12. Lipid droplets were examined by Oil Red O (ORO) staining using microscopy and then quantified by elution assay. Gene expression were assessed with real-time quantitative polymerase chain reaction (qRT-PCR) and intracellular triglycerides were quantified using commercial kit (Abcam, UK) and radiochemical assay. Fatty acid composition was measured by gas chromatography and mitochondrial function by seahorse XF24 flux assay. Results: HepG2 cells in low B12 had more lipid droplets that were intensely stained with ORO compared with control. The total intracellular triglyceride and incorporation of radio-labelled-fatty acid in triglyceride synthesis were increased. Expression of genes regulating fatty acid, triglyceride and cholesterol biosynthesis were upregulated. Absolute concentrations of total fatty acids, saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), trans-fatty acids and individual even-chain and oddchain fatty acids were significantly increased. Also, low B12 impaired fatty acid oxidation and mitochondrial functional integrity in HepG2 compared with control. Conclusion: Our data provide novel evidence that low B12 increases fatty acid synthesis and levels of individual fatty acids, and decreases fatty acid oxidation and mitochondrial respiration, thus resulting in dysregulation of lipid metabolism in HepG2. This highlights the potential significance of de novo lipogenesis and warrants possible epigenetic mechanisms of low B12.