Trivalent chromium alleviates oleic acid induced steatosis in SMMC-7721 cells by decreasing fatty acid uptake and triglyceride synthesis

BioMetals ◽  
2016 ◽  
Vol 29 (5) ◽  
pp. 881-892 ◽  
Author(s):  
Song Wang ◽  
Jian Wang ◽  
Xiaonan Zhang ◽  
Linlin Hu ◽  
Zhijia Fang ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Fatty Acid ◽  
Fatty Acid Uptake ◽  
Trivalent Chromium ◽  
Acid Uptake ◽  
Triglyceride Synthesis

Studies on the uptake of fatty acids by brush border membranes of the rabbit intestine

1985 ◽  
Vol 63 (4) ◽  
pp. 249-256 ◽  
Author(s):  
P. Proulx ◽  
H. Aubry ◽  
I. Brglez ◽  
D. G. Williamson
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Fatty Acid ◽  
Palmitic Acid ◽  
Bile Salt ◽  
Chain Length ◽  
Brush Border ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Egg Lecithin

Initial studies revealed that the uptake of palmitic acid and oleic acid into brush border membranes was similar when these were isolated from either whole small intestine, jejunum, or ileum. The uptake of these fatty acids was somewhat lower with membranes obtained from duodenum. Subsequent studies, all with membranes obtained from whole intestine, indicated an increase in binding with chain length of fatty acid of up to 16 carbons. Unsaturation decreased this uptake somewhat. Taurocholate and 1-palmitoyl lysolecithin had a moderate stimulatory effect on the binding of oleic acid and palmitic acid at concentrations of 10 and 0.5 mM, respectively, and inhibited at higher concentrations. Addition of 1.4 mM egg lecithin to the fatty acid – bile salt micelles, such that the lecithin – bile salt ratio was 0.2, decreased the uptake of fatty acids generally, but did not significantly affect the pattern of binding by membrane fractions isolated from different segments nor did it change the pattern of labelling when fatty acid chain length and unsaturation were varied. At lower concentrations, egg lecithin had little effect on the uptake of oleic acid, whereas dipalmitoyl phosphatidylcholine stimulated binding of both palmitic acid and oleic acid over the entire range of concentrations tested. Preincubation of the membranes with this saturated phospholipid stimulated the uptake of oleic acid, and addition of this choline lipid to the oleic acid – bile salt containing micelles did not substantially enhance fatty acid uptake in lipid-treated membranes. The binding of fatty acid was very rapid either in the presence or the absence of Ca2+, such that even in zero-time controls essentially equilibrium bindings were obtained. The presence of Ca2+ stimulated the incorporation substantially. The results as a whole indicate that fatty acid uptake into brush border membrane is very responsive to a variety of conditions which could prevail in the gut during the absorption process.

Valproate induced hepatic steatosis by enhanced fatty acid uptake and triglyceride synthesis

2017 ◽  
Vol 324 ◽  
pp. 12-25 ◽  
Author(s):  
Xupeng Bai ◽  
Weipeng Hong ◽  
Peiheng Cai ◽  
Yibei Chen ◽  
Chuncao Xu ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Hepatic Steatosis ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Triglyceride Synthesis

Z-ligustilide and n-Butylidenephthalide Isolated from the Aerial Parts of Angelica tenuissima Inhibit Lipid Accumulation In Vitro and In Vivo

Planta Medica ◽  
2019 ◽  
Vol 85 (09/10) ◽  
pp. 719-728 ◽  
Author(s):  
Wonseok Lee ◽  
Hye Ryoung Koo ◽  
You-Jin Choi ◽  
Jin Gyu Choi ◽  
Myung Sook Oh ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Fatty Acid ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Target Genes ◽  
Regulatory Element ◽  
Fatty Acid Uptake ◽  
Acid Uptake

AbstractAbnormal lipid metabolism, such as increased fatty acid uptake and esterification, is associated with nonalcoholic fatty liver disease (NAFLD). The aqueous extract of the aerial part of Angelica tenuissima Nakai (ATX) inhibited high-fat diet–induced hepatic steatosis in mice as well as oleic acid–induced neutral lipid accumulation in HepG2 cells. ATX decreased the mRNA and protein levels of CD36 and diglyceride acyltransferase 2 (DGAT2), the maturation of sterol regulatory element-binding proteins (SREBP), and the expression of the lipogenic target genes fasn and scd1. The ATX components, Z-ligustilide and n-butylidenephthalide, inhibited the expression of FATP5 and DGAT2 and thus oleic acid–induced lipid accumulation in HepG2 cells. These results suggest that ATX and its active components Z-ligustilide and n-butylidenephthalide inhibit fatty acid uptake and esterification in mice and have potential as therapeutics for NAFLD.

scholarly journals Myo-inositol alters 13C-labeled fatty acid metabolism in human placental explants

2019 ◽  
Vol 243 (1) ◽  
pp. 73-84 ◽  
Author(s):  
Oliver C Watkins ◽  
Mohammed Omedul Islam ◽  
Preben Selvam ◽  
Reshma Appukuttan Pillai ◽  
Amaury Cazenave-Gassiot ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Fatty Acid ◽  
Docosahexaenoic Acid ◽  
Palmitic Acid ◽  
Acid Metabolism ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Liquid Chromatography Mass Spectrometry ◽  
Acid Processing ◽  
Clinical Consequences

We postulate that myo-inositol, a proposed intervention for gestational diabetes, affects transplacental lipid supply to the fetus. We investigated the effect of myo-inositol on fatty acid processing in human placental explants from uncomplicated pregnancies. Explants were incubated with 13C-labeled palmitic acid, 13C-oleic acid and 13C-docosahexaenoic acid across a range of myo-inositol concentrations for 24 h and 48 h. The incorporation of labeled fatty acids into individual lipids was quantified by liquid chromatography mass spectrometry. At 24 h, myo-inositol increased the amount of 13C-palmitic acid and 13C-oleic-acid labeled lipids (median fold change relative to control = 1). Significant effects were seen with 30 µM myo-inositol (physiological) for 13C-palmitic acid-lysophosphatidylcholines (1.26) and 13C-palmitic acid-phosphatidylethanolamines (1.17). At 48 h, myo-inositol addition increased 13C-oleic-acid-lipids but decreased 13C-palmitic acid and 13C-docosahexaenoic-acid lipids. Significant effects were seen with 30 µM myo-inositol for 13C-oleic-acid-phosphatidylcholines (1.25), 13C-oleic-acid-phosphatidylethanolamines (1.37) and 13C-oleic-acid-triacylglycerols (1.32) and with 100 µM myo-inositol for 13C-docosahexaenoic-acid-triacylglycerols (0.78). Lipids labeled with the same 13C-fatty acid showed similar responses when tested at the same time point, suggesting myo-inositol alters upstream processes such as fatty acid uptake or activation. Myo-inositol supplementation may alter placental lipid physiology with unknown clinical consequences.

The transcription factor HNF-4α: a key factor of the intestinal uptake of fatty acids in mouse

2012 ◽  
Vol 302 (11) ◽  
pp. G1253-G1263 ◽  
Author(s):  
Vincent Frochot ◽  
Malik Alqub ◽  
Anne-Laure Cattin ◽  
Véronique Carrière ◽  
Anne Houllier ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Oleic Acid ◽  
Fatty Acid ◽  
Intestinal Absorption ◽  
Fatty Acid Uptake ◽  
Dietary Lipids ◽  
Fatty Acid Transport ◽  
Acid Uptake ◽  
Intestinal Uptake ◽  
Key Factor

With an excessive postprandial accumulation of intestine-derived, triglyceride-rich lipoproteins being a risk factor of cardiovascular diseases, it is essential to characterize the mechanisms controlling the intestinal absorption of dietary lipids. Our aim was to investigate the role of the transcription factor hepatocyte nuclear factor (HNF)-4α in this process. We used transgenic mice with a specific and inducible intestinal knockout of Hnf-4α gene. One hour after a lipid bolus, in the presence of the lipase inhibitor tyloxapol, lower amounts of triglycerides were found in both plasma and intestinal epithelium of the intestine-specific Hnf-4α knockout (Hnf-4αintΔ) mice compared with the Hnf-4αloxP/loxP control mice. These discrepancies were due to a net decrease of the intestinal uptake of fatty acid in Hnf-4αintΔ mice compared with Hnf-4αloxP/loxP mice, as assessed by the amount of radioactivity that was recovered in intestine and plasma after gavage with labeled triolein or oleic acid, or in intestinal epithelial cells isolated from jejunum after a supply of labeled oleic acid-containing micelles. This decreased fatty acid uptake was associated with significant lower levels of the fatty acid transport protein-4 mRNA and protein along the intestinal tract and with a lower acyl-CoA synthetase activity in Hnf-4αintΔ mice compared with the control mice. We conclude that the transcription factor HNF-4α is a key factor of the intestinal absorption of dietary lipids, which controls this process as early as in the initial step of fatty acid uptake by enterocytes.

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