Abstract | BACKGROUND: METHODS: Mice were fed a control diet, or diets containing 0.3 %, 0.6 %, or 0.9 % (w/w) TTP for 14 days. Blood and liver samples were collected, enzyme activities and gene expression were analyzed in liver, lipid and fatty acid composition in liver and plasma, one- carbon metabolites, B-vitamin status, carnitine and acylcarnitines were analyzed in plasma. RESULTS: Liver mitochondrial fatty acid oxidation decreased by 40 % and steatosis was induced in a dose dependent manner; total lipids increased 1.6-fold in animals treated with 0.3 % TTP, 2-fold with 0.6 % TTP and 2.1 fold with 0.9 % TTP compared to control. The higher hepatic concentration of fatty acids was associated with shortening of carbon-length. Furthermore, the inhibited fatty acid oxidation led to a 30-fold decrease in plasma carnitine and 9.3-fold decrease in acetylcarnitine at the highest dose of TTP, whereas an accumulation of palmitoylcarnitine resulted. Compared to the control diet, TTP administration was associated with elevated plasma total Hcy (control: 7.2 ± 0.3 umol/L, 0.9 % TTP: 30.5 ± 5.9 umol/L) and 1.4-1.6 fold increase in the one- carbon metabolites betaine, dimethylglycine, sarcosine and glycine, accompanied by changes in gene expression of the different B-vitamin dependent pathways of Hcy and choline metabolism. A positive correlation between total Hcy and hepatic triacylglycerol resulted. CONCLUSIONS:
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Authors | Rolf K Berge, Bodil Bjørndal, Elin Strand, Pavol Bohov, Carine Lindquist, Jan Erik Nordrehaug, Asbjørn Svardal, Jon Skorve, Ottar Nygård |
Journal | Lipids in health and disease
(Lipids Health Dis)
Vol. 15
Pg. 24
(Feb 05 2016)
ISSN: 1476-511X [Electronic] England |
PMID | 26846427
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Propionates
- Sulfides
- Homocysteine
- 1-(carboxyethylthio)tetradecane
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Topics |
- Animals
- Fatty Liver
(chemically induced, metabolism)
- Homocysteine
(blood)
- Liver
(drug effects, metabolism)
- Male
- Mice
- Mitochondria
(drug effects, metabolism)
- Non-alcoholic Fatty Liver Disease
(chemically induced, metabolism)
- Propionates
(pharmacology)
- Sulfides
(pharmacology)
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