Mechanisms for competitively reducing ruminal methanogenesis

1999 ◽  
Vol 50 (8) ◽  
pp. 1299 ◽  
Author(s):  
R. S. Hegarty
Keyword(s):  
Fatty Acids ◽  
Methane Production ◽  
Hydrogen Gas ◽  
Dietary Fatty Acids ◽  
Long Chain Fatty Acids ◽  
End Use ◽  
Long Chain ◽  
Chain Fatty Acids ◽  
Reducing Equivalents

Methane production is the principal end use of hydrogen gas derived by phosphoroclastic reactions or the release of protons from reducing equivalents by hydrogenases in the rumen. It should therefore be possible to reduce methanogenesis by (1) inhibiting H2 liberating reactions, (2) promoting alternative reactions which accept H+ during reoxidation of reducing equivalents, and (3) promoting alternative H2-using reactions. Strategies to reduce methanogenesis by these means are discussed. Particular attention is given to increasing synthesis of propionate and long chain fatty acids in the rumen, to acetogenesis, and to the actions of chemicals such as monensin and dietary fatty acids.

scholarly journals Waste lipids to energy: how to optimize methane production from long-chain fatty acids (LCFA)

2009 ◽  
Vol 2 (5) ◽  
pp. 538-550 ◽  
Author(s):  
M. Madalena Alves ◽  
M. Alcina Pereira ◽  
Diana Z. Sousa ◽  
Ana J. Cavaleiro ◽  
Merijn Picavet ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Methane Production ◽  
Long Chain Fatty Acids ◽  
Long Chain ◽  
Chain Fatty Acids

Inhibitory effects of long-chain fatty acids on VFA degradation and β-oxidation

2003 ◽  
Vol 47 (10) ◽  
pp. 139-146 ◽  
Author(s):  
H.-S. Shin ◽  
S.-H. Kim ◽  
C.-Y. Lee ◽  
S.-Y. Nam
Keyword(s):  
Fatty Acids ◽  
Methane Production ◽  
Substrate Inhibition ◽  
Long Chain Fatty Acids ◽  
Inhibitory Effects ◽  
Inhibition Model ◽  
Propionate Degradation ◽  
Acetate Degradation ◽  
Long Chain ◽  
Chain Fatty Acids

The inhibitory effects of major long-chain fatty acids (LCFA), which have 16 or 18 carbons, not only on acetate degradation, but also on propionate degradation and β-oxidation were examined in anaerobic serum bottle tests at 35°C with the acclimated granular sludges. A modified Gompertz equation described cumulative methane production to assess the rates of VFA degradation and β-oxidation, which were applied to a simplified noncompetitive model and a simplified substrate inhibition model, respectively. The specific methane production rates on acetate decreased as LCFA concentration increased, which was in good agreement with the noncompetitive inhibition model. Unsaturated oleate (C18:1) and linoleate (C18:2) were more inhibitory than saturated stearate (C18:0) and palmitate (C16:0) on acetate degradation. LCFA inhibition on propionate degradation was similar to that for acetate; however, propionate degradation was less inhibited than acetate degradation. β-oxidation was the rate-limiting step in LCFA degradation in most cases. As LCFA concentration increased, β-oxidation rate reached the maximum value, and then decreased, which confirmed the substrate inhibition of LCFA. Oleate, the most abundant LCFA in wastewater, could be degraded more quickly than saturated LCFA containing the same or even less carbon in spite of relatively high toxicity on acetate degradation.

Postprandial Activation of Coagulant Factor VII by Long-chain Dietary Fatty Acids

1996 ◽  
Vol 76 (03) ◽  
pp. 369-371 ◽  
Author(s):  
T A B Sanders ◽  
G J Miller ◽  
Tamara de Grassi ◽  
Najat Yahia
Keyword(s):  
Fatty Acids ◽  
Dietary Fatty Acids ◽  
Factor Vii ◽  
Fat Intake ◽  
Long Chain Fatty Acids ◽  
Postprandial Lipaemia ◽  
Increased Risk ◽  
Coagulant Activity ◽  
Long Chain Triglycerides ◽  
Long Chain

SummaryFactor VII coagulant activity (FVIIc) is associated with an increased risk of fatal ischaemic heart disease (IHD). Several reports have suggested that dietary fat intake or hypertriglyceridaemia are associated with elevated levels of FVII. This study demonstrates that an intake of long-chain fatty acids sufficient to induce postprandial lipaemia in healthy subjects leads to a substantial elevation in both FVIIc and the concentration of FVII circulating in the activated form. Such an increase in FVIIc could not be induced by medium-chain triglycerides. These results suggest that the consumption of a sufficient amount of long-chain triglycerides to induce postprandial lipaemia induces the activation of FVII.

scholarly journals Differential Effects of Fatty Acid Saturation and Chain Length on NASH in Juvenile Iberian Pigs

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 682-682 ◽  
Author(s):  
Kayla Dillard ◽  
Morgan Coffin ◽  
Gabriella Hernandez ◽  
Victoria Smith ◽  
Catherine Johnson ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Body Weight ◽  
Fatty Acid ◽  
Liver Injury ◽  
Olive Oil ◽  
Coconut Oil ◽  
Long Chain Fatty Acids ◽  
Medium Chain ◽  
Long Chain ◽  
Chain Fatty Acids

Abstract Objectives Non-alcoholic fatty liver disease (NAFLD) represents the major cause of pediatric chronic liver pathology in the United States. The objective of this study was to compare the relative effect of inclusion of isocaloric amounts of saturated medium-chain fatty acids (hydrogenated coconut oil), saturated long-chain fatty acids (lard) and unsaturated long-chain fatty acids (olive oil) on endpoints of NAFLD and insulin resistance. Methods Thirty-eight 15-d-old Iberian pigs were fed 1 of 4 diets containing (g/kg body weight × d) 1) control (CON; n = 8): 0 g fructose, 10.5 g fat, and 187 kcal metabolizable energy (ME), 2) lard (LAR; n = 10): 21.6 g fructose, 17.1 g fat (100% lard) and 299 kcal ME, 3) hydrogenated coconut oil (COCO; n = 10): 21.6 g fructose, 16.9 g fat (42.5% lard and 57.5% coconut oil) and 299 kcal ME, and 4) olive oil (OLV, n = 10): 21.6 g fructose, 17.1 g fat (43.5% lard and 56.5% olive oil) and 299 kcal ME, for 9 consecutive weeks. Body weight was recorded every 3 d. Serum markers of liver injury and dyslipidemia were measured on d 60 at 2 h post feeding, with all other serum measures assessed on d 70. Liver tissue was collected on d 70 for histology, triacylglyceride (TG) quantification, and metabolomics analysis. Results Tissue histology indicated the presence of steatosis in LAR, COCO and OLV compared with CON (P ≤ 0.001), with a further increase in in non-alcoholic steatohepatitis (NASH) in OLV and COCO compared with LAR (P ≤ 0.01). Alanine and aspartate aminotransferases were higher in COCO and OLV (P ≤ 0.01) than CON. All treatment groups had lower liver concentrations of methyl donor's choline and betaine versus CON, while bile acids were differentially changed (P ≤ 0.05). COCO had higher levels of TGs with less carbons (Total carbons < 52) than all other groups (P ≤ 0.05). Several long-chain acylcarnitines involved in fat oxidation were higher in OLV versus all other groups (P ≤ 0.05). Conclusions Inclusion of fats enriched in medium-chain saturated and long-chain unsaturated fatty acids in a high-fructose high-fat diet increased liver injury, compared with fats with a long-chain saturated fatty acid profile. Further research is required to investigate the mechanisms causing this difference in physiological response to these dietary fat sources. Funding Sources ARI, AcornSeekers.

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