Effects of Chain Length and Degree of Unsaturation of Fatty Acids on Structure and in Vitro Digestibility of Starch–Protein–Fatty Acid Complexes

2018 ◽  
Vol 66 (8) ◽  
pp. 1872-1880 ◽  
Author(s):  
Mengge Zheng ◽  
Chen Chao ◽  
Jinglin Yu ◽  
Les Copeland ◽  
Shuo Wang ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Chain Length ◽  
In Vitro Digestibility ◽  
Degree Of Unsaturation

Effect of fatty acid structure on esterification by the small intestine in vitro

1963 ◽  
Vol 204 (5) ◽  
pp. 821-824 ◽  
Author(s):  
Alvin M. Gelb ◽  
Jacques I. Kessler
Keyword(s):  
Fatty Acids ◽  
Small Intestine ◽  
Fatty Acid ◽  
Small Bowel ◽  
Chain Length ◽  
Degree Of Unsaturation ◽  
Fatty Acid Structure ◽  
Acid Structure

The effect of chain length and degree of unsaturation of fatty acids (FA) on in vitro esterification by slices of hamster small intestine was observed in a medium containing C14-labeled FA. After incubation, lipids were extracted and separated and the radioactivity in the esterified lipids was measured. Comparative experiments, in which results were expressed as per cent of substrate esterified per 100 mg tissue, indicate that for saturated FA, maximal esterification occurred with myristic acid, 14 carbons. As chain length was either increased or decreased, percentage esterification decreased. FA with 8 carbons or less were only minimally esterified. Among 18-carbon FA, two unsaturated bonds significantly decreased percentage esterification, although one unsaturated bond did not. These results suggest that, at least in vitro, the small bowel esterifies FA at varying rates depending upon chain length and degree of unsaturation. These differences are in the same direction as differences in absorption and partition of FA in vivo previously reported by others.

FATTY ACID INHIBITION OF CHOLESTEROL SYNTHESIS

1956 ◽  
Vol 34 (1) ◽  
pp. 861-868 ◽  
Author(s):  
J. D. Wood ◽  
B. B. Migicovsky
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Chain Length ◽  
Rat Liver ◽  
Cholesterol Synthesis ◽  
Rapid Decrease ◽  
Acid Inhibition ◽  
Degree Of Unsaturation ◽  
Liver Homogenates ◽  
Fatty Acid Inhibition

Fatty acids inhibit cholesterol synthesis by rat liver homogenates. Inhibition occurs with acids containing either an even or an odd number of carbon atoms in the chain, and with saturated and unsaturated acids, the inhibition increasing with the degree of unsaturation of the acid. In the case of acids with an even number of carbon atoms the inhibition increases with chain length to a maximum at 12 carbons after which a rapid decrease occurs. The presence of fatty acid during cholesterol synthesis increases the acetate incorporated into fatty acids to a slight extent. This increase is small compared with the decrease in the amount incorporated into cholesterol. A possible mechanism for the inhibition is discussed.

FATTY ACID INHIBITION OF CHOLESTEROL SYNTHESIS

1956 ◽  
Vol 34 (5) ◽  
pp. 861-868 ◽  
Author(s):  
J. D. Wood ◽  
B. B. Migicovsky
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Chain Length ◽  
Rat Liver ◽  
Cholesterol Synthesis ◽  
Rapid Decrease ◽  
Acid Inhibition ◽  
Degree Of Unsaturation ◽  
Liver Homogenates ◽  
Fatty Acid Inhibition

Fatty acids inhibit cholesterol synthesis by rat liver homogenates. Inhibition occurs with acids containing either an even or an odd number of carbon atoms in the chain, and with saturated and unsaturated acids, the inhibition increasing with the degree of unsaturation of the acid. In the case of acids with an even number of carbon atoms the inhibition increases with chain length to a maximum at 12 carbons after which a rapid decrease occurs. The presence of fatty acid during cholesterol synthesis increases the acetate incorporated into fatty acids to a slight extent. This increase is small compared with the decrease in the amount incorporated into cholesterol. A possible mechanism for the inhibition is discussed.

The short-term effect of fatty acids on glucagon secretion is influenced by their chain length, spatial configuration, and degree of unsaturation: studies in vitro

Metabolism ◽  
2005 ◽  
Vol 54 (10) ◽  
pp. 1329-1336 ◽  
Author(s):  
Jing Hong ◽  
Reziwanggu Abudula ◽  
Jianguo Chen ◽  
Per B. Jeppesen ◽  
Stig E.U. Dyrskog ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Chain Length ◽  
Spatial Configuration ◽  
Glucagon Secretion ◽  
Term Effect ◽  
Short Term ◽  
Short Term Effect ◽  
Degree Of Unsaturation

Formation of debranched wheat starch-fatty acid inclusion complexes using saturated fatty acids with different chain length

LWT ◽  
2021 ◽  
pp. 110867
Author(s):  
Min Hyeock Lee ◽  
Ha Ram Kim ◽  
Woo Su Lim ◽  
Min-Cheol Kang ◽  
Hee-Don Choi ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Chain Length ◽  
Inclusion Complexes ◽  
Saturated Fatty Acids ◽  
Wheat Starch

TetR-family transcriptional repressor Thermus thermophilus FadR controls fatty acid degradation

Microbiology ◽  
2011 ◽  
Vol 157 (6) ◽  
pp. 1589-1601 ◽  
Author(s):  
Yoshihiro Agari ◽  
Kazuko Agari ◽  
Keiko Sakamoto ◽  
Seiki Kuramitsu ◽  
Akeo Shinkai
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Target Genes ◽  
Thermus Thermophilus ◽  
Acyl Chain ◽  
Metabolic Energy ◽  
Straight Chain ◽  
Fatty Acid Degradation ◽  
Acid Degradation

In the extremely thermophilic bacterium Thermus thermophilus HB8, one of the four TetR-family transcriptional regulators, which we named T. thermophilus FadR, negatively regulated the expression of several genes, including those involved in fatty acid degradation, both in vivo and in vitro. T. thermophilus FadR repressed the expression of the target genes by binding pseudopalindromic sequences covering the predicted −10 hexamers of their promoters, and medium-to-long straight-chain (C10–18) fatty acyl-CoA molecules were effective for transcriptional derepression. An X-ray crystal structure analysis revealed that T. thermophilus FadR bound one lauroyl (C12)-CoA molecule per FadR monomer, with its acyl chain moiety in the centre of the FadR molecule, enclosed within a tunnel-like substrate-binding pocket surrounded by hydrophobic residues, and the CoA moiety interacting with basic residues on the protein surface. The growth of T. thermophilus HB8, with palmitic acid as the sole carbon source, increased the expression of FadR-regulated genes. These results indicate that in T. thermophilus HB8, medium-to-long straight-chain fatty acids can be used for metabolic energy under the control of FadR, although the major fatty acids found in this strain are iso- and anteiso-branched-chain (C15 and 17) fatty acids.

scholarly journals Effects of propionate and carnitine on the hepatic oxidation of short- and medium-chain-length fatty acids

1988 ◽  
Vol 250 (3) ◽  
pp. 819-825 ◽  
Author(s):  
E P Brass ◽  
R A Beyerinck
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Organic Acid ◽  
Chain Length ◽  
Ketone Body ◽  
Acetyl Coa ◽  
Body Formation ◽  
Medium Chain ◽  
Medium Chain Length ◽  
Hepatic Oxidation

Accumulation of propionate, or its metabolic product propionyl-CoA, can disrupt normal cellular metabolism. The present study examined the effects of propionate, or propionyl-CoA generated during the oxidation of odd-chain-length fatty acids, on hepatic oxidation of short- and medium-chain-length fatty acids. In isolated hepatocytes, ketone-body formation from odd-chain-length fatty acids was slow as compared with even-chain-length fatty acid substrates, and increased as the carbon chain length was increased from five to seven to nine. In contrast, rates of ketogenesis from butyrate, hexonoate and octanoate were all approximately equal. Propionate (10 mM) inhibited ketogenesis from butyrate, hexanoate and octanoate by 81%, 53% and 18% respectively. Addition of carnitine had no effect on ketogenesis from the even-chain-length fatty acids, but increased the rate of ketone-body formation from pentanoate (by 53%), heptanoate (by 28%) and from butyrate or hexanoate in the presence of propionate. The inhibitory effect of propionate could not be explained by shunting acetyl-CoA into the tricarboxylic acid cycle, as CO2 formation from butyrate was also decreased by propionate. Examination of the hepatocyte CoA pool during oxidation of butyrate demonstrated that addition of propionate decreased acetyl-CoA and CoA as propionyl-CoA accumulated. Addition of carnitine decreased propionyl-CoA by 50% (associated with production of propionylcarnitine) and increased acetyl-CoA and CoA. Similar changes in the CoA pool were seen during the oxidation of pentanoate. These results demonstrate that accumulation of propionyl-CoA results in inhibition of short-chain fatty acid oxidation. Carnitine can partially reverse this inhibition. Changes in the hepatocyte CoA pool are consistent with carnitine acting by generating propionylcarnitine, thereby decreasing propionyl-CoA and increasing availability of free CoA. The data provide further evidence of the potential cellular toxicity from organic acid accretion, and supports the concept that carnitine's interaction with the cellular CoA pool can have a beneficial effect on cellular metabolism and function under conditions of unusual organic acid accumulation.

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