Inducing Effect of Clofibric Acid on Stearoyl‐CoA Desaturase in Intestinal Mucosa of Rats

Abstract

Fibrates have been reported to elevate the hepatic proportion of oleic acid (18:1n-9) through inducing stearoyl-CoA desaturase (SCD). Despite abundant studies on the regulation of SCD in the liver, little is known about this issue in the small intestine. The present study aimed to investigate the effect of clofibric acid on the fatty acid profile, particularly monounsaturated fatty acids (MUFA), and the SCD expression in intestinal mucosa. Treatment of rats with a diet containing 0.5% (w/w) clofibric acid for 7 days changed the MUFA profile of total lipids in intestinal mucosa; the proportion of 18:1n-9 was significantly increased, whereas those of palmitoleic (16:1n-7) and cis-vaccenic (18:1n-7) acids were not changed. Upon the treatment with clofibric acid, SCD was induced and the gene expression of SCD1, SCD2, and fatty acid elongase (Elovl) 6 was up-regulated, but that of Elovl5 was unaffected. Fat-free diet feeding for 28 days increased the proportions of 16:1n-7 and 18:1n-7, but did not effectively change that of 18:1n-9, in intestinal mucosa. Fat-free diet feeding up-regulated the gene expression of SCD1, but not that of SCD2, Elovl6, or Elovl5. These results indicate that intestinal mucosa significantly changes its MUFA profile in response to challenges by clofibric acid and a fat-free diet and suggest that up-regulation of the gene expression of SCD along with Elovl6 is indispensable to elevate the proportion of 18:1n-9 in intestinal mucosa.

Western and heart healthy dietary patterns differentially affect the expression of genes associated with lipid metabolism, interferon signaling and inflammation in the jejunum of Ossabaw pigs

“…High hepatic SCD activity has been observed in several disease states, including obesity, atherosclerosis, diabetes, and cancer in humans and animal models [ 37 – 39 ]. Despite abundant investigations of hepatic SCD expression, the regulation of this gene in the small intestine is not well-understood [ 40 ]. In our study, FADS1 gene expression was higher in pigs fed the HHD compared to the WD in the jejunal mucosa, and these data were consistent with the estimated D5D enzyme activity in serum.…”

“…Altered estimated enzyme activity or expression of FADS1 gene has been implied in several disease states, including CAD and insulin resistance [ 42 , 43 ]. Most studies that have investigated fatty acid metabolism in the small intestine focused on absorption, esterification and chylomicrons formation, rather than desaturation activities [ 40 ]. Our data suggest that dietary patterns altered gene expression associated with fatty acids desaturation in the jejunal mucosa.…”

Reduction in Secretion of Very Low Density Lipoprotein–Triacylglycerol by a Matrix Metalloproteinase Inhibitor in a Rat Model of Diet-Induced Hypertriglyceridemia

“…FA methyl esters were prepared using sodium methoxide/methanol. FA methyl esters were measured by gas-liquid chromatography (Shimadzu GC-2014; Shimadzu, Kyoto, Japan) as described previously (Yamazaki et al, 2014).…”

The PPAR pan-agonist tetradecylthioacetic acid promotes redistribution of plasma cholesterol towards large HDL

“…Peroxisome proliferators have previously been shown to regulate expression of the Scd1 gene in liver [68,69] and in the small intestine [54,70]. Upregulation of Scd1 gene expression in the liver by TTA resulted in increased oleic acid content in liver and VLDL as well as accumulation of a delta 9-desaturated metabolite of TTA [1].…”