Tissue-dependent effects of cis-9,trans-11- and trans-10,cis-12-CLA isomers on glucose and lipid metabolism in adult male mice

Abstract

Mixtures of the two major conjugated linoleic acid (CLA) isomers trans-10,cis-12-CLA and cis-9,trans-11-CLA are used as over the counter supplements for weight loss. Because of the reported adverse effects of CLA on insulin sensitivity in some mouse studies, we sought to compare the impact of dietary t10c12-CLA and c9t11-CLA on liver, adipose tissue, and systemic metabolism of adult lean mice. We fed 8 week-old C57Bl/6J male mice with low fat diets (10.5% Kcal from fat) containing 0.8% t10c12-CLA or c9t11-CLA for 9 or 38 days. Diets containing c9t11-CLA had minimal impact on the endpoints studied. However, 7 days after starting the t10c12-CLA diet, we observed a dramatic reduction in fat mass measured by NMR spectroscopy, which interestingly rebounded by 38 days. This rebound was apparently due to a massive accumulation of lipids in the liver, because adipose tissue depots were visually undetectable. Hepatic steatosis and the disappearance of adipose tissue after t10c12-CLA feeding was associated with elevated plasma insulin levels and insulin resistance, compared to mice fed a control diet or c9t11-CLA diet. Unexpectedly, despite being insulin resistant, mice fed t10c12-CLA had normal levels of blood glucose, without signs of impaired glucose clearance. Hepatic gene expression and fatty acid composition suggested enhanced hepatic de novo lipogenesis without an increase in expression of gluconeogenic genes. These data indicate that dietary t10c12-CLA may alter hepatic

Effects of in ovo feeding of t10,c12-conjugated linoleic acid on hepatic lipid metabolism and subcutaneous adipose tissue deposition in newly hatched broiler chicks

“…It should be noted that the delipidation effect of t10,c12-CLA on adipose tissue and the adipose tissue-dependent effect induced by t10,c12-CLA was fully investigated by previous studies. However, several studies also found that the antiobesity effect of t10,c12-CLA might promote fatty liver by enhancing fatty acid transport to the liver ( Clement et al., 2002 ; Vyas et al., 2012 ; Cordoba-Chacon et al., 2019 ). Interestingly, these findings were closely associated with the animal models used.…”

Loss of Hepatocyte-Specific PPARγ Expression Ameliorates Early Events of Steatohepatitis in Mice Fed the Methionine and Choline-Deficient Diet

“…To assess hepatic fatty acid composition, total lipids were extracted using the Bligh and Dyer method [30]. An aliquot of extracted lipids was transmethylated with BF3-methanol (Sigma-Aldrich) to quantify specific methyl esters of fatty acids using GC/MS, as we previously reported [31,32], using 17 : 1 as the internal standard to quantify the amount of each fatty acid in the sample. In addition, we used a commercial sample of polyunsaturated fatty acid mixture (PUFA-2, Supelco) to identify the different fatty acids in the samples.…”

Transgenic female mice producingtrans10,cis12-conjugated linoleic acid present excessive prostaglandin E2, adrenaline, corticosterone, glucagon, and FGF21

“…Previous studies on mice have yielded conflicting results on whether dietary t10c12-CLA leads to hepatic steatosis [15,[29][30][31]. The current observation of fatty liver and hypertriglyceridemia in pai/pai mice, which may be associated with t10c12-CLAinduced excess corticosterone for the overproduction of corticosterone can lead to Cushing syndrome, corticosteroid-induced lipodystrophy, hypertriglyceridemia, or hepatic steatosis [32,33].…”