Linseed Oil Attenuates Liver Inflammation, Fatty Acid Accumulation, and Lipid Distribution in Periportal and Perivenous Hepatocytes Induced by a High-Carbohydrate Diet in Mice.

We evaluated whether linseed oil (LO) modulates the effects of a high-carbohydrate diet (HCD) on liver inflammation, fatty acid (FA) accumulation, and lipid distribution in periportal and perivenous hepatocytes. The control group (control high-carbohydrate diet [HCD-C]) received an HCD with lard and soybean oil as the lipid source. The L10 and L100 groups received the HCD with 10% and 100% of LO as the lipid source, respectively. The animals were killed by decapitation before (day 0) and after receiving the diets. Liver FA composition, inflammation, and fibrogenesis gene expression were evaluated. Also, the percentage of lipid-occupied area in periportal end perivenous hepatocytes were measured. The L100 group exhibited a higher (P < .05) liver amount of omega-3 polyunsaturated FA (n-3 PUFA) and lower (P < .05) amounts of saturated FA (SFA), monounsaturated FA (MUFA), and omega-6 polyunsaturated FA (n-6 PUFA) compared with L10 or HCD-C mice. On day 56, interleukin 10 and type IV collagen gene expression were significantly upregulated and downregulated, respectively in L100. Also, the L100 group showed lower (P < .05) FA accumulation (i.e., total FA, SFA, MUFA, and n-6 PUFA). Also, L10 and L100 presented lower (P < .05) percentage of high lipid-containing portion in periportal and perivenous hepatocytes. We concluded that LO attenuation of liver inflammation promoted by an HCD is associated with increased liver n-3 PUFA levels, so modulating FA composition, deposition, and distribution in periportal and perivenous hepatocytes.

The Dietary Replacement of Soybean Oil by Canola Oil Does Not Prevent Liver Fatty Acid Accumulation and Liver Inflammation in Mice.

A high-carbohydrate diet (HCD) is a well-established experimental model of accelerated liver fatty acid (FA) deposition and inflammation. In this study, we evaluated whether canola oil can prevent these physiopathological changes. We evaluated hepatic FA accumulation and inflammation in mice fed with a HCD (72.1% carbohydrates) and either canola oil (C group) or soybean oil (S group) as a lipid source for 0, 7, 14, 28, or 56 days. Liver FA compositions were analyzed by gas chromatography. The mRNA expression of acetyl-CoA carboxylase 1 (ACC1) was measured as an indicator of lipogenesis. The mRNA expression of F4/80, tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, IL-6, and IL-10, as mediators of liver inflammation, were also measured. The C group stored less n-6 polyunsaturated FAs (n-6 PUFAs) and had more intense lipid deposition of monounsaturated FAs (MUFAs), n-3 PUFAs, and total FAs. The C group also showed higher ACC1 expression. Moreover, on day 56, the C group showed higher expressions of the inflammatory genes F4/80, TNF-α, IL-1ß, and IL-6, as well as the anti-inflammatory IL-10. In conclusion, a diet containing canola oil as a lipid source does not prevent the fatty acid accumulation and inflammation induced by a HCD.