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Abstract
Long-chain n-3 polyunsaturated fatty acids (PUFA) can have beneficial effects against fat deposition, cardiovascular diseases, and liver steatosis. We investigated how diets based on lard (predominantly saturated and monounsaturated fatty acids) or flaxseed oil (rich in 18:3n-3) affect liver fat-% and fatty acid profiles of tundra voles (Microtus oeconomus). We also studied potential participation of hyaluronan (HA) in the pathology of fatty liver and whether the development and recovery of fasting-induced steatosis are influenced by n-3 PUFA. The dietary fatty acid composition was manifested in the liver fatty acid signatures. Fasting for 18 h induced macrovesicular steatosis and the liver fat-% increased to 22% independent of the preceding diet. Fasting-induced steatosis did not involve inflammation or connective tissue activation indicated by the absence of both leukocyte accumulation and increased HA. Food deprivation modified the liver fatty acid signatures to resemble more closely the diets. Fasting reduced the proportions of long-chain n-3 PUFA in both dietary regimes and n-3/n-6 PUFA ratios in the lard-fed voles. Decreases in long-chain n-3 PUFA may promote lipid accumulation by modulating the expression of lipid-metabolizing genes. Dietary 18:3n-3 did not prevent the development or attenuate the manifestation of steatosis in the fasted voles or promote the recovery.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is a major health burden in Western countries, affecting20%–30% of the general population [1,2]
The specific aims of this study were to examine: (i) how diets based on lard or flaxseed oil affect the food intake, body fat stores, liver fat-%, and fatty acid (FA) profiles of voles, (ii) whether the different diets could have effects on the rate of weight loss and the responses of liver biochemistry and histology to 18 h of fasting, (iii) if signs of inflammation and connective tissue activation are present in steatotic livers of voles, and (iv) how body composition and liver characteristics recover from food deprivation
Fasting for 18 h caused a decrease in the body masses (BM)
Summary
Non-alcoholic fatty liver disease (NAFLD) is a major health burden in Western countries, affecting20%–30% of the general population [1,2]. Non-alcoholic fatty liver disease (NAFLD) is a major health burden in Western countries, affecting. NAFLD is characterized by pathological accumulation of lipids in the liver in the absence of alcohol abuse, but its pathogenesis is still inadequately understood. Fat accumulation arises from an imbalance between hepatic lipid uptake, oxidation, export of lipids from the liver, and de novo lipogenesis [3]. This has been considered the first hit in NAFLD predisposing the liver to injury mediated by second hits, such as inflammatory cytokines/adipokines, mitochondrial dysfunction, and oxidative stress, leading to NASH and fibrosis [4]. The dietary n-3/n-6 polyunsaturated FA (PUFA) ratio should be approximately 1:3, but the modern diet is rich in n-6
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