Low concentrations of serum n-3 polyunsaturated fatty acids in non-alcoholic fatty liver disease patients with liver injury

Kishino, Tomonori; Ohnìshì, H.; Ohtsuka, Kouki; Matsushima, Satsuki; Urata, Tsuyoshi; Watanebe, Keiko; Honda, Yukihisa; Mine, Yoshitaka; Matsumoto, Motoko; Nishikawa, Kaori; Mori, Hiromu; Takahashi, Shinichi; Ishida, Hideyuki; Watanabe, Takashi

doi:10.1515/cclm.2011.020

Cited by 11 publications

(6 citation statements)

References 10 publications

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“…Studies have associated a higher consumption of fish rich in omega-3 with a reduced risk of NAFLD [ 10 ]. This has been supported by case-control studies reporting a significantly lower concentration of omega-3 PUFA, especially DHA, in NAFLD patients than in healthy individuals [ 54 , 55 , 56 ]. There are few data concerning hepatic fatty acid composition in patients with NAFLD.…”

Section: Observations Of Dietary Composition and Patterns In Nafldmentioning

confidence: 71%

Dietary Composition Independent of Weight Loss in the Management of Non-Alcoholic Fatty Liver Disease

2017

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Poor dietary composition is an important factor in the progression of non-alcoholic fatty liver disease (NAFLD). The majority of NAFLD patients follow diets with overconsumption of simple carbohydrates, total and saturated fat, with reduced intake of dietary fiber and omega-3 rich foods. Although lifestyle modifications including weight loss and exercise remain the keystone of NAFLD management, modifying dietary composition with or without a calorie-restricted diet may also be a feasible and sustainable strategy for NAFLD treatment. In the present review article, we highlight the potential therapeutic role of a “high quality healthy diet” to improve hepatic steatosis and metabolic dysfunction in patients with NAFLD, independent of caloric restriction and weight loss. We provide a literature review evaluating the evidence behind dietary components including fiber-, meat- and omega-3-rich diets and, pending further evidence, we concur with the EASL-EASD-EASO Clinical Guidelines recommendation of the Mediterranean diet as the diet of choice in these patients.

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Section: Observations Of Dietary Composition and Patterns In Nafldmentioning

confidence: 71%

Dietary Composition Independent of Weight Loss in the Management of Non-Alcoholic Fatty Liver Disease

2017

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“…This is highly relevant because dietary 3 PUFAs are being evaluated as treatment strategies for NAFLD/NASH in children and adults (30)(31)(32)(33)(34)(35)63 ). Although these clinical studies show that dietary 3 PUFAs reduce liver fat (30)(31)(32)(33)(34)(35)(36)(37), some clinical trials have reported that 3 PUFAs, like fi sh oil ( 36 ) or EPA-ethyl esters ( 37 ), fail to improve fi brosis scores associated with NASH. Our previous report established that DHA was more effective than EPA at attenuating WD-induced hepatic fat, infl ammation, and fi brosis ( 17 ).…”

Section: Discussionmentioning

confidence: 99%

“…Omega-3 PUFAs have well-defi ned effects on hepatic lipid metabolism and infl ammation ( 29,73 ), and more recently their effects on hepatic fi brosis have been noted ( 17,28,69 ). Although several human studies have provided evidence in support of using supplemental 3 PUFAs to treat NAFLD (30)(31)(32)(33)(34)(35)(36)(37), other studies suggest there may be limitations for their use in NASH treatment ( 36,37 ). In trials using either fi sh oil or EPA-ethyl ester supplements, investigators report that 3 PUFA supplements failed to improve fi brosis scores.…”

Section: Can 3 Pufa Be Used To Treat Human Nash?mentioning

confidence: 99%

Docosahexaenoic acid attenuates Western diet-induced hepatic fibrosis in Ldlr mice by targeting the TGFβ-Smad3 pathway

Lytle

Depner

Wong

et al. 2015

Journal of Lipid Research

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This article is available online at http://www.jlr.org mainly as neutral lipids consisting of triacylglycerols, cholesterol esters, and diacylglycerols. NAFLD ranges in severity from benign hepatosteatosis to nonalcoholic steatohepatitis (NASH) ( 1 ). NASH is defi ned as hepatosteatosis with infl ammation and hepatic injury ( 2 ). Although simple hepatosteatosis is considered clinically benign, NASH is the progressive form of the disease that can lead to significant changes in hepatic morphology (hepatocyte ballooning) and injury (cell death and fi brosis).The incidence of NAFLD has increased in parallel with the obesity epidemic in Western societies. In the general population, the prevalence of NAFLD is estimated to range from 6 to 33% ( 3 ), and ‫ف‬ 30-40% of individuals with hepatic steatosis progress to NASH ( 4 ). The prevalence of NASH ranges from 3 to 5% in the general population ( 3 ). NAFLD and NASH have high prevalence ( у 60%) in patients with type 2 diabetes ( 5 ). Additionally, NASH patients have higher mortality rates than NAFLD patients ( 6-8 ), and over a 10 year period, cirrhosis and liver-related death occurs in 20 and 12% of NASH patients, respectively ( 9 ). Because NASH can progress to cirrhosis, hepatocellular cancer, and liver failure ( 4,(10)(11)(12)(13)(14), it is the third most common cause for liver transplantation. NASH is projected to be the leading cause of liver transplantation in the United States by 2020 ( 15 ).Hepatic fi brosis involves the increased production of extracellular matrix (ECM) from activated hepatic stellate cells and myofi broblasts infi ltrating the liver. The liver has an underlayment of connective tissue composed of several Nonalcoholic fatty liver disease (NAFLD) is a signifi cant public health burden in Western societies. NAFLD is defi ned as excess accumulation of liver fat (hepatosteatosis),

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“…On the basis of the well-established effects of C20-22 (n-3) PUFA to regulate hepatic lipid metabolism, dyslipidemia, and inflammation (12)(13)(14), we tested the hypothesis that dietary (n-3) PUFA prevents high-fat (HF) diet-induced fatty liver disease in mice. Recent clinical studies have indicated that dietary (n-3) PUFA have the potential to reduce hepatic lipid content in children and adults (15)(16)(17)(18)(19). Our studies, however, go beyond the analysis of hepatic lipids and examine the capacity of (n-3) PUFA to regulate markers of NASH, such as hepatic damage, inflammation, oxidative stress, and fibrosis.…”

Section: Introductionmentioning

confidence: 98%

Menhaden Oil Decreases High-Fat Diet–Induced Markers of Hepatic Damage, Steatosis, Inflammation, and Fibrosis in Obese Ldlr−/− Mice

Depner

Torres-Gonzalez

Tripathy

et al. 2012

The Journal of Nutrition

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The frequency of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) has increased in parallel with obesity in the United States. NASH is progressive and characterized by hepatic damage, inflammation, fibrosis, and oxidative stress. Because C20-22 (n-3) PUFA are established regulators of lipid metabolism and inflammation, we tested the hypothesis that C20-22 (n-3) PUFA in menhaden oil (MO) prevent high-fat (HF) diet-induced fatty liver disease in mice. Wild-type (WT) and Ldlr(-/-) C57BL/6J mice were fed the following diets for 12 wk: nonpurified (NP), HF with lard (60% of energy from fat), HF-high-cholesterol with olive oil (HFHC-OO; 54.4% of energy from fat, 0.5% cholesterol), or HFHC-OO supplemented with MO (HFHC-MO). When compared with the NP diet, the HF and HFHC-OO diets induced hepatosteatosis and hepatic damage [elevated plasma alanine aminotransferase (ALT) and aspartate aminotransferases] and elevated hepatic expression of markers of inflammation (monocyte chemoattractant protein-1), fibrosis (procollagen 1α1), and oxidative stress (heme oxygenase-1) (P ≤ 0.05). Hepatic damage (i.e., ALT) correlated (r = 0.74, P < 0.05) with quantitatively higher (>140%, P < 0.05) hepatic cholesterol in Ldlr(-/-) mice fed the HFHC-OO diet than WT mice fed the HF or HFHC-OO diets. Plasma and hepatic markers of liver damage, steatosis, inflammation, and fibrosis, but not oxidative stress, were lower in WT and Ldlr(-/-) mice fed the HFHC-MO diet compared with the HFHC-OO diet (P < 0.05). In conclusion, MO [C20-22 (n-3) PUFA at 2% of energy] decreases many, but not all, HF diet-induced markers of fatty liver disease in mice.

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Low concentrations of serum n-3 polyunsaturated fatty acids in non-alcoholic fatty liver disease patients with liver injury

Cited by 11 publications

References 10 publications

Dietary Composition Independent of Weight Loss in the Management of Non-Alcoholic Fatty Liver Disease

Dietary Composition Independent of Weight Loss in the Management of Non-Alcoholic Fatty Liver Disease

Docosahexaenoic acid attenuates Western diet-induced hepatic fibrosis in Ldlr mice by targeting the TGFβ-Smad3 pathway

Menhaden Oil Decreases High-Fat Diet–Induced Markers of Hepatic Damage, Steatosis, Inflammation, and Fibrosis in Obese Ldlr−/− Mice

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