ω-3 Fatty acids reverse lipotoxity through induction of autophagy in nonalcoholic fatty liver disease

Chen, Yi; Xu, Chengfu; Yan, Tang; Yu, Chaohui; Li, Youming

doi:10.1016/j.nut.2015.05.022

Cited by 29 publications

(19 citation statements)

References 55 publications

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“…FO treatment promoted a total reversion of this effect, reaching similar values to the CO group. It is known that elevated levels of FFA are associated to higher deposition of these lipids in other organs and, more aggressively, it is correlated to central adiposity (associated with the viscera), which corroborates for fat accumulation in heart and liver (lipotoxic effects) (Chen et al, ; Su, Lee, Cheng, & Huang, ).…”

Section: Discussionmentioning

confidence: 87%

“…FO is rich in long-chain omega-3 polyunsaturated fatty acids (LC n − 3 PUFAs). LC n − 3 PUFAs, including eicosapentaenoic acid (EPA 20:5) and docosahexaenoic acid (DHA 22:6), have long been shown to improve insulin sensitivity and to play a potent anti-inflammatory, hypolipidemic, and body weight (BW) reducing effects (Chen, Xu, Yan, Yu, & Li, 2015;Couet, Delarue, Ritz, Antoine, & Lamisse, 1997;Kopecky et al, 2009;de Sá et al, 2016;Serhan, 2014). The most important source of EPA and DHA is marine fish, such as salmon, sardines, tuna, and mullet (Rustan, Hustvedt, & Drevon, 1993).…”

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confidence: 99%

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Fish oil reverses metabolic syndrome, adipocyte dysfunction, and altered adipokines secretion triggered by high‐fat diet‐induced obesity

et al. 2020

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The effect of fish oil (FO) treatment on high‐fat (HF) diet‐induced obesity and metabolic syndrome was addressed by analyzing dysfunctions in cells of different adipose depots. For this purpose, mice were initially induced to obesity for 8 weeks following a treatment with FO containing high concentration of EPA compared to DHA (5:1), for additional 8 weeks (by gavage, 3 times per week). Despite the higher fat intake, the HF group showed lower food intake but higher body weight, glucose intolerance and insulin resistance, significant dyslipidemia and increased liver, subcutaneous (inguinal‐ING) and visceral (retroperitoneal‐RP) adipose depots mass, accompanied by adipocyte hypertrophy and decreased cellularity in both adipose tissue depots. FO treatment reversed all these effects, as well as it improved the metabolic activities of isolated adipocytes, such as glucose uptake and lipolysis in both depots, and de novo synthesis of fatty acids in ING adipocytes. HF diet also significantly increased both the pro and anti‐inflammatory cytokines expression by adipocytes, while HF + FO did not differ from control group. Collectively, these data show that the concomitant administration of FO with the HF diet is able to revert metabolic changes triggered by the diet‐induced obesity, as well as to promote beneficial alterations in adipose cell activities. The main mechanism underlying all systemic effects involves direct and differential effects on ING and RP adipocytes.

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Section: Discussionmentioning

confidence: 87%

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confidence: 99%

Fish oil reverses metabolic syndrome, adipocyte dysfunction, and altered adipokines secretion triggered by high‐fat diet‐induced obesity

et al. 2020

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“…Autophagy is also used by H. pylori to survive 78,79 CD Defect/ active MAP1S, NOD2, CLEC12A, ATG16L, NDP52, IRGM NOD2 direct ATG16L1 on the plasma membrane and initiate autophagy. Onset of CD is triggered by dysfunction of autophagy [80][81][82] Fatty liver disease Defect SREBP-2, PNPLA8, FGF21 Impairment of autophagy decreases insulin resistance and enhances oxidative stress and deteriorates hepatocyte damage [83][84][85] Alcoholic liver disease Defect CNR2, ATG5…”

Section: Becn1 Cftrmentioning

confidence: 99%

Modulation of autophagy in human diseases strategies to foster strengths and circumvent weaknesses

Sui

Zhang

et al. 2019

Medicinal Research Reviews

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Autophagy is central to the maintenance of intracellular homeostasis across species. Accordingly, autophagy disorders are linked to a variety of diseases from the embryonic stage until death, and the role of autophagy as a therapeutic target has been widely recognized. However, autophagy‐associated therapy for human diseases is still in its infancy and is supported by limited evidence. In this review, we summarize the landscape of autophagy‐associated diseases and current autophagy modulators. Furthermore, we investigate the existing autophagy‐associated clinical trials, analyze the obstacles that limit their progress, offer tactics that may allow barriers to be overcome along the way and then discuss the therapeutic potential of autophagy modulators in clinical applications.

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“…Nutrient excess has also been shown to inhibit autophagy in the liver of high fat diet (HFD)-fed mice. Conversely, treatment of the LO2 hepatocyte cell line with ω-3 fatty acids decreased cellular lipid accumulation partly by increasing autophagic flux and downregulation of lipogenesis genes (Chen et al, 2015). This finding suggests that in the setting of excess fat accumulation in the liver, autophagy is down regulated, leading to an additional increase of lipid accumulation in liver.…”

Section: Nafld Pathogenesismentioning

confidence: 99%

Molecular mechanisms of nonalcoholic fatty liver disease: Potential role for 12-lipoxygenase

Samala

Tersey

Anderson³

et al. 2017

Journal of Diabetes and its Complications

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Nonalcoholic fatty liver disease (NAFLD) is a spectrum of pathologies associated with fat accumulation in the liver. NAFLD is the most common cause of liver disease in the United States, affecting up to a third of the general population. It is commonly associated with features of metabolic syndrome, particularly insulin resistance. NAFLD shares the basic pathogenic mechanisms with obesity and insulin resistance, such as mitochondrial, oxidative and endoplasmic reticulum stress. Lipoxygenases catalyze the conversion of poly-unsaturated fatty acids in the plasma membrane—mainly arachidonic acid and linoleic acid—to produce oxidized pro-inflammatory lipid intermediates. 12-Lipoxygenase (12-LOX) has been studied extensively in setting of inflammation and insulin resistance. As insulin resistance is closely associated with development of NAFLD, the role of 12-LOX in pathogenesis of NAFLD has received increasing attention in recent years. In this review we discuss the role of 12-LOX in NAFLD pathogenesis and its potential role in emerging new therapeutics.

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ω-3 Fatty acids reverse lipotoxity through induction of autophagy in nonalcoholic fatty liver disease

Cited by 29 publications

References 55 publications

Fish oil reverses metabolic syndrome, adipocyte dysfunction, and altered adipokines secretion triggered by high‐fat diet‐induced obesity

Fish oil reverses metabolic syndrome, adipocyte dysfunction, and altered adipokines secretion triggered by high‐fat diet‐induced obesity

Modulation of autophagy in human diseases strategies to foster strengths and circumvent weaknesses

Molecular mechanisms of nonalcoholic fatty liver disease: Potential role for 12-lipoxygenase

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