Dietary Supplementation of Genistein Alleviates Liver Inflammation and Fibrosis Mediated by a Methionine-Choline-Deficient Diet in <i>db</i>/<i>db</i> Mice

Yoo, Na-young; Jeon, Sookyoung; Nam, Yerim; Park, Youn‐Jin; Won, Sungjun; Kwon, Young Hye

doi:10.1021/acs.jafc.5b00398

Cited by 43 publications

(29 citation statements)

References 46 publications

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“…This biological effect of isofl avones occurs by indirect rather than direct action in mammalian cells. In fact, mice fed a methionine-cholinedefi cient diet, which is associated with development of nonalcoholic steatohepatitis, exhibit increased levels of TBARS and heme oxygenase-1 mRNA, which are significantly mitigated by genistein supplementation, resulting in prevention of liver infl ammation and fi brosis (29). Furthermore, genistein inhibited H2O2-induced activation of the JNK and ERK signaling pathway, leading to protection of cortical neurons against oxidative stress (30).…”

Section: Discussionmentioning

confidence: 99%

Dietary Supplementation with Isoflavones Prevents Muscle Wasting in Tumor-Bearing Mice

Hirasaka

Saito

Yamaguchi

et al. 2016

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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Summary Proinfl ammatory cytokines contribute to the progression of muscle wasting caused by ubiquitin-proteasome-dependent proteolysis. We have previously demonstrated that isofl avones, such as genistein and daidzein, prevent TNF-␣-induced muscle atrophy in C2C12 myotubes. In this study, we examined the effect of dietary fl avonoids on the wasting of muscle. Mice were divided into the following four groups: vehicle-injected (control) mice fed the normal diet (CN); tumor-bearing mice fed the normal diet (TN); control mice fed the isofl avone diet (CI); and tumor-bearing mice fed the isofl avone diet (TI). There were no significant differences in the intake of food or body weight gain among these four groups. The wet weight and myofi ber size of gastrocnemius muscle in TN signifi cantly decreased, compared with those in CN. Interestingly, the wet weight and myofi ber size of gastrocnemius muscle in TI were nearly the same as those in CN and CI, although isofl avone supplementation did not affect the increased tumor mass or concentrations of proinfl ammatory cytokines, such as TNF-␣ and IL-6, in the blood. Moreover, increased expression of muscle-specifi c ubiquitin ligase genes encoding MAFbx/Atrogin-1 and MuRF1 in the skeletal muscle of TN was signifi cantly inhibited by the supplementation of isofl avones. In parallel with the expression of muscle-specifi c ubiquitin ligases, dietary isofl avones signifi cantly suppressed phosphorylation of ERK in tumor-bearing mice. These results suggest that dietary isofl avones improve muscle wasting in tumor-bearing mice via the ERK signaling pathway mediated-suppression of ubiquitin ligases in muscle cells.

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Section: Discussionmentioning

confidence: 99%

Dietary Supplementation with Isoflavones Prevents Muscle Wasting in Tumor-Bearing Mice

Hirasaka

Saito

Yamaguchi

et al. 2016

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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“…Genistein is an isoflavone and its beneficial effects on metabolic disorders and inflammatory state have been indicated. Despite no inhibition of hepatic steatosis, genistein can attenuate steatohepatitis induced in methionine‐choline‐deficient (MCD) diet‐fed mice by alleviating AMPK inactivation and suppressing inflammation . In a recently conducted trial, oral supplementation with genistein could reduce insulin resistance, oxidative, and inflammatory indices along with improvement in fat metabolism in patients with NAFLD .…”

Section: Nafld Therapeutics From a Mitochondria‐centric Perspectivementioning

confidence: 99%

Mitochondria‐Mediated Pathogenesis and Therapeutics for Non‐Alcoholic Fatty Liver Disease

Zhang

et al. 2019

Molecular Nutrition Food Res

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Non‐alcoholic fatty liver disease (NAFLD) has become a worldwide epidemic over the last decade. Remarkable progress has been made in understanding the pathogenesis of NAFLD and, subsequently, in developing medications to treat this disease. Although the mechanisms of NAFLD are complex and multifactorial, accumulating and emerging evidence indicates that mitochondria play a critical role in the pathogenesis and progression of NAFLD. Pharmacologic therapies acting on mitochondria may therefore pave the way to novel strategies for the prevention and protection against NAFLD. This review focuses on new insights into the role of hepatic mitochondrial dysfunction in NAFLD, and summarizes recent studies on mitochondria‐centric therapies for NAFLD utilizing new medications or repurposing of currently available drugs. Although some studies presented may feature controversial results or are still in lack of clinical verification, it is undoubted that medications that may spare the mitochondria from multiple levels of damage are highly promising, and have begun to be used with some degree of success.

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“…In contrast to the aforementioned benefits from isoflavones in fatty liver disease, there are studies that isoflavones have been effective in inhibition of hepatic inflammation and injury but not steatosis. For instance, genistein did not prevent liver steatosis but reduced oxidative stress, fibrosis, and inflammatory gene expression in mice (Yoo et al, ). Likewise, a mixture of polyphenols, containing resveratrol, genistein, and quercetin, increased hepatic lipids but did not activate expression of genes relative to apoptosis, cell repair, or tissue remodeling (Miller et al, ).…”

Section: Treatment Of Non‐alcoholic Fatty Liver Diseasementioning

confidence: 99%

Non-alcoholic Fatty Liver Disease: Beneficial Effects of Flavonoids

Akhlaghi

2016

Phytother. Res.

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Non-alcoholic fatty liver disease (NAFLD) has been known as the hepatic feature of metabolic syndrome. Extra fat depots, especially in visceral areas, develop insulin resistance as a result of mild oxidation and inflammation. Insulin resistance induces lipolysis and releases free fatty acids into the circulation, where they are transported to the liver. In the liver, free fatty acids are converted to triglycerides and accumulate, causing simple steatosis that, if left untreated, can lead to steatohepatitis, and subsequently liver necrosis and cirrhosis.Flavonoids, a group of plant compounds with incredible biological characteristics, have shown advantages in pathological conditions. Beneficial effects of flavonoids against NAFLD and its related disorders have been observed in both animal and human studies. Various mechanisms have been found for their protection. Flavonoids prevent hepatosteatosis by increasing fatty acid oxidation in the liver. They can also reduce caloric intake and decrease body weight and fat deposition in visceral tissues. Flavonoids are unique antioxidants that exert their beneficial effects through inhibition of nuclear factor κB, thereby attenuating release of inflammatory cytokines, which are triggers of insulin resistance. Finally, flavonoids have shown to increase adiponectin, improve insulin sensitivity and glucose tolerance, correct dyslipidemia, and reduce blood pressure in patients with NAFLD. Copyright © 2016 John Wiley & Sons, Ltd.

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Dietary Supplementation of Genistein Alleviates Liver Inflammation and Fibrosis Mediated by a Methionine-Choline-Deficient Diet in db/db Mice

Cited by 43 publications

References 46 publications

Dietary Supplementation with Isoflavones Prevents Muscle Wasting in Tumor-Bearing Mice

Dietary Supplementation with Isoflavones Prevents Muscle Wasting in Tumor-Bearing Mice

Mitochondria‐Mediated Pathogenesis and Therapeutics for Non‐Alcoholic Fatty Liver Disease

Non-alcoholic Fatty Liver Disease: Beneficial Effects of Flavonoids

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