Effects of taurine on hepatic lipid metabolism and anti-inflammation in chronic alcohol-fed rats

Chou, Chung‐Hsi; Chang, Yuan Yen; Tzang, Bor‐Show; Hsu, Chin‐Lin; Lin, Yi-Ling; Lin, Hui-Wen; Chen, Yi‐Chen

doi:10.1016/j.foodchem.2012.04.036

Cited by 19 publications

(9 citation statements)

References 28 publications

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“…Taurine supplementation increased the expression of PPAR-α and LPL mRNA. Taurine supplementation can lower liver triacylglycerol levels in alcohol-fed rats via downregulation of FAS gene expression and upregulation of PPAR-α gene expression (Chou et al, 2012). This indicates that free-range housing and taurine supplementation increase the expression of lipolytic genes and decrease the expression of liposynthetic genes to decrease hepatocellular fat accumulation, as previously described (Schoonjans et al, 1996).…”

Section: Discussionsupporting

confidence: 75%

“…The development of adipose tissue depends on the availability of plasma TG that are hydrolyzed before their uptake by adipocytes along with de novo-synthesized fatty acids (Huang et al, 2008). Serum content of TG, TC, LDL-C, and HDL-C are parameters used to measure serum lipid levels (Huang et al, 2008;Chou et al, 2012;Hu et al, 2012). Our data indicate that serum concentrations of TG, TC, and LDL-C in the highdensity group increased compared with the low-density and free-range groups, whereas serum concentrations of HDL-C in the high-density groups decreased.…”

Section: Discussionmentioning

confidence: 99%

“…Metabolic lipid disorders leading to liver injury are common and most often occur during the most productive egg-laying cycles (Chou et al, 2012). The mechanism of hepatic lipidosis is similar to nonalcoholic fatty liver disease in humans, which is defined as pathological fat deposition in hepatocytes (Di Minno et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

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The influence of dietary taurine and reduced housing density on hepatic functions in laying hens

Zhi-gang

Zhang

et al. 2014

Poultry Science

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To investigate the influence of dietary taurine and reduced housing density on hepatic functions in laying hens, green-shell laying hens were randomly assigned to 3 groups: a free-range group, a caged group with low-density, and a caged group with high-density. Each group was further divided into the control (C) and taurine-treatment (T) groups. All the test birds were fed the same basic diet, except that the T groups were supplemented with 0.1% taurine. After 15 d, sera and liver were aseptically collected. The results show that dietary taurine supplementation and reduced housing density significantly attenuated physiopathological changes in the liver. When compared with the free-range group, serum alanine aminotransterase and aspartate aminotransterase in the caged hens were significantly higher and were deceased by taurine (P< 0.05). Serum inducible nitric oxide synthase activity in caged hens was higher than that in free-range hens, and taurine reduced serum inducible nitric oxide synthase activities in the low-density group (P < 0.05). Nuclear factor-κB DNA-binding activity increased significantly in the high-density housing group when compared with the other 2 housing patterns and was decreased by taurine (P < 0.05). Taurine reduced the expression of tumor necrosis factor-α mRNA in all 3 rearing patterns, IL-4 mRNA expression in the high-density group, and IL-10 in the low-density group (P < 0.05). Malondialdehyde levels decreased in serum and liver from T groups and serum total antioxidation capability levels increased significantly (P < 0.05) in the low-density group. Dietary taurine supplementation decreased acetyl-CoA and sterol regulatory element-binding protein-1c mRNA expression in the high-density groups (P < 0.05). Taurine significantly increased lipoprotein lipase mRNA expression in the high-density group and peroxisome proliferator receptor mRNA expression both in the low- and high-density groups (P < 0.05). Taurine supplementation reduced total cholesterol levels in the low- and high-density groups, decreased triglyceride and low-density lipoprotein cholesterol levels in high-density groups, and increased high-density lipoprotein cholesterol levels in all 3 rearing patterns (P < 0.05). Our data demonstrate that dietary taurine and reduced housing density offer significant protection from hepatic damage in laying hens.

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Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 99%

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The influence of dietary taurine and reduced housing density on hepatic functions in laying hens

Zhi-gang

Zhang

et al. 2014

Poultry Science

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“…18 For example, in a rat model of chronic alcohol consumption, rats given taurine supplements at a dosage of 1 g Tau/kg body weight showed that alcohol metabolism was accelerated by upregulation of alcohol dehydrogenase, catalase, and aldehyde dehydrogenase activities, whereas microvesicular steatosis and necrotic cells in the liver were reduced. 19 Our recent study indicated that taurine downregulates lipogenesis, oxidative stress, and inflammatory cytokines in a rat model of chronic alcohol consumption. 20 However, the precise signaling involved in the beneficial effect of taurine on alcohol-induced liver injury is still obscure.…”

Section: Introduction Ementioning

confidence: 98%

Taurine Attenuates Hepatic Inflammation in Chronic Alcohol-Fed Rats Through Inhibition of TLR4/MyD88 Signaling

Lin

Chiu

Chen

et al. 2015

Journal of Medicinal Food

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Accumulating evidence indicates that overconsumption of ethanol contributes in many ways to the pathogenesis of hepatic injury. Although studies indicate that taurine decreases lipogenesis, oxidative stress, and inflammatory cytokines, the protective effect of taurine against alcohol-induced liver injury is still unclear. To clarify the precise signaling involved in the beneficial effect of taurine on alcohol-induced liver injury, rats were randomly divided into four treatment groups: (1) control (Ctl), (2) alcohol (Alc), (3) Alc + taurine (Tau), and (4) Alc + silymarin (Sil). The Tau and Sil groups had lower lymphocyte infiltration and significantly lower TLR-4/MyD88 and IjB/NFjB compared to the Alc group. The inducible nitric oxide synthase (iNOS), C-reactive protein (CRP), tumor necrosis factors (TNF)-a, interleukin (IL)-6, and IL-1b were also significantly lower in the Tau and Sil groups than in the Alc group. The experimental results indicated that hepatoprotection against alcohol-induced inflammation may be mediated by decreased TLR-4/MyD88 signaling.

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“…Slight-to-severe alcoholic liver injury models were usually established by different doses (2–8 g/kg/day) of alcohol in murine [17, 18]. To avoid the accumulated effects of the individual toxicity on liver, we specifically chose the low dose of alcohol (2 g/kg/day) and iron (300 mg/kg), based on our previous study [19] rather than high dose to investigate the synergistic interaction of them [20].…”

Section: Introductionmentioning

confidence: 99%

Synergistic Interaction of Light Alcohol Administration in the Presence of Mild Iron Overload in a Mouse Model of Liver Injury: Involvement of Triosephosphate Isomerase Nitration and Inactivation

Gao¹,

Zhao²,

Gao³

et al. 2017

PLoS ONE

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It is well known that iron overload promotes alcoholic liver injury, but the doses of iron or alcohol used in studies are usually able to induce liver injury independently. Little attention has been paid to the coexistence of low alcohol consumption and mild iron overload when either of them is insufficient to cause obvious liver damage, although this situation is very common among some people. We studied the interactive effects and the underlining mechanism of mild doses of iron and alcohol on liver injury in a mouse model. Forty eight male Kunming mice were randomly divided into four groups: control, iron (300 mg/kg iron dextran, i.p.), alcohol (2 g/kg/day ethanol for four weeks i.g.), and iron plus alcohol group. After 4 weeks of treatment, mice were sacrificed and blood and livers were collected for biochemical analysis. Protein nitration level in liver tissue was determined by immunoprecipitation and Western blot analysis. Although neither iron overload nor alcohol consumption at our tested doses can cause severe liver injury, it was found that co-administration of the same doses of alcohol and iron resulted in liver injury and hepatic dysfunction, accompanied with elevated ratio of NADH/NAD+, reduced antioxidant ability, increased oxidative stress, and subsequent elevated protein nitration level. Further study revealed that triosephosphate isomerase, an important glycolytic enzyme, was one of the targets to be oxidized and nitrated, which was responsible for its inactivation. These data indicate that even under low alcohol intake, a certain amount of iron overload can cause significant liver oxidative damage, and the modification of triosephosphate isomerasemight be the important underlining mechanism of hepatic dysfunction.

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Effects of taurine on hepatic lipid metabolism and anti-inflammation in chronic alcohol-fed rats

Cited by 19 publications

References 28 publications

The influence of dietary taurine and reduced housing density on hepatic functions in laying hens

The influence of dietary taurine and reduced housing density on hepatic functions in laying hens

Taurine Attenuates Hepatic Inflammation in Chronic Alcohol-Fed Rats Through Inhibition of TLR4/MyD88 Signaling

Synergistic Interaction of Light Alcohol Administration in the Presence of Mild Iron Overload in a Mouse Model of Liver Injury: Involvement of Triosephosphate Isomerase Nitration and Inactivation

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