Black Tea Prevents High Fat Diet‐induced Non‐alcoholic Steatohepatitis

Karmakar, Subhra; Das, Dolan; Maiti, Anasuya; Majumdar, Sangita; Mukherjee, Piyal; Das, Asankur Sekhar; Mitra, Chandan

doi:10.1002/ptr.3466

Cited by 19 publications

(10 citation statements)

References 53 publications

(51 reference statements)

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“…As also reported by other investigators 43 44 , we found that DIO mice exhibited higher total and direct bilirubin levels than did Chow controls or DIO mice treated with exogenous bilirubin. The increased bilirubin in DIO animals may reflect blockage of bilirubin excretion due to impaired liver function in these mice.…”

Section: Discussionsupporting

confidence: 91%

Bilirubin Increases Insulin Sensitivity by Regulating Cholesterol Metabolism, Adipokines and PPARγ Levels

Liu

Dong

Zhang

et al. 2015

Sci Rep

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Obesity can cause insulin resistance and type 2 diabetes. Moderate elevations in bilirubin levels have anti-diabetic effects. This study is aimed at determining the mechanisms by which bilirubin treatment reduces obesity and insulin resistance in a diet-induced obesity (DIO) mouse model. DIO mice were treated with bilirubin or vehicle for 14 days. Body weights, plasma glucose, and insulin tolerance tests were performed prior to, immediately, and 7 weeks post-treatment. Serum lipid, leptin, adiponectin, insulin, total and direct bilirubin levels were measured. Expression of factors involved in adipose metabolism including sterol regulatory element-binding protein (SREBP-1), insulin receptor (IR), and PPARγ in liver were measured by RT-PCR and Western blot. Compared to controls, bilirubin-treated mice exhibited reductions in body weight, blood glucose levels, total cholesterol (TC), leptin, total and direct bilirubin, and increases in adiponectin and expression of SREBP-1, IR, and PPARγ mRNA. The improved metabolic control achieved by bilirubin-treated mice was persistent: at two months after treatment termination, bilirubin-treated DIO mice remained insulin sensitive with lower leptin and higher adiponectin levels, together with increased PPARγ expression. These results indicate that bilirubin regulates cholesterol metabolism, adipokines and PPARγ levels, which likely contribute to increased insulin sensitivity and glucose tolerance in DIO mice.

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Section: Discussionsupporting

confidence: 91%

Bilirubin Increases Insulin Sensitivity by Regulating Cholesterol Metabolism, Adipokines and PPARγ Levels

Liu

Dong

Zhang

et al. 2015

Sci Rep

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“…32 Increased NO · production along with changes of antioxidant enzyme status and liver histopathological changes were also observed in non-diabetic high-fat fed rats. 33 Therefore, our data about lack of NO · production increase differ from previously published data. However, it should be noted that published results about NO · concentration measurements in high-fat fed rats confer to usage of indirect methods, such as Griess reaction, when metabolites of nitric oxide nitrate and nitrite (NOx) are assessed or evaluation of nitrotyrosine.…”

Section: Discussioncontrasting

confidence: 99%

“…Increased nitrotyrosine levels were detected in livers of lean female Zucker rats fed with high‐fat diet for short term (4 weeks) . Increased NO · production along with changes of antioxidant enzyme status and liver histopathological changes were also observed in non‐diabetic high‐fat fed rats . Therefore, our data about lack of NO · production increase differ from previously published data.…”

Section: Discussioncontrasting

confidence: 92%

Changes in glucose transporter expression and nitric oxide production are associated with liver injury in diabetes

Sokolovska

Isajevs

Rostoka

et al. 2015

Cell Biochemistry & Function

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In diabetes mellitus (DM), both hyperglycaemia and hyperlipidaemia can initiate accumulation of fat in the liver, which might be further mediated by inducible nitric oxide synthase. We have studied changes in GLUT1, nitric oxide (NO(·)) concentration and liver damage in two rat DM models. STZ model was induced by strepozotocin 50 mg/kg. HS model was induced by high-fat diet and 30 mg/kg streptozotocin. GLUT1 expression was studied by means of real-time RT-PCR and immunohistochemistry. Production of NO(·) was monitored by means of erythrocyte sedimentation rate spectroscopy of Fe-DETC-NO complex. Liver damage was assessed using histological activity index (HAI). NO(·) concentration was increased in the liver of STZ rats, but it did not change in HS rats (control 36.8 ± 10.3; STZ 142.1 ± 31.1; HS 35.4 ± 9.8 ng/g). Liver HAI was higher in STZ group, 8.6 ± 0.17 versus HS 4.7 ± 0.31, p < 0.05. GLUT1 protein expression was elevated only in STZ group, 16 ± 3 cells/mm(2) versus Control 5 ± 2 cells/mm(2), p = 0.007. Hyperglycaemia sooner causes severe liver damage in rat models of DM, compared with hyperlipidaemia, and is associated with increased NO(·) production. GLUT1 transporter expression might be involved in toxic effects of glucose in the liver. We have obtained novel data about association of GLUT1 expression and NO(·) metabolism in the pathogenesis of liver injury in DM. Increased GLUT1 expression was observed together with overproduction of NO(·) and pronounced liver injury in severely hyperglycaemic rats. On the contrary, moderately hyperglycaemic hyperlipidaemic rats developed only moderate liver steatosis and no increase in GLUT1 and NO(·). GLUT1 overexpression might be implicated in the toxic effects of glucose in the liver. Glycotoxicity is associated with oxidative stress and NO(·) hyperproduction. GLUT1 and NO(·) metabolism might become novel therapeutic targets in liver steatosis.

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“…These data are in consequence with Singh and Sharma (2011) who reported that pretreatment and posttreatment with CMN prevented histological alterations in liver including marked histological disturbances. Karmakar et al (2011) found that oral administration of aqueous black tea in high fat diet Wistar rats prevented the histological alterations in liver and hepatocellular damage. Therefore, the present data together with the previous data show that supplementation of black tea extract or CMN showed an efficient role in repairing the distortion of the biochemical and histological changes induced by AFB1 in liver.…”

Section: Discussionmentioning

confidence: 99%

Synergistic effect of black tea and curcumin in improving the hepatotoxicity induced by aflatoxin B1 in rats

et al. 2013

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Aflatoxin B1 (AFB1) is a toxic compound commonly found as a contaminant in human food. It is carcinogenic due its potential in inducing the oxidative stress and distortion of the most antioxidant enzymes. Since black tea possesses strong antioxidant activity, it protects cells and tissues against oxidative stress. Curcumin (CMN), a naturally occurring agent, has a combination of biological and pharmacological properties that include antioxidant activity. Therefore, the present study was carried out to investigate the possible role of separate and mixed supplementation of black tea extract and CMN in the hepatotoxicity induced by AFB1 in rats. A total of 48: adult male Sprague Dawley rats were randomly divided into eight groups with six rats in each group. Group 1 (normal control) includes rats that received no treatment. Groups 2, 3, and 4 (positive control) include rats that received olive oil, black tea extract, and CMN, respectively. Group 5 includes rats that received AFB1 at a dose of 750 μg/kg body weight (b.w.) dissolved in olive oil. Groups 6, 7, and 8 include rats that received AFB1 along with 2% black tea extract, CMN at a dose of 200 mg/kg b.w., and both black tea extract and CMN at the same previous doses, respectively. After 90 days, biochemical and histopathological examination was carried out for the blood samples and liver tissues. A significant decrease in the antioxidant enzymes and a significant increase in the lipid peroxidation and hydrogen peroxide in the rats treated with AFB1 were observed. Moreover, there were dramatic changes in the liver function biomarkers, lipid profile, and liver architecture. Supplementation of black tea extract or CMN showed an efficient role in repairing the distortion of the biochemical and histological changes induced by AFB1 in liver. This improvement was more pronounced when both CMN and black tea were used together.

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Black Tea Prevents High Fat Diet‐induced Non‐alcoholic Steatohepatitis

Cited by 19 publications

References 53 publications

Bilirubin Increases Insulin Sensitivity by Regulating Cholesterol Metabolism, Adipokines and PPARγ Levels

Bilirubin Increases Insulin Sensitivity by Regulating Cholesterol Metabolism, Adipokines and PPARγ Levels

Changes in glucose transporter expression and nitric oxide production are associated with liver injury in diabetes

Synergistic effect of black tea and curcumin in improving the hepatotoxicity induced by aflatoxin B1 in rats

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