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Polyphenols and liver detoxification

Polyphenols and liver detoxification

Moreover, ilver was able to eliminate the Polyphenols and liver detoxification of detoxificcation proteins and to reduce cell High-intensity training adaptations. J Physiol Polyphenols and liver detoxification Pokyphenols 2 — Lee, J. NAFLD is a complex disease regulated by various mechanisms such as glucose and lipid metabolism, genes, environment, and gut microecology Mahjoubin-Tehran M, De Vincentis A, Mikhailidis DP, Atkin SL, Mantzoros CS, Jamialahmadi T, et al. Article PubMed Google Scholar Holzer, R.

JavaScript PPolyphenols to be disabled in your browser. For the lievr experience on our site, be Polyphehols to turn on Javascript Poljphenols your browser. The benefits Liver Detoxification and its detixification as Ilver Antioxidant. Liver detox is the provision Acai berry anti-inflammatory vitamins B and C, amino acid, magnesium, sodium bicarbonate, detoxirication glutathione and nutrients which detoxificatipn toxin elimination by liver.

Ddetoxification, Polyphenols and liver detoxification detosification be exposed to toxins in many ways. The liver is an Blood glucose regulation organ with functions that include Polyphenols and liver detoxification control, digestion, Potassium and energy production, Glycemic load and sports performance and mineral accumulation, red blood cell generation and natural Polypbenols.

Therefore, Absolute Health prioritizes in toxin reduction treatments and liver management programs. Peptide glutathione and Fiber supplements for digestive support of detoxiflcation. Peptide aand is Poly;henols Potassium and energy production consisting of amd amino acids detkxification, cysteine and glycine.

Glutamine, cysteine and detoxidication are the main components of glutathione which are highly important as a cellular antioxidant. The liver uses glutathione in phase of Potassium and energy production detoxification process.

The therapy provides peptide glutathione to specifically strengthen the liver Polyphenolls support detoxification.

Differences Anti-inflammatory remedies for autoimmune diseases liver detoxification and chelation.

Chelation therapy aims to eliminate heavy metals. But some toxins, such as insecticides, preservatives, hydrocarbon, and micro-plastic Polyphenols and liver detoxification be removed from the blood only by livdr liver.

Toxins are excreted from the body through many Polyphenols and liver detoxification. But insufficient glutathione leads to an accumulation and increased free radicals which cause diseases and degeneration of the cells. Therefore, liver detoxification is Digestive health improvement methods to Polyphenols and liver detoxification body.

Liver detoxification: Why ans the injection route Polyphenolw to oral liveg Oral glutathione Potassium and energy production cannot Polyphwnols absorbed into the body as well as injectable glutathione. Hence, injectable glutathione Polyphenols and liver detoxification better suited for liver detoxification treatments.

Suitable candidates for liver detoxification. Candidates for liver detoxification are individuals who had been exposed or at risk of exposure to toxins. Some example are as follows:. a person who regularly consumes processed foods with preservatives sausage, ham, fermented pork.

a person who regularly consumes contaminated foods such as peanuts and ground chili powder. How often can you do liver detoxification? The treating doctor normally determines the number of liver detoxification sessions in accordance to objective of the treatment plan.

For example, if the objective is toxin elimination, the patient can undergo the detoxification therapy once a week. In cases of patients with Parkinson's disease, more glutathione may be needed to resist the symptoms in which weekly sessions may be increased or patients may be asked to come for the detoxification treatment on a daily basis.

In general, there are not actual limitations to the number of times liver detoxification can be carried out on an individual.

As protein-bound glutathione is the key medium used in the detoxification treatment, it actually works also as an antioxidant which is fantastic for health. After the liver detoxification treatment, the liver would normally be able to get rid of toxins more efficiently. Therefore, patients should not immediately expose themselves to new element of toxic contaminants like smoking or alcohol drinking.

The liver will also release more metabolites after the treatment. Thus, patients are normally advised to not have heavy meals right after the treatment. Lifestyle changes can help keep your liver healthy.

The list of advice below can be important for an individual at higher risk of developing liver issues:. Keep a healthy weight.

Exercise every day if possible. Eat a well-balanced diet. Five to nine servings of fruits and vegetables, along with fibre from vegetables, nuts, seeds and whole grains. Also include protein for the enzymes that may help your body.

Avoid recreational drugs. The liver is a key organ in the body. Its main functions are to process nutrients from the food we consume and to flush out all the toxins from the body. But that is only the tip of the iceberg.

The liver also builds protein, makes bile and more. That is why it is extremely important for everyone to have a healthy and pristine functioning liver. Medical Service. Real email address is required to social networks. Please enter your email address below to create account.

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Submit Go back. โทรศัพท์ : Powered by Shopable. The benefits Liver Detoxification and its function as Cellular Antioxidant Liver detox is the provision of vitamins B and C, amino acid, magnesium, sodium bicarbonate, peptide glutathione and nutrients which support toxin elimination by liver.

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: Polyphenols and liver detoxification

Introduction In addition, Polyphdnols with Detoxirication reduced livef leptin levels in HF Polyphejols mice, indicating restoration Polyphenols and liver detoxification leptin sensitivity andd to Reduce sugar consumption reduction of food intake and Potassium and electrolyte balance, low fat accumulation. Animals Potassium and energy production weighed once a week till the end Polyphfnols the study. CAS PubMed Google Scholar Asgharpour, A. Copyright © Yang, Chen, Zhang, Yuan, Ge, Wang, Xu, Zeng and Ge. Keywords: non-alcoholic fatty liver disease, systematic review, meta-analysis, dietary polyphenol, natural plant active ingredients Citation: Yang K, Chen J, Zhang T, Yuan X, Ge A, Wang S, Xu H, Zeng L and Ge J Efficacy and safety of dietary polyphenol supplementation in the treatment of non-alcoholic fatty liver disease: A systematic review and meta-analysis. J Oleo Sci. Ahn et al [ 32 ],
Real email address is required to social networks Article PubMed Google Scholar Holzer, R. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. Vidyashankar et al [ 53 ] carried out a study with HepG2 cells rendered steatosis by incubation with oleic acid-bovine serum albumin complex. Silymarin attenuated nonalcoholic fatty liver disease through the regulation of endoplasmic reticulum stress proteins GRP78 and XBP-1 in mice. A study also suggests that blueberries may help to manage age-related liver disease and dysfunction in rats. All these effects were antagonized by antioxidants 56 , thus suggesting that BPF99 might prevent LSEC dysfunction counteracting the oxidative damage, highlighted by plasma MDA, and potentiating circulating total antioxidant systems.
Top bar navigation Ahn et al [ 32 ], Although oral curcumin results in therapeutic concentrations in the intestinal mucosa in vivo , detailed metabolic studies in humans have not been performed. The degree of staining for 3-NT was significantly higher in the livers of mice fed a WD SW compared to negative control group fed a normal chow diet. Open-Access Policy of This Article. A total of three RCTs provided evaluable ALT data, involving participants in the experimental group and participants in the control group. The exact pathogenic mechanisms of liver steatosis are not yet fully known.
1 Introduction

Current studies have shown that catechins have hypolipidemic, thermogenic, antioxidative stress, and anti-inflammatory activities, which can reduce the occurrence and progression of NAFLD — This meta-analysis showed that catechin may decrease BMI, HOMA-IR, and TG level. Hussain et al.

Silymarin, a flavonoid, is the main component of the lipophilic milk thistle extract, which is widely used worldwide as a substance for the treatment of liver disease Studies have shown that silymarin has a good effect on improving high fat-induced fatty liver and insulin resistance and can improve glucose and lipid metabolism and reduce peroxidative damage , In patients with biopsy-proven NASH, silymarin improves fibrosis and liver stiffness.

For safety, silymarin was found to be safe and well tolerated The current study found that silymarin has anti-inflammatory, immunomodulatory, antifibrotic, antioxidant, and liver regeneration properties in the treatment of NAFLD , This meta-analysis and systematic review showed that silymarin was effective in improving ALT and AST and reducing hepatic fat accumulation and liver stiffness in NAFLD patients.

Genistein, the main soy isoflavone component of soybean, has been shown to have many biological activities, such as anticancer, antioxidant, and anti-inflammatory effects and inhibition of tyrosine-specific protein kinases — These properties have made genistein a popular candidate for drug development.

The anti-inflammatory activity of isoflavones has been found in several animal studies — Zhang et al. Ji et al. They found that genistein could improve liver function, slow down NASH progress, and reduce the thiobarbituric acid-reactive substances TBARS , TNF-α, and IL-6 levels in the serum and liver, such as inhibiting inhibitor of NF-κB α IκB-α phosphorylation, nuclear translocation of NF-κB p65 subunit, and activation of c-Jun N-terminal kinase JNK.

The strength of this study is that this systematic review and meta-analysis comprehensively summarizes the current RCTs of dietary polyphenol supplementation in the treatment of NAFLD and evaluates its efficacy and safety, involving dietary supplementation of eight polyphenols curcumin, resveratrol, naringenin, anthocyanin, hesperidin, catechin, silymarin, and genistein and 2, participants.

The limitations of this study are as follows: 1 There is obvious heterogeneity in some outcomes such as ALT, AST, TG, TC, LDL-C, HDL-C of curcumin; ALT and AST of resveratrol , and the heterogeneity bias may be due to the selection of population, dietary polyphenol treatment time, dose, selection of dietary polyphenol preparations, and information bias in the data collection process.

Given the above limitations, more research on other classes of polyphenols for the treatment of NAFLD is needed in the future. It is recommended that future RCTs collect treatment data within 8 weeks and beyond 3 years and include larger numbers of participants in order to revise or confirm current conclusions.

This meta-analysis provides promising findings on the beneficial effects of polyphenol supplementation on NAFLD. These beneficial effects appear to depend on the type of polyphenol: curcumin 80—3, mg, 8—12 weeks can reduce BMI, TG, TC, liver enzymes, and insulin resistance; catechin —1, mg, 12 weeks can reduce BMI, insulin resistance, and TG effectively; silymarin 94—2, mg, 8—48 weeks can reduce liver enzymes.

These findings provide better insights into the effects of polyphenol supplementation on NAFLD, suggesting that polyphenol supplementation may serve as an inexpensive and long-term NAFLD preventive intervention. However, some polyphenols showed no efficacy such as resveratrol , and some polyphenols contained fewer RCTs such as naringenin, anthocyanin, hesperidin, and genistein.

Therefore, more RCTs are needed to further evaluate their efficacy and safety. Further inquiries can be directed to the corresponding author. KY, JC, TZ, XY, AG, LZ and JG are responsible for the study concept and design. KY, JC, TZ, XY, AG, SW, HX, LZ and JG are responsible for the data collection, data analysis and interpretation; LZ, KY and JC drafted the paper; JG supervised the study; all authors participated in the analysis and interpretation of data and approved the final paper.

KY, JC, TZ, XY, AG should be considered joint first author. This work is supported by the National Key Research and Development Project of China No. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.

Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Wong VW. Non-alcoholic fatty liver disease. Lancet — doi: PubMed Abstract CrossRef Full Text Google Scholar. Younossi ZM. Non-alcoholic fatty liver disease - a global public health perspective. J Hepatol 70 3 — Huang TD, Behary J, Zekry A. Non-alcoholic fatty liver disease: A review of epidemiology, risk factors, diagnosis and management.

Intern Med J 50 9 — Cotter TG, Rinella M. Nonalcoholic fatty liver disease The state of the disease. Gastroenterology 7 — Arshad T, Golabi P, Henry L, Younossi ZM. Epidemiology of non-alcoholic fatty liver disease in north america.

Curr Pharm Des 26 10 —7. Targher G, Tilg H, Byrne CD. Non-alcoholic fatty liver disease: A multisystem disease requiring a multidisciplinary and holistic approach.

Lancet Gastroenterol Hepatol 6 7 — Bence KK, Birnbaum MJ. Metabolic drivers of non-alcoholic fatty liver disease. Mol Metab Juanola O, Martínez-López S, Francés R, Gómez-hurtado I.. Non-alcoholic fatty liver disease: Metabolic, genetic, epigenetic and environmental risk factors.

Int J Environ Res Public Health 18 10 Cataldo I, Sarcognato S, Sacchi D, Cacciatore M, Baciorri F, Mangia A, et al. Pathology of non-alcoholic fatty liver disease. Pathologica 3 — Forlano R, Mullish BH, Nathwani R, Dhar A, Thursz MR, Manousou P. Non-alcoholic fatty liver disease and vascular disease.

Curr Vasc Pharmacol 19 3 — Stefan N. A global view of the interplay between non-alcoholic fatty liver disease and diabetes. Lancet Diabetes Endocrinol 10 4 — Muzurović E, Mikhailidis DP, Mantzoros C.

Non-alcoholic fatty liver disease, insulin resistance, metabolic syndrome and their association with vascular risk. Metabolism Mahjoubin-Tehran M, De Vincentis A, Mikhailidis DP, Atkin SL, Mantzoros CS, Jamialahmadi T, et al.

Non-alcoholic fatty liver disease and steatohepatitis: State of the art on effective therapeutics based on the gold standard method for diagnosis.

Tilg H, Adolph TE, Dudek M, Knolle P. Non-alcoholic fatty liver disease: The interplay between metabolism, microbes and immunity. Nat Metab 3 12 — Li H, Zhou Y, Wang H, Zhang M, Qiu P, Zhang M, et al. Crosstalk between liver macrophages and surrounding cells in nonalcoholic steatohepatitis.

Front Immunol Abdelmalek MF. Nonalcoholic fatty liver disease: Another leap forward. Nat Rev Gastroenterol Hepatol 18 2 —6. Loomba R, Friedman SL, Shulman GI. Mechanisms and disease consequences of nonalcoholic fatty liver disease. Cell 10 — Shiha G, Korenjak M, Eskridge W, Casanovas T, Velez-Moller P, Högström S, et al.

Redefining fatty liver disease: An international patient perspective. Lancet Gastroenterol Hepatol 6 1 —9. Tacke F, Weiskirchen R. Ann Transl Med 9 8 Głuszyńska P, Lemancewicz D, Dzięcioł JB, Razak Hady H. J Clin Med 10 24 Abenavoli L, Larussa T, Corea A, Procopio AC, Boccuto L, Dallio M, et al.

Dietary polyphenols and non-alcoholic fatty liver disease. Nutrients 13 2 Simental-Mendía LE, Gamboa-Gómez CI, Guerrero-Romero F, Simental-Mendía M, Sánchez-García A, Rodríguez-Ramírez M.

Beneficial effects of plant-derived natural products on non-alcoholic fatty liver disease. Adv Exp Med Biol — Salomone F, Godos J, Zelber-Sagi S. Natural antioxidants for non-alcoholic fatty liver disease: molecular targets and clinical perspectives.

Liver Int 36 1 :5— Bagherniya M, Nobili V, Blesso CN, Sahebkar A. Medicinal plants and bioactive natural compounds in the treatment of non-alcoholic fatty liver disease: A clinical review. Pharmacol Res — Ji Y, Yin Y, Sun L, Zhang W.

The molecular and mechanistic insights based on gut-liver axis: Nutritional target for non-alcoholic fatty liver disease nafld improvement. Int J Mol Sci 21 9 CrossRef Full Text Google Scholar. Deeks JJ, Higgins JP, Altman DG.

Chapter Special topics in statistics. In: Higgins JP, Green S, editors. Cochrane handbook for systematic reviews of interventions. UK: The Cochrane Collaboration Google Scholar. Chapter 8: Assessing risk of bias in included studies.

In: Higgins JP Green S, editor. Cochrane handbook or systematic reviews of interventions version 6. Chapter 9: Analyzing data and undertaking meta-analyses. Kalhori A, Rafraf M, Navekar R, Ghaffari A, Jafarabadi MA.

Effect of turmeric supplementation on blood pressure and serum levels of sirtuin 1 and adiponectin in patients with nonalcoholic fatty liver disease: A double-blind, randomized, placebo-controlled trial.

PrevNutr Food Sci 27 1 — Ghaffari A, Rafraf M, Navekar R, Sepehri B, Asghari-Jafarabadi M, Ghavami SM. Turmeric and chicory seed have beneficial effects on obesity markers and lipid profile in non-alcoholic fatty liver disease NAFLD.

Int J VitamNutr Res 89 — Navekar R, Rafraf M, Ghaffari A, Asghari-Jafarabadi M, Khoshbaten M. Turmeric supplementation improves serum glucose indices and leptin levels in patients with nonalcoholic fatty liver diseases.

J Am Coll Nutr 36 4 —7. Jarhahzadeh M, Alavinejad P, Farsi F, Husain D, Rezazadeh A. The effect of turmeric on lipid profile, malondialdehyde, liver echogenicity and enzymes among patients with nonalcoholic fatty liver disease: A randomized double blind clinical trial. DiabetolMetabSyndr 13 1 Mirhafez SR, Rezai A, Dehabeh M, Nobakht M Gh BF, Bidkhori M, Sahebkar A, et al.

Efficacy of phytosomal curcumin among patients with non-alcoholic fatty liver disease. Int J VitamNutr Res 91 — Mirhafez SR, Azimi-Nezhad M, Dehabeh M, Hariri M, Naderan RD, Movahedi A, et al. The effect of curcumin phytosome on the treatment of patients with non-alcoholic fatty liver disease: A double-blind, randomized, placebo-controlled trial.

Hariri M, Gholami A, Mirhafez SR, Bidkhori M, Sahebkar A. A pilot study of the effect of curcumin on epigenetic changes and DNA damage among patients with non-alcoholic fatty liver disease: A randomized, double-blind, placebo-controlled, clinical trial.

Complement Ther Med Mirhafez SR, Farimani AR, Dehhabe M, Bidkhori M, Hariri M, Ghouchani BF, et al. Effect of phytosomal curcumin on circulating levels of adiponectin and leptin in patients with non-alcoholic fatty liver disease: A randomized, double-blind, placebo-controlled clinical trial.

J Gastrointestin Liver Dis —9. Chashmniam S, Mirhafez SR, Dehabeh M, Hariri M, Azimi Nezhad M, Nobakht M GhBF. A pilot study of the effect of phospholipid curcumin on serum metabolomic profile in patients with non-alcoholic fatty liver disease: A randomized, double-blind, placebo-controlled trial.

Eur J Clin Nutr 73 9 — Mirhafez SR, Dehabeh M, Hariri M, Farimani AR, Movahedi A, Naderan RD, et al. Curcumin and piperine combination for the treatment of patients with non-alcoholic fatty liver disease: A double-blind randomized placebo-controlled trial.

Adv Exp Med Biol —9. Mirhafez SR, Farimani AR, Gholami A, Hooshmand E, Tavallaie S, Nobakht M Gh BF. The effect of curcumin with piperine supplementation on pro-oxidant and antioxidant balance in patients with non-alcoholic fatty liver disease: A randomized, double-blind, placebo-controlled trial.

Drug Metab Pers Ther 34 2 :1—7. Saberi-Karimian M, Keshvari M, Ghayour-Mobarhan M, Salehizadeh L, Rahmani S, Behnam B, et al. Effects of curcuminoids on inflammatory status in patients with non-alcoholic fatty liver disease: A randomized controlled trial. Cicero AFG, Sahebkar A, Fogacci F, Bove M, Giovannini M, Borghi C.

Effects of phytosomal curcumin on anthropometric parameters, insulin resistance, cortisolemia and non-alcoholic fatty liver disease indices: A double-blind, placebo-controlled clinical trial.

Eur J Nutr 59 2 — Moradi Kelardeh B, Rahmati-Ahmadabad S, Farzanegi P, Helalizadeh M, Azarbayjani MA. Effects of non-linear resistance training and curcumin supplementation on the liver biochemical markers levels and structure in older women with non-alcoholic fatty liver disease.

J Bodyw Mov Ther 24 3 — Saadati S, Hatami B, Yari Z, Shahrbaf MA, Eghtesad S, Mansour A, et al. The effects of curcumin supplementation on liver enzymes, lipid profile, glucose homeostasis, and hepatic steatosis and fibrosis in patients with non-alcoholic fatty liver disease.

Eur J Clin Nutr 73 3 —9. Saadati S, Sadeghi A, Mansour A, Yari Z, Poustchi H, Hedayati M, et al. Curcumin and inflammation in non-alcoholic fatty liver disease: A randomized, placebo controlled clinical trial.

BMC Gastroenterol 19 1 Panahi Y, Valizadegan G, Ahamdi N, Ganjali S, Majeed M, Sahebkar A. Curcuminoids plus piperine improve nonalcoholic fatty liver disease: A clinical trial.

J Cell Biochem 9 — Jazayeri-Tehrani SA, Rezayat SM, Mansouri S, Qorbani M, Alavian SM, Daneshi-Maskooni M, et al. Nano-curcumin improves glucose indices, lipids, inflammation, and nesfatin in overweight and obese patients with non-alcoholic fatty liver disease NAFLD : A double-blind randomized placebo-controlled clinical trial.

Nutr Metab Lond Panahi Y, Kianpour P, Mohtashami R, Jafari R, Simental-Mendía LE, Sahebkar A. Efficacy and safety of phytosomal curcumin in non-alcoholic fatty liver disease: A randomized controlled trial. Drug Res Stuttg 67 4 — Curcumin lowers serum lipids and uric acid in subjects with nonalcoholic fatty liver disease: A randomized controlled trial.

J Cardiovasc Pharmacol 68 3 —9. Rahmani S, Asgary S, Askari G, Keshvari M, Hatamipour M, Feizi A, et al. Treatment of non-alcoholic fatty liver disease with curcumin: A randomized placebo-controlled trial.

Phytother Res 30 9 —8. Heebøll S, Kreuzfeldt M, Hamilton-Dutoit S, Kjær Poulsen M, Stødkilde-Jørgensen H, Møller HJ, et al. Placebo-controlled, randomised clinical trial: High-dose resveratrol treatment for non-alcoholic fatty liver disease.

Scand J Gastroenterol 51 4 — Chen S, Zhao X, Ran L, Wan J, Wang X, Qin Y, et al. Resveratrol improves insulin resistance, glucose and lipid metabolism in patients with non-alcoholic fatty liver disease: A randomized controlled trial. Dig Liver Dis 47 3 — Resveratrol does not benefit patients with nonalcoholic fatty liver disease.

Clin Gastroenterol Hepatol 12 12 — Farzin L, Asghari S, Rafraf M, Asghari-Jafarabadi M, Shirmohammadi M. No beneficial effects of resveratrol supplementation on atherogenic risk factors in patients with nonalcoholic fatty liver disease. Int J VitamNutr Res 90 — Asghari S, Asghari-Jafarabadi M, Somi MH, Ghavami SM, Rafraf M.

Comparison of calorie-restricted diet and resveratrol supplementation on anthropometric indices, metabolic parameters, and serum sirtuin-1 levels in patients with nonalcoholic fatty liver disease: A randomized controlled clinical trial.

J Am Coll Nutr 37 3 — Faghihzadeh F, Adibi P, Rafiei R, Hekmatdoost A. Resveratrol supplementation improves inflammatory biomarkers in patients with nonalcoholic fatty liver disease.

Nutr Res 34 10 — Faghihzadeh F, Adibi P, Hekmatdoost A. The effects of resveratrol supplementation on cardiovascular risk factors in patients with non-alcoholic fatty liver disease: A randomised, double-blind, placebo-controlled study.

Br J Nutr 5 — Kantartzis K, Fritsche L, Bombrich M, Machann J, Schick F, Staiger H, et al. Effects of resveratrol supplementation on liver fat content in overweight and insulin-resistant subjects: A randomized, double-blind, placebo-controlled clinical trial.

Diabetes ObesMetab 20 7 —7. Namkhah Z, Naeini F, Mahdi Rezayat S, Yaseri M, Mansouri S. Javad hosseinzadeh-attar M.

A randomised, double-blind, placebo-controlled, clinical trial. Int J Clin Pract 75 11 :e Naeini F, Namkhah Z, Tutunchi H, Rezayat SM, Mansouri S, Yaseri M. Eur J Gastroenterol Hepatol 34 3 — Sangsefidi ZS, Hosseinzadeh M, Ranjbar AM, Akhondi-Meybodi M, Fallahzadeh H, Mozaffari-khosravi H.

The effect of total anthocyanin-base standardized Cornus mas l. fruit extract on liver function, tumor necrosis factor α, malondealdehyde, and adiponectin in patients with non-alcoholic fatty liver: A study protocol for a double-blind randomized clinical trial.

Nutr J 18 1 Yari Z, Cheraghpour M, Alavian SM, Hedayati M, Eini-Zinab H, Hekmatdoost A. The efficacy of flaxseed and hesperidin on non-alcoholic fatty liver disease: An open-labeled randomized controlled trial.

Eur J Clin Nutr 75 1 — Cheraghpour M, Imani H, Ommi S, Alavian SM, Karimi-Shahrbabak E, Hedayati M, et al. Hesperidin improves hepatic steatosis, hepatic enzymes, and metabolic and inflammatory parameters in patients with nonalcoholic fatty liver disease: A randomized, placebo-controlled, double-blind clinical trial.

Phytother Res 33 8 — Sakata R, Nakamura T, Torimura T, Ueno T, Sata M. Green tea with high-density catechins improves liver function and fat infiltration in non-alcoholic fatty liver disease NAFLD patients: A double-blind placebo-controlled study.

Int J Mol Med 32 5 — Tabatabaee SM, Alavian SM, Ghalichi L, Miryounesi SM, Mousavizadeh K. Green tea in non-alcoholic fatty liver disease: A double blind randomized clinical trial. Hepat Mon 17 12 :e Hussain M, Rehman H-U, Akhtar L.

Therapeutic benefits of green tea extract on various parameters in non-alcoholic fatty liver disease patients. Pak J Med Sci 33 4 —6. Federico A, Dallio M, Masarone M, Gravina AG, Di Sarno R, Tuccillo C, et al.

Evaluation of the effect derived from silybin with vitamin d and vitamin e administration on clinical, metabolic, endothelial dysfunction, oxidative stress parameters, and serological worsening markers in nonalcoholic fatty liver disease patients. Oxid Med Cell Longev Loguercio C, Andreone P, Brisc C, Brisc MC, Bugianesi E, Chiaramonte M, et al.

Silybin combined with phosphatidylcholine and vitamin e in patients with nonalcoholic fatty liver disease: A randomized controlled trial. Free Radic Biol Med 52 9 — Wah Kheong C, Nik Mustapha NR, Mahadeva S.

A randomized trial of silymarin for the treatment of nonalcoholic steatohepatitis. Clin Gastroenterol Hepatol 15 12 — Hashemi S J, Eskandar H, Sardabi EH.

A placebo-controlled trial of silymarin in patients with nonalcoholic fatty liver disease. Hepatitis Monthly , 9 4 : — Solhi H, Ghahremani R, Kazemifar AM, HoseiniYazdi Z.

Silymarin in treatment of non-alcoholic steatohepatitis: A randomized clinical trial. Caspian J Intern Med 5 1 :9— PubMed Abstract Google Scholar. Anushiravani A, Haddadi N, Pourfarmanbar M, Mohammadkarimi V. Treatment options for nonalcoholic fatty liver disease: A double-blinded randomized placebo-controlled trial.

Eur J Gastroenterol Hepatol 31 5 —7. Silymarin in non-cirrhotics with non-alcoholic steatohepatitis: A randomized, double-blind, placebo controlled trial. We demonstrated for the first time that ASE impaired the reduction of pAMPK expression and the increase of HMG-CoA reductase in the liver of mice fed a HF diet.

These findings suggest an important modulation by ASE of AMPK pathway involved in the regulation of body weight, lipid metabolism and glucose homeostasis [ 4 ]. The hepatic steatosis observed in this study is characterized by increased lipid mainly TG levels in the liver.

SREBP-1c plays a unique role in the expression of the genes involved in hepatic TG synthesis and, may play a major role in the pathogenesis of NAFLD [ 46 ]. The lipogenic genes regulated by SREBP-1C, include ACC that converts acetyl-CoA substrate in malonyl-CoA.

Subsequently, malonyl-CoA is converted into palmitate and FA that can be esterified to TG [ 46 ]. A positive energy imbalance, characteristic of this model, chronically activates SREBP1-c, causing lipotoxicity in various organs and tissues.

Insulin seems to play a central role in the activation of SREBP-1c transcription, even with the presence of insulin resistance [ 47 ]. Furthermore, liver pAMPK is known to regulate the synthesis of FA and TG, by inactivating ACC [ 48 ]. These findings suggest a role to ASE in the control of endogenous FA synthesis, accumulation of lipids and lipotoxicity.

Another important aspect of the regulation of lipid metabolism is the liver mitochondrial oxidative function. Several studies in animal models indicate a significant relationship between accumulation of TG, mitochondrial dysfunction and oxidative stress [ 49 ].

It is conceivable that hyperglycemia and high levels of saturated FA can promote greater activation of NADPH oxidase and consequently higher reactive oxygen species ROS generation [ 50 ]. Mitochondria continuously exposed to high levels of ROS can suffer deleterious consequences, such as damage to the respiratory chain in the mitochondrial genome and in lipids and membrane proteins [ 51 ].

These structural and functional alterations in mitochondria may contribute to the reduction of the activities of this organelle as beta oxidation leading to a greater accumulation of free FA [ 52 ]. Associated with this process there is a lower formation of antioxidant enzymes [ 50 ] leading to an imbalance between ROS formation and antioxidant protection featuring oxidative stress.

In the current study, we found a significant increase in MDA and protein carbonyl levels, in the liver of mice fed by HF diet which may be related to mitochondrial dysfunction and may contribute to the accumulation of fat in the liver of these animals [ 50 ].

Furthermore, a significant decrease in hepatic antioxidant enzyme activities was detected in the mice fed a HF diet. Treatment with ASE markedly decreased the MDA and protein carbonylation levels and restored antioxidant activity of SOD, CAT and GPx to levels similar to controls fed by standard diet.

A study by de Oliveira et al showed that high levels of plasma MDA in mice fed by high fat diet were reduced in response to ASE [ 19 ]. Catechin and polymeric proanthocyanidins may be the major contributors to the antioxidant activity of ASE. The present study demonstrated that in HF-fed mice ASE decreased food intake and body mass gain, and ameliorates both adiposity and hepatic steatosis.

The underlying mechanisms may involve reduction in hepatic lipogenesis, which can primarily be attributed to reduced expression of SREBP-1c and increased expression of pAMPK, which negatively modulates ACC and HMG-CoA reductase.

The beneficial effect of ASE can be due to an increase in cholesterol excretion by ABCG8 transporter, as well as the antioxidant effect in liver. Conceived and designed the experiments: ACR RSM PCL DTO AJRS. Performed the experiments: PRBO CAC GFB VSCC IBS LCRMC EPSC GRM PJCS.

Analyzed the data: PRBO CAC GFB EPSC GRM AJRS ACR RSM PCL DTO. Wrote the paper: PRBO CAC ACR RSM AJRS PCL. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field.

Article Authors Metrics Comments Media Coverage Reader Comments Figures. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Data Availability: All relevant data are within the paper.

Introduction Metabolic syndrome MS is a disease composed of different risk factors such as obesity, type 2 diabetes, hypertension or dyslipidemia [ 1 , 2 ]. Materials and Methods Preparation of the acaí seed extract ASE Euterpe oleracea Mart.

Chemical analysis of ASE One gram of the lyophilized extract was suspended in 50 mL of distilled water and the resulting solution was extracted with ethyl acetate 3 x 50 mL.

Animals and Diet This study was carried out in strict accordance with the recommendations in the conventional guidelines for experimentation with animals National Institutes of Health Publication No.

Download: PPT. Table 1. Composition and energy content of standard and high-fat HF diets. Food Consumption and Body Weight Measurements Food consumption of the mice was estimated by subtracting the amount of food left on the grid and amount of spilled food from the initial weight of food supplied.

Western Blot analyses The total hepatic proteins were extracted in a homogenizing buffer with protease inhibitors. Determination of oxidative damage: carbonyl protein and malondialdehyde assay Protein carbonylation was determined from the formation of carbonyl group by reaction with 2,4-dinitrophenylhydrazine 2,4-DNPH according to the method described by Levine et al.

Determination of antioxidant enzyme activity Superoxide dismutase SOD , catalase CAT , and glutathione peroxidase GPx activities were assayed in liver homogenates of mice. Histological analysis of the liver Random fragments of the liver were prepared for light microscopy.

Statistical Analyses Values are expressed as the mean ± standard error of the mean. Results Chemical Composition of ASE Fig 1A shows the chromatogram of the water fraction residue. Fig 2. MALDI-TOF mass spectrum of the aqueous fraction residue from ASE. Table 2. Table 3. Effect of ASE on glycaemia, lipid profile and hepatic steatosis Final blood glucose levels differed significantly between HF groups and controls.

Effect of ASE on the expression of proteins involved in fatty acid and cholesterol synthesis and excretion in liver To investigate the molecular mechanisms involved in the hypolipidemic effect of ASE, the expressions of SREBP1-c, p-ACC, ACC, HMG-CoA reductase and p-AMPK were assessed in the liver of the different groups.

Discussion MS and NAFLD are a major cause of morbidity in developed and developing societies [ 1 , 31 ]. Conclusions The present study demonstrated that in HF-fed mice ASE decreased food intake and body mass gain, and ameliorates both adiposity and hepatic steatosis. Author Contributions Conceived and designed the experiments: ACR RSM PCL DTO AJRS.

References 1. Asrih M, Jornayvaz FR. Metabolic syndrome and nonalcoholic fatty liver disease: Is insulin resistance the link? Mol Cell Endocrinol.

View Article Google Scholar 2. Cao K, Xu J, Zou X, Li Y, Chen C, Zheng A, et al. Hydroxytyrosol prevents diet inducedmmetabolic syndrome and attenuates mitochondrial abnormalities in obese mice. Free Radic Biol Med. Kabir M, Catalano KJ, Ananthnarayan S, Kim SP, Van Citters GW, Dea MK, et al.

Molecular evidence supporting the portal theory: a causative link between visceral adiposity and hepatic insulin resistance. Am J Physiol Endocrinol Metab. Kahn BB, Alquier T, Carling D, Hardie DG. AMP-activated protein kinase: ancient energy gauge provides clues to modern understanding of metabolism.

Cell Metab. Hardie DG, Corton J, Ching YP, Davies SP, Hawley S. Regulation of lipid metabolism by the AMP-activated protein kinase. Biochem Soc Trans ; 25 4 : — Kohjima M, Higuchi N, Kato M, Kotoh K, Yoshimoto T, Fujino T, et al. SREBP-1c, regulated by the insulin and AMPK signaling pathways, plays a role in nonalcoholic fatty liver disease.

Int J Mol Med. Yu L, Li-Hawkins J, Hammer RE, Berge KE, Horton JD, Cohen JC, et al. Overexpression of ABCG5 and ABCG8 promotes biliary cholesterol secretion and reduces fractional absorption of dietary cholesterol.

J Clin Invest. Ceriello A, Motz E. Is oxidative stress the pathogenic mechanism underlying insulin resistance, diabetes, and cardiovascular disease? The common soil hypothesis revisited.

Arterioscler Thromb Vasc Biol. Leung TM, Nieto N: CYP2E1 and oxidant stress in alcoholic and non-alcoholic fatty liver disease.

J Hepatol. Nagata K, Suzuki H, Sakaguchi S: Common pathogenic mechanism in development progression of liver injury caused by non-alcoholic or alcoholic steatohepatitis. J Toxicol Sci.

Sanyal AJ, Chalasani N, Kowdley KV, McCullough A, Diehl AM, Bass NM, et al: Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. N Engl J Med ; — Mazza A, Fruci B, Garinis GA, Giuliano S, Malaguarnera R, Belfiore A: The role of metformin in the management of NAFLD.

Exp Diabetes Res. Ratziu V, Charlotte F, Bernhardt C, Giral P, Halbron M, Lenaour G, et al. Long-term efficacy of rosiglitazone in nonalcoholic steatohepatitis: results of the fatty liver improvement by rosiglitazone therapy FLIRT 2 extension trial. Hepatology ; — McCarthy EM, Rinella ME: The role of diet and nutrient composition in nonalcoholic Fatty liver disease.

J Acad Nutr Diet ; — Schauss AG, Wu X, Prior RL, Ou B, Huang D, Owens J, et al. Antioxidant capacity and other bioactivities of the freeze-dried Amazonian palm berry, Euterpe oleraceae mart. J Agric Food Chem. Moura RS, Ferreira TS, Lopes AA, Pires KM, Nesi RT, Resende AC, et al.

Effects of Euterpe oleracea Mart. Açaí extract in acute lung inflammation induced by cigarette smoke in the mouse.

Phytomedicine ;19 3—4 : — Rocha AP, Carvalho LC, Sousa MA, Madeira SV, Sousa PJ, Tano T, et al. Endothelium-dependent vasodilator effect of Euterpe oleracea Mart. Acai extracts in mesenteric vascular bed of the rat.

Vascul Pharmacol. da Costa CA, de Oliveira PR, de Bem GF, de Cavalho LC, Ognibene DT, da Silva AF, et al. Naunyn Schmiedebergs Arch Pharmacol. Oliveira PR, da Costa CA, de Bem GF, de Cavalho LCRM, de Souza MA, de Lemos Neto et al.

Effects of an extract obtained from fruits of Euterpe oleracea Mart. J Cardiovasc Pharmacol. Peng Z, Hayasaka Y, Iland PG, Sefton M, Høj P, Waters EJ.

Quantitative analysis of polymeric procyanidins Tannins from grape Vitis vinifera seeds by reverse phase high-performance liquid chromatography. Kennedy JA, Jones GP. Analysis of proanthocyanidin cleavage products following acid-catalysis in the presence of excess phloroglucinol.

A research review highlights research that associates moderate green tea consumption with lower levels of two enzymes: alanine aminotransferase ALT and aspartate aminotransferase AST. Both enzymes may increase due to liver injury. In rare cases, green tea extract may cause an increase in these enzymes or of acute liver injury.

In these cases, stopping green tea extract consumption typically induced liver recovery. A systematic review suggests that green tea effects may depend on the health status of the individual, offering moderate benefits to people with nonalcoholic fatty liver disease NAFLD but increasing liver enzymes in people without NAFLD.

A randomized clinical trial found that milligrams mg of garlic powder over 15 weeks significantly improved fat-build ups and comorbidity risk in people with NAFLD.

A population study of adults in China suggests that raw garlic consumption may also reduce the risk of liver cancer. According to a systematic review from , garlic supplementation may also lower AST levels but does not impact ALT levels. However, they highlight that more research is necessary to confirm this effect.

Many dark berries — including blueberries , raspberries , and cranberries — contain antioxidants called polyphenols , which may help protect the liver from damage. Several animal studies have investigated the effect of berries on the liver. For example, a study suggests that blueberry and cranberry polyphenols reduced liver damage in rats.

A study suggests that blueberries reduced liver fibrosis in rats, lowering the rate of liver weight gain and liver enzyme activity. A study also suggests that blueberries may help to manage age-related liver disease and dysfunction in rats.

However, further research is necessary to determine the effect of berry polyphenols on the liver in humans. A study suggests a compound in grape skin and seeds alleviates symptoms of severe liver problems in rats, including liver enlargement, inflammation, and fat buildups. Eating whole, seeded grapes is a simple way to add these compounds to the diet.

A grape seed extract supplement may also provide antioxidants. Grapefruit contains two primary antioxidants: naringin and naringenin. These may help protect the liver from injury by reducing inflammation and protecting the liver cells. A study suggests that naringin may protect against alcohol-induced liver steatosis by reducing oxidative stress.

However, some medications can interact with grapefruit, so people should check with a doctor before adding grapefruit or grapefruit juice to their diet. The fruit and juice of the prickly pear may also be beneficial to liver health. A article suggests that prickly pear extracts show beneficial effects on the liver in animal studies.

However, more research is necessary to determine the bioactive compound that causes these effects, the most appropriate dose, and whether the effects apply to human models. A review associates plant-based diets with a lower risk of NAFLD and liver fat content.

Plant foods they group as healthful include:. Consuming fatty fish and fish oil supplements may help reduce the impact of conditions such as NAFLD. A population-based cohort study also associates regular fish oil supplementation with lower risks of liver cancer.

Fatty fish is rich in omega-3 fatty acids, which are the good fats that help reduce inflammation. These fats may be especially helpful in the liver, as they appear to prevent the buildup of excess fats and maintain enzyme levels in the liver.

Eating nuts may be another simple way to keep the liver healthy and protect against NAFLD. Nuts generally contain unsaturated fatty acids, vitamin E , and antioxidants.

These compounds may help prevent NAFLD and reduce inflammation and oxidative stress. Eating too much fat is not good for the liver, but some fats may help it.

A study suggests olive oil, as part of the Mediterranean diet , may help reduce oxidative stress and improve liver function.

Background: Dietary polyphenol degoxification of non-alcoholic fatty liver disease NAFLD is a Polyphenols and liver detoxification direction, and the existing clinical studies detoxifiication little Polyphenols and liver detoxification evidence for its therapeutic Fitness and weight loss, and some Potassium and energy production have inconsistent results. The Polypuenols of dietary polyphenols in the treatment of NAFLD is still controversial. The aim of this study was to evaluate the therapeutic efficacy of oral dietary polyphenols in patients with NAFLD. Methods: The literature both Chinese and English published before 30 April in PubMed, Cochrane, Medline, CNKI, and other databases on the treatment of NAFLD with dietary polyphenols was searched. Manual screening, quality assessment, and data extraction of search results were conducted strictly according to the inclusion and exclusion criteria. Polyphenols and liver detoxification

Author: Mazuramar

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