Liver Cleanse & Detox
Milk Thistle
Milk thistle in liver diseases: past, present, future
Abstract
Silybum marianum or milk thistle (MT) is the most well-researched plant in the treatment of liver disease. The active complex of MT is a lipophilic extract from the seeds of the plant and is composed of three isomer flavonolignans (silybin, silydianin, and silychristin) collectively known as silymarin. Silybin is a component with the greatest degree of biological activity and makes up 50% to 70% of silymarin. Silymarin is found in the entire plant but it is concentrated in the fruit and seeds. Silymarin acts as an antioxidant by reducing free radical production and lipid peroxidation, has antifibrotic activity and may act as a toxin blockade agent by inhibiting binding of toxins to the hepatocyte cell membrane receptors. In animals, silymarin reduces liver injury caused by acetaminophen, carbon tetrachloride, radiation, iron overload, phenylhydrazine, alcohol, cold ischaemia and Amanita phalloides. Silymarin has been used to treat alcoholic liver disease, acute and chronic viral hepatitis and toxin-induced liver diseases.
Source: Ludovico Abenavoli, Raffaele Capasso, Natasa Milic, and Francesco Capasso. “Milk thistle in liver diseases: past, present, future” Physiotherapy Research (2010): 24(10):1423-32.
Dandelion
Purification, Preliminary Characterization and Hepatoprotective Effects of Polysaccharides from Dandelion Root
Abstract
In this study, purification, preliminary characterization and hepatoprotective effects of water-soluble polysaccharides from dandelion root (DRP) were investigated. Two polysaccharides, DRP1 and DRP2, were isolated from DRP. The two polysaccharides were α-type polysaccharides and didn’t contain protein. DRP1, with a molecular weight of 5695 Da, was composed of glucose, galactose and arabinose, whereas DRP2, with molecular weight of 8882 Da, was composed of rhamnose, galacturonic acid, glucose, galactose and arabinose. The backbone of DRP1 was mainly composed of (1→6)-linked-α-d-Glc and (1→3,4)-linked-α-d-Glc. DRP2 was mainly composed of (1→)-linked-α-d-Ara and (1→)-linked-α-d-Glc. A proof-of-concept study was performed to assess the therapeutic potential of DRP1 and DRP2 in a mouse model that mimics acetaminophen (APAP) -induced liver injury (AILI) in humans. The present study shows DRP1 and DRP2 could protect the liver from APAP-induced hepatic injury by activating the Nrf2-Keap1 pathway. These conclusions demonstrate that the DRP1 and DRP2 might be suitable as functional foods and natural drugs in preventing APAP-induced liver injury.
Source: Liangliang Cai, Dongwei Wan, Fanglian Yi, and Libiao Luan. “Purification, Preliminary Characterization and Hepatoprotective Effects of Polysaccharides from Dandelion Root” Molecules – Advances in Natural Polysaccharides Research (2017): 22(9), 1409.
L-Methionine
Methionine metabolism in chronic liver diseases: an update on molecular mechanism and therapeutic implication
Abstract
As one of the bicyclic metabolic pathways of one-carbon metabolism, methionine metabolism is the pivot linking the folate cycle to the transsulfuration pathway. In addition to being a precursor for glutathione synthesis, and the principal methyl donor for nucleic acid, phospholipid, histone, biogenic amine, and protein methylation, methionine metabolites can participate in polyamine synthesis. Methionine metabolism disorder can aggravate the damage in the pathological state of a disease. In the occurrence and development of chronic liver diseases (CLDs), changes in various components involved in methionine metabolism can affect the pathological state through various mechanisms. A methionine-deficient diet is commonly used for building CLD models. The conversion of key enzymes of methionine metabolism methionine adenosyltransferase (MAT) 1 A and MAT2A/MAT2B is closely related to fibrosis and hepatocellular carcinoma. In vivo and in vitro experiments have shown that by intervening related enzymes or downstream metabolites to interfere with methionine metabolism, the liver injuries could be reduced. Recently, methionine supplementation has gradually attracted the attention of many clinical researchers. Most researchers agree that adequate methionine supplementation can help reduce liver damage. Retrospective analysis of recently conducted relevant studies is of profound significance. This paper reviews the latest achievements related to methionine metabolism and CLD, from molecular mechanisms to clinical research, and provides some insights into the future direction of basic and clinical research.
Source: Zhanghao Li, Feixia Wang Baoyu Liang, Ying Su, Sumin Sun, Siwei Xia, Jiangjuan Shao, Zili Zhang, Min Hong, Feng Zhang, and Shizhong Zheng. “Methionine metabolism in chronic liver diseases: an update on molecular mechanism and therapeutic implication” Signals Transduction and Targeted Therapy (2020): 5(1):280.
Artichoke
Effects of Artichoke Supplementation on Liver Enzymes: A Systematic Review and Meta-Analysis of Randomized Controlled Trials
Abstract
Studies examining the effect of artichoke on liver enzymes have reported inconsistent results. This systematic review and meta-analysis aimed to assess the effects of artichoke administration on the liver enzymes. PubMed, Embase, the Cochrane Library, and Scopus databases were searched for articles published up to January 2022. Standardized mean difference (Hedges’ g) were analyzed using a random-effects model. Heterogeneity, publication bias, and sensitivity analysis were assessed for the liver enzymes. Pooled analysis of seven randomized controlled trials (RCTs) suggested that the artichoke administration has an effect on both alanine aminotransferase (ALT) (Hedges’ g, −1.08; 95% confidence interval [CI], −1.76 to −0.40; p = 0.002), and aspartate aminotransferase (AST) (Hedges’ g, −1.02; 95% CI, −1.76 to −0.28; p = 0.007). Greater effects on ALT were detected in trials that lasted ≤8 weeks. Also, greater effects on AST were detected in trials using > 500 mg artichoke. Overall, this meta-analysis demonstrated artichoke supplementation decreased ALT and AST.
Source: Mohammad Reza Amini, Fatemeh Sheikhhossein, Alireza Talebyan, Elham Bazshahi, Farhang Djafari, and Azita Hekmatdoost. “Effects of Artichoke Supplementation on Liver Enzymes: A Systematic Review and Meta-Analysis of Randomized Controlled Trials” Clinical Nutrition Research (2022): 11(3): 228–239.
Curcumin (Turmeric)
Curcumin in Liver Diseases: A Systematic Review of the Cellular Mechanisms of Oxidative Stress and Clinical Perspective
Abstract
Oxidative stress has been considered a key causing factor of liver damage induced by a variety of agents, including alcohol, drugs, viral infections, environmental pollutants and dietary components, which in turn results in progression of liver injury, non-alcoholic steatohepatitis, non-alcoholic liver disease, liver fibrosis and cirrhosis. During the past 30 years and even after the major progress in the liver disease management, millions of people worldwide still suffer from an acute or chronic liver condition. Curcumin is one of the most commonly used indigenous molecules endowed by various shielding functionalities that protects the liver. The aim of the present study is to comprehensively review pharmacological effects and molecular mechanisms, as well as clinical evidence, of curcumin as a lead compound in the prevention and treatment of oxidative associated liver diseases. For this purpose, electronic databases including “Scopus,” “PubMed,” “Science Direct” and “Cochrane library” were extensively searched with the keywords “curcumin or curcuminoids” and “hepatoprotective or hepatotoxicity or liver” along with “oxidative or oxidant.” Results showed that curcumin exerts remarkable protective and therapeutic effects of oxidative associated liver diseases through various cellular and molecular mechanisms. Those mechanisms include suppressing the proinflammatory cytokines, lipid perodixation products, PI3K/Akt and hepatic stellate cells activation, as well as ameliorating cellular responses to oxidative stress such as the expression of Nrf2, SOD, CAT, GSH, GPx and GR. Taking together, curcumin itself acts as a free radical scavenger over the activity of different kinds of ROS via its phenolic, β-diketone and methoxy group. Further clinical studies are still needed in order to recognize the structure-activity relationships and molecular mechanisms of curcumin in oxidative associated liver diseases.
Source: Mohammad Hosein Farzaei, Mahdi Zobeiri, Fatemeh Parvizi, Fardous F. El-Senduny, Ilias Marmouzi, Ericsson Coy-Barrera, Rozita Naseri, Seyed Mohammad Nabavi, Roja Rahimi, and Mohammad Abdollahi. “Curcumin in Liver Diseases: A Systematic Review of the Cellular Mechanisms of Oxidative Stress and Clinical Perspective” Nutrients (2018): 10(7): 855.
Beet Root
Beta vulgaris L. (Beetroot) Methanolic Extract Prevents Hepatic Steatosis and Liver Damage in T2DM Rats by Hypoglycemic, Insulin-Sensitizing, Antioxidant Effects, and Upregulation of PPARα
Abstract
The present study examined if methanolic beetroot extract (BE) could prevent dyslipidemia and hepatic steatosis and damage in a type-2 diabetes mellitus (T2DM) rat model and studied some mechanisms of action. T2DM was induced in adult male Wistar rats by a low single dose of streptozotocin (STZ) (35 mg/kg, i.p) and a high-fat diet (HFD) feeding for 5 weeks. Control or T2DM rats then continued on standard or HFDs for another 12 weeks and were treated with the vehicle or BE (250 or 500 mg/kg). BE, at both doses, significantly improved liver structure and reduced hepatic lipid accumulation in the livers of T2DM rats. They also reduced body weight gain, serum glucose, insulin levels, serum and hepatic levels of cholesterol, triglycerides, free fatty acids, and serum levels of low-density lipoproteins in T2DM rats. In concomitant, they significantly reduced serum levels of aspartate and alanine aminotransferases, hepatic levels of malondialdehyde, tumor-necrosis factor-α, interleukin-6, and mRNA of Bax, cleaved caspase-3, and SREBP1/2. However, both doses of BE significantly increased hepatic levels of total glutathione, superoxide dismutase, and mRNA levels of Bcl2 and PPARα in the livers of both the control and T2DM rats. All of these effects were dose-dependent and more profound with doses of 500 mg/kg. In conclusion, chronic feeding of BE to STZ/HFD-induced T2DM in rats prevents hepatic steatosis and liver damage by its hypoglycemic and insulin-sensitizing effects and its ability to upregulate antioxidants and PPARα.Source: Laila Naif Al-Harbi, Ghedeir M Alshammari, Alhanouf Mohammed Al-Dossari, Pandurangan Subash-Babu, Manal Abdulaziz Binobead, Maha H Alhussain, Sahar Abdulaziz AlSedairy, Doha M Al-Nouri, and Ghalia Shamlan. “Beta vulgaris L. (Beetroot) Methanolic Extract Prevents Hepatic Steatosis and Liver Damage in T2DM Rats by Hypoglycemic, Insulin-Sensitizing, Antioxidant Effects, and Upregulation of PPARα” Biology (Basel) (2021): 10(12):1306.
Chicory Root & Turmeric
Turmeric and chicory seed have beneficial effects on obesity markers and lipid profile in non-alcoholic fatty liver disease (NAFLD)
Abstract
In an attempt to investigate new strategies aimed at reducing risk factors of non-alcoholic fatty liver disease (NAFLD), effects of turmeric (Curcuma longa L.) and chicory seed (Cichorium intybus L.) supplementation was evaluated in these patients. In this double-blind, randomized, controlled clinical trial, 92 patients with NAFLD aged 20-60 year with body mass index (BMI) ranged 24.9-40 kg/m2 was randomly assigned to 4 groups as follows. 1) Turmeric supplementation (3 g/d) (n = 23, TUR); 2) Chicory seed supplementation (infused 9 g/d (4.5 g /100mL)) (n = 23, CHI); 3) Turmeric and chicory seed supplementation (3 g/d turmeric + infused 9 g/d chicory seed (n = 23, TUR + CHI); 4) Placebo (n = 23, PLA). All intervention periods were 12 weeks. Fasting blood samples, anthropometric measurements, dietary records and physical activity were collected at baseline and at the end of the trial. Significant decreases were observed in BMI and waist circumference (WC) of subjects in CHI and TUR + CHI groups, compared with PLA group (p < 0.05). Combination of turmeric and chicory seed significantly decreased serum alkaline phosphatase level (p < 0.05). Serum levels of HDL-C increased considerably in TUR and TUR + CHI groups (p < 0.05 vs. placebo). Turmeric supplementation alone and plus chicory seed led to significant reduction in serum levels of TG/HDL-C and LDL-C/HDL-C ratio in TUR and TUR + CHI groups in comparison with placebo (p < 0.05). In conclusion, turmeric and chicory seed supplementation can be significantly useful in management of NAFLD risk factors.
Source: Aida Ghaffari, Maryam Rafraf, Roya Navekar, Bita Sepehri, Mohammad Asghari-Jafarabadi, and Seyyed-Mostafa Ghavami. “Turmeric and chicory seed have beneficial effects on obesity markers and lipid profile in non-alcoholic fatty liver disease (NAFLD)” International Journal of Biological Macromolecules (2019): 89(5-6):293-302.
Black Pepper (Piperine)
Piperine attenuates cardiovascular, liver and metabolic changes in high
Abstract
Black pepper is used worldwide to enhance food flavor. We investigated dietary supplementation with piperine, the active principle of black pepper, to high carbohydrate, high fat (HCHF) diet-fed rats as a model of human metabolic syndrome. Rats were fed with either HCHF diet (carbohydrate, 52%; fat, 24%; 25% fructose in drinking water) or cornstarch (CS) diet for a total of 16 weeks. Diets of the treatment groups (CS + piperine and HCHF + piperine) were supplemented with piperine for the last 8 weeks of this protocol. After 16 weeks, rats fed with HCHF diet developed hypertension, elevated oxidative stress and inflammation-induced cardiac changes (infiltration of inflammatory cells in heart, increase in count and degranulation of mast cells in heart, cardiac fibrosis and increase in ventricular stiffness), reduced responsiveness of aortic rings, impaired glucose tolerance, abdominal obesity together with liver fibrosis, fat deposition and increased plasma liver enzymes. Supplementation with piperine (375 mg/kg food; approximately 30 mg/kg/day) in HCHF-fed rats normalized blood pressure, improved glucose tolerance and reactivity of aortic rings, reduced plasma parameters of oxidative stress and inflammation, attenuated cardiac and hepatic inflammatory cell infiltration and fibrosis and improved liver function. These changes clearly suggest that piperine reduces symptoms of human metabolic syndrome in HCHF-fed rats by reducing inflammation and oxidative stress.
Source: Vishal Diwan, Hemant Poudyal, and Lindsay Brown. “Piperine attenuates cardiovascular, liver and metabolic changes in high carbohydrate, high fat-fed rats” Cell Biochemistry and Biophysics (2013): 67(2):297-304.
Ginger
Ginger Supplementation in Nonalcoholic Fatty Liver Disease: A Randomized, Double-Blind, Placebo-Controlled Pilot Study
Abstract
Background: Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases worldwide. The pathogenesis of this disease is closely associated with obesity and insulin resistance. Ginger can have hypolipidemic and antioxidant effects, and act as an insulin sensitizer.
Objectives: The aim of this study was to evaluate the effects of ginger supplementation in NAFLD management. Patients and Methods: In a randomized, double-blind, placebo-controlled clinical trial, 44 patients with NAFLD were assigned to take either two grams per day of a ginger supplement or the identical placebo, for 12 weeks. In both groups, patients were advised to follow a modified diet and physical activity program. The metabolic parameters and indicators of liver damage were measured at study baseline and after the 12 week intervention.
Results: Ginger supplementation resulted in a significant reduction in alanine aminotransferase, γ-glutamyl transferase, inflammatory cytokines, as well as the insulin resistance index and hepatic steatosis grade in comparison to the placebo. We did not find any significant effect of taking ginger supplements on hepatic fibrosis and aspartate aminotransferase.
Conclusions: Twelve weeks of two grams of ginger supplementation showed beneficial effects on some NAFLD characteristics. Further studies are recommended to assess the long-term supplementation effects.
Source: Mehran Rahimlou, Zahra Yari, Azita Hekmatdoost, Seyed Moayed Alavian, and Seyed Ali Keshavarz. “Ginger Supplementation in Nonalcoholic Fatty Liver Disease: A Randomized, Double-Blind, Placebo-Controlled Pilot Study” (2016): 16(1): e34897.
Zinc
Long-Term Zinc Supplementation Improves Liver Function and Decreases the Risk of Developing Hepatocellular Carcinoma
Abstract
Zinc plays a pivotal role in various zinc enzymes, which are crucial in the maintenance of liver function. Patients with chronic liver diseases (CLDs) usually have lower concentrations of zinc, which decrease further as liver fibrosis progresses. Whether long-term zinc supplementation improves liver function and reduces the risk of hepatocellular carcinoma (HCC) development remains unknown. Two hundred and sixty-seven patients with CLDs who received a zinc preparation (Zn-group; 196 patients), or who did not receive zinc (no Zn-treatment group; 71 patients), were retrospectively analyzed in this study. The Zn-group was divided into 4 groups according to their serum Zn concentrations at 6 months after the start of Zn treatment. Liver function significantly deteriorated in the no Zn-treatment group, while no notable change was observed in the Zn-group. The cumulative incidence rates of events and HCC at 3 years were observed to be lower in the Zn-group (9.5%, 7.6%) than in the no Zn-treatment group (24.9%, 19.2%) (p < 0.001). According to serum Zn concentrations, the cumulative incidence rates of events and HCC were significantly decreased in patients with Zn concentrations ≥ 70 µg/dL (p < 0.001). Zinc supplementation appears to be effective at maintaining liver function and suppressing events and HCC development, especially among patients whose Zn concentration is greater than 70 µg/dL.
Source: Atsushi Hosui, Eiji Kimura, Sumiko Abe, Takashi Tanimoto, Kousaku Onishi, Yukihiro Kusumoto, Yuka Sueyoshi, Kengo Matsumoto, Motohiro Hirao, Takuya Yamada, and Naoki Hiramatsu. “Long-Term Zinc Supplementation Improves Liver Function and Decreases the Risk of Developing Hepatocellular Carcinoma” Nutrients (2018): 10(12): 1955.
Celery
Inhibitory effect of celery seeds extract on chemically induced hepatocarcinogenesis: modulation of cell proliferation, metabolism and altered hepatic foci development
Abstract
The chemopreventive activity of methanolic extract of Apium graveolens seeds (celery seeds) has been investigated against Solt Farber protocol of hepatocarcinogenesis, oxidative stress and induction of positive foci of gamma-GT in the liver of Wistar rats. The prophylactic treatment of celery seeds extract protected dose dependently against diethylnitrosoamine (DEN)+2-acetylaminofluorine (AAF)+partial hepatectomy (PH) induced hepatocarcinogenesis and other related events such as induction of gamma-GT positive foci (P<0.001). 2-AAF administration in diet with PH in rats resulted in increased hepatic ornithine decarboxylase (ODC) activity and a consequent increase in the rate of DNA synthesis when compared to saline treated control group while pretreatment of rats with celery seeds extract resulted in inhibition of aforementioned parameters dose dependently. The augmentation of quinone reductase (QR), glutathione-S-transferase (GST) and serum gamma-glutamyl transpeptidase (GGT) activities; and depletion of the tissue GSH content after 2-AAF (i.p. injection) for five consecutive days was prevented with the administration of celery seed extract. On the basis of the above results it can be said that A. graveolens is a potent plant against experimentally induced hepatocarcinogenesis in Wistar rats.
Source: Sarwat Sultana, Salahuddin Ahmed, Tamanna Jahangir, and Sonia Sharma. “Inhibitory effect of celery seeds extract on chemically induced hepatocarcinogenesis: modulation of cell proliferation, metabolism and altered hepatic foci development” Cancer Letters (2005): 221(1):11-20.
Red Raspberry
Antioxidant properties of red raspberry extract alleviate hepatic fibrosis via inducing apoptosis and transdifferentiation of activated hepatic stellate cells
Abstract
Hepatic fibrosis is a wound-healing process caused by prolonged liver damage and often occurs due to hepatic stellate cell activation in response to reactive oxygen species (ROS). Red raspberry has been found to attenuate oxidative stress, mainly because it is rich in bioactive components. In the current study, we investigated the inhibitory effects and associated molecular mechanisms of red raspberry extract (RBE) upon activated hepatic stellate cell (aHSC) in cellular and rat models. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were increased in the dimethylnitrosamine (DMN)-applied samples, whereas treatment of RBE significantly suppressed the activities of these enzymes. In addition, a histopathological analysis demonstrated that RBE could substantially diminish the hepatic collagen content and alpha-smooth muscle actin (α-SMA) expression induced by DMN. Administration of 250 μg/mL RBE could also arrest the growth and enhance the apoptosis of activated HSC-T6 cells, which was accompanied with elevated levels of activated caspases and poly (ADP-ribose) polymerase (PARP) cleavage. Particularly, RBE application remarkably abolished oxidative damage within the cells and reduced the carbonylation of proteins, which was attributed to the upregulation of catalase, nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1). Moreover, the knockdown of Nrf2 together with the RBE treatment synergistically abrogated the expression of α-SMA and promoted the level of peroxisome proliferator-activated receptor gamma (PPAR-γ), suggesting that RBE could mitigate the transdifferentiation of HSC in a Nrf2-independent manner. These findings implied that the application of RBE could effectively remove oxidative stress and relieve the activation of HSC via modulating the caspase/PARP, Nrf2/HO-1 and PPAR-γ pathways, which may allow the development of novel therapeutic strategies against chemical-caused liver fibrogenesis.
Source: Tung-Ho Wu, Pei-Wen Wang, Tung-Yi Lin, Pei-Ming Yang, Wen-Tai Li, Chau-Ting Yeh and ai-Long Pan. “Antioxidant properties of red raspberry extract alleviate hepatic fibrosis via inducing apoptosis and transdifferentiation of activated hepatic stellate cells” Biomedicine and Pharmacotherapy (2021): 144:112284.
Berberine
Therapeutic Effects of Berberine on Liver Fibrosis are associated With Lipid Metabolism and Intestinal Flora
Abstract
Liver cirrhosis is a form of liver fibrosis resulting from chronic hepatitis caused by various liver diseases, such as viral hepatitis, alcoholic liver damage, nonalcoholic steatohepatitis, autoimmune liver disease, and by parasitic diseases such as schistosomiasis. Liver fibrosis is the common pathological base and precursors of cirrhosis. Inflammation and disorders of lipid metabolism are key drivers in liver fibrosis. Studies have determined that parts of the arachidonic acid pathway, such as its metabolic enzymes and biologically active products, are hallmarks of inflammation, and that aberrant peroxisome proliferator-activated receptor gamma (PPARγ)-mediated regulation causes disorders of lipid metabolism. However, despite the ongoing research focus on delineating the mechanisms of liver fibrosis that underpin various chronic liver diseases, effective clinical treatments have yet to be developed. Berberine (BBR) is an isoquinoline alkaloid with multiple biological activities, such as anti-inflammatory, anti-bacterial, anti-cancer, and anti-hyperlipidemic activities. Many studies have also found that BBR acts via multiple pathways to alleviate liver fibrosis. Furthermore, the absorption of BBR is increased by nitroreductase-containing intestinal flora, and is strengthened via crosstalk with bile acid metabolism. This improves the oral bioavailability of BBR, thereby enhancing its clinical utility. The production of butyrate by intestinal anaerobic bacteria is dramatically increased by BBR, thereby amplifying butyrate-mediated alleviation of liver fibrosis. In this review, we discuss the effects of BBR on liver fibrosis and lipid metabolism, particularly the metabolism of arachidonic acid, and highlight the potential mechanisms by which BBR relieves liver fibrosis through lipid metabolism related and intestinal flora related pathways. We hope that this review will provide insights on the BBR-based treatment of liver cirrhosis and related research in this area, and we encourage further studies that increase the ability of BBR to enhance liver health.
Source: Liu Xianzhi, Wang Lifu, Tan Siwei, Chen Zebin, Wu Bin, and Wu Xiaoying. “Therapeutic Effects of Berberine on Liver Fibrosis are associated With Lipid Metabolism and Intestinal Flora” Frontiers in Pharmacology Sec. Gastrointestinal and Hepatic Pharmacology (2022): Vol 13. https://doi.org/10.3389/fphar.2022.814871
Grape Seed
Grape seed extract to improve liver function in patients with nonalcoholic fatty liver change
Abstract
Background/aim: Therapeutic interventions in nonalcoholic fatty liver disease are limited, while anti-oxidative materials have shown benefits in animal models. This study aimed to evaluate grape seed extract as an anti-oxidative material in this process. Therapeutic effects of grape seed extract were evaluated in comparison to vitamin C in a double-blind setting.
Materials and methods: Fifteen patients were enrolled in each group. Liver function tests were done; also, grade of steatosis and pattern of echogenicity of the liver were determined. Patients were followed up by the same evaluation repeated in first, second and third months.
Results: Mean age +/- standard deviation was 43.2 +/- 10.3 years. Grape seed extract (GSE) significantly improved the grade of fatty liver change; and resulted in significant decrease in alanine aminotransferase in patients receiving the concentrate compared to those receiving vitamin C independently, from the initial grade of steatosis.
Conclusions: This study describes the beneficial effect of using grape seed extract for three months in patients with nonalcoholic fatty liver disease. These results may improve with a longer period of follow-up.
Source: Manouchehr Khoshbaten, Akbar Aliasgarzadeh, Koorosh Masnadi, Sara Farhang, Mohammad K Tarzamani, Hosain Babaei, Javad Kiani, Maryam Zaare, and Farzad Najafipoor. “Grape seed extract to improve liver function in patients with nonalcoholic fatty liver change” Saudi Journal of Gastroenterology (2010): 16(3):194-7.
References:
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