Evaluation of L-Carnitine Efficacy in the Treatment of Non-Alcoholic Fatty Liver Disease among Diabetic Patients: A Randomized Double Blind Pilot Study

Pezhman Alavinejad, Mehrnoosh Zakerkish, Eskandar Hajiani, Seyed Jalal Hashemi, Mahmoud Chobineh, Elham Karimi Moghaddam

Pezhman Alavinejad, Eskandar Hajiani, Seyed Jalal Hashemi, Research Center for Infectious Diseases of Digestive System, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Pezhman Alavinejad, Assistant Professor of Gastroenterology and Hepatology, GI Department, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Mehrnoosh Zakerkish, Assistant Professor of Endocrinology, Department of Endocrinology, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Eskandar Hajiani, Seyed Jalal Hashemi, Associate Professor of Gastroenterology and Hepatology, GI Department, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Mahmoud Chobineh, Resident of Internal Medicine, Department of Internal Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Elham Karimi Moghaddam, Assistant Professor of Gynecology, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

Correspondence to: Pezhman Alavinejad, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Email: pezhmanalavinejad@gmail.com
Telephone: +0037068463001
Received: July 26, 2016
Revised: September 25, 2016
Accepted: October 7, 2016
Published online: October 21, 2016


AIM: Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases worldwide and while its pathophysiology is still unverified, most of the present theories are based on Insulin resistance and oxidative stress as key factors. According to role of L-Carnitine in the process of fatty acid oxidation and glucose metabolism, it seems that this drug could be potentially effective in the treatment of diabetic patients suffering from NAFLD. This study has been designed to evaluate this potential therapeutic effect.

METHOD: 60 type 2 diabetic patients with NAFLD based on sonographic findings and elevated serum transaminases randomly divided into 2 groups. The intervention group (A) treated with L-Carnitine 750mg TDS while the control group (B) received placebo. After 3 months intervention the level of liver transaminases and sonographic degree of fatty liver compared between 2 groups.

RESULT: After three months of intervention, in group A the level of AST decreased from 122.7 ± 13.6 to 96.3 ± 7 while in group B raised from 125 ± 14 to 126 ± 11 (p < 0.001). The level of ALT in group A declined from 124.5 ± 11.3 to 82.1 ± 5.2 and in placebo group decreased from 120 ± 10.8 to 115.1 ± 6.3 (p < 0.001) In comparison of average level of AST and ALT between 2 groups, we found a meaningful decline in the serum level of liver transaminases in group A (p < 0.001) while there were no significant reduction in serum level of Cholesterol, TG and FBS (p > 0.05) and also the sonographic degree of fatty liver didn't change among 2 groups.

CONCLUSION: It seems that L-Carnitine is effective in treatment of NAFLD among diabetic patients and could be a potential therapeutic approach in such patients. We recommend these findings to further be verified in future studies (www.irct.ir: IRCT2014020316348N2).

Key words: NAFLD; L-Carnitine; Liver transaminases; Diabetic patients

© 2016 The Authors. Published by ACT Group Ltd.

Alavinejad P, Zakerkish M, Hajiani E, Hashemi SJ, Chobineh M, Moghaddam EK. Evaluation of L-Carnitine Efficacy in the Treatment of Non-Alcoholic Fatty Liver Disease among Diabetic Patients: A Randomized Double Blind Pilot Study. Journal of Gastroenterology and Hepatology Research 2016; 5(5): 2191-2195 Available from: URL: http: //www.ghrnet.org/index.php/joghr/article/view/1804


TDS: tree times / day

TG: triglyceride

FBS: fasting blood sugar


Nonalcoholic fatty liver disease (NAFLD) results from accumulation of fatty droplets in human hepatocytes and its prevalence is increasing worldwide due to overweight and obesity epidemic and sedentary life style among communities[1,2]. NAFLD represent a spectrum of clinical and pathologic situations and range from simple steatosis to nonalcoholic steatohepatitis (NASH), liver fibrosis, cirrhosis and finally hepatocellular carcinoma[3-5]. This condition is one of the most common liver diseases among western countries, currently 2 to 3 times more prevalent than hepatitis B, C and or alcohol related liver disorders and consider as the most common reason of disturbed liver function tests[6,7]. Its prevalence has been reported to be about 10 to 24% in general population and up to 75% among obese subjects[3,8,9]. Recent surveys in eastern countries have also revealed an increasing incidence of fatty liver due to changes in life style, tendency toward sedentary life, low physical activity, central obesity and diabetes Mellitus type 2 and population based studies estimated its prevalence about 15 to 30% of community and comparable to western countries[5,10-14].

The term of NASH is used to show the severity of hepatocytes injury and its similarity to alcoholic steatohepatitis without any history of alcohol consumption[3,8]. The risk factors of NASH include insulin resistance, oxidative stress, stellate cell activation, cellular apoptosis and infiltration of inflammatory cytokines[3,9,15-18]. Concomitance of NASH with abdominal obesity, hypertension, dyslipidemia and glucose intolerance has been known as Metabolic or X syndrome and Diabetes Mellitus type 2 (T2DM) as a complication of obesity has been found in 34 to 74% of cases of NASH[9,19-21].

The most common clinical presentation of these patients include elevation of liver transaminases during routine laboratory exams though hepatomegaly is also prevalent. ALT and AST have been elevated in 70-100% of patients and usually the AST/ALT ratio is less than 1 although a normal transaminase level cannot exclude histological involvement of liver[4,10,22].

The higher plasma concentration of free fatty acids among obese people per se could be a risk factor for T2DM and based on overlap of insulin resistance and obesity between NASH and T2DM, it is supposable that effective medications on each condition be able to affect positively the other one[23,24]. L-Carnitine affects intracellular reactions and could decrease response of inflammatory mediators by restriction of oxidative stress. It also stabilize the cellular wall by inhibiting transmission of fatty acids, detoxification of their toxic metabolites, regulation of intra mitochondrial Acyl CoA/CoA ratio and increasing catabolism of glucose[25-28].

Based on increasing prevalence of non-alcoholic fatty liver and T2DM, their concordance and recent alteration of nutritional and life style among communities, evaluation of these conditions is important and according to role of L-Carnitine in fatty acid oxidation and glucose catabolism, it seems that this drug be able to positively affect the type II diabetic patients who concomitantly involved by nonalcoholic fatty liver. So this randomized pilot study designed to evaluate the potential therapeutic effects of L-Carnitine on fatty liver of diabetic patients.


In this randomized double blind pilot study, 60 type 2 diabetic patients whom also diagnosed concomitantly as non-alcoholic fatty liver based on sonographic findings and elevated liver transaminases included during a 2 months period. The target community selected from diabetic patients who attended in endocrinology outpatient clinics of Ahvaz Jundishapur University. Inclusion criteria included known history of diabetes Mellitus type 2, AST and ALT elevation, sonographic findings compatible with fatty liver, absence of any history of viral hepatitis, hemochromatosis, Wilson disease, autoimmune hepatitis, alpha 1 antitrypsin deficiency and or and chronic liver disease and elevated serum TG and cholesterol level. Exclusion criteria included any history of significant chronic liver disease, history of gastroplasty of jejunoileal bypass surgery, consumption of hepatotoxic medication during last 6 months and significant alcohol consumption (more than 10 g for female and 20 g for male/ day). Before study, every participants requested to sign an informed consent and then, they randomly divided into two groups. The randomization performed by using random numbers which allocated to consecutive participants.

The patients allocated in intervention group (group A) received L Carnitine tablet 750 mg TDS for 3 months while the other group (group B) treated with placebo. The serum levels of FBS, TG, Cholesterol, AST and ALT determined at the beginning of the study and also the sonographic grade of fatty liver recorded. After 3 months, at the end of study again, the serum level of fasting blood sugar, lipid profile and liver transaminases measured and a liver sonography performed for the patients. Then the collected DATA analyzed by using paired t test and SPSS software. During study period, the patients were requested to contact and report their physician any side effect or any other unpredicted problem and also they were free to leave study any time if they want. During the study, all of the authors had access to the study data and reviewed and approved the final manuscript and study protocol arranged based on CONSORT check list. This study has been approved by ethical committee of Ahvaz Jundishapur University of Medical Sciences (AJUMS.REC.1392.199) and also registered in Iran Registration of Clinical Trials as IRCT2014020316348N2.


Overall in this randomized clinical pilot study 60 patients included and during study 6 patients did not completed the study due to lack of attendance in regular visits, incompleteness of their DATA and/or their own demand. So finally 54 patients finished the study course and considered for final analysis (Figure 1) of them 38 patients (70.4%) were male. Based on their sonographic reports, 10 of participants had grade1 of fatty liver, 20 allocated as grade 2 and 24 diagnosed as grade 3. Their blood sugar was under control with oral agents. The participants randomly divided into 2 groups. The demographic and baseline laboratory characters of two groups had not any significant difference statistically (Table 1).

The patients in intervention group (group A) treated with L- Carnitine 750 mg TDS while group B received placebo. We did not make any change in their therapeutic regimen for diabetes Mellitus and or hypercholesterolemia. After three months of intervention, the serum level of liver transaminases, Cholesterol, TG and FBS of participants in 2 groups determined (Table 2). In group A the level of AST decreased from 122.7 ± 13.6 to 96.3 ± 7 while in group B raised from 125 ± 14 to 126 ± 11 (p < 0.001). The level of ALT in group A declined from 124.5 ± 11.3 to 82.1 ± 5.2 and in placebo group decreased from 120 ± 10.8 to 115.1 ± 6.3 (p < 0.001) (Figure 2). The serum cholesterol level before and after study period were 213 ± 40 and 189 ± 34 in group A and 224 ± 54 and 193 ± 24 in group B and did not reveal any significant decline (p = 0.814). Results of serum TG as well as fasting blood sugar in two groups were also comparable and did not show any meaningful result (p > 0.05, Table 2). In addition, their follow up ultrasonography did not show any significant change in comparison with baseline reports.


The pathogenesis of fatty liver is multifactorial and it seems that insulin resistance and oxidative stress have an important role in accumulation of fatty droplets in hepatocytes[6,7,9,16-18]. Based on this multifactorial pathogenesis, most efforts for management of fatty liver have been focused on treating the risk factors that are commonly associated with metabolic syndrome and beside lifestyle modification and encourage to weight loss as fundamental steps[29-33], a number of medical and supplementary therapies have been studied. These include antioxidants such as vitamin E, Co Q10 and Dark chocolate, insulin sensitizers such as pioglitazone and metformin and cytoprotective agents such as ursodeoxycholic acid[34-38]. In the current study, we evaluated any potential efficacy of L-Carnitine 750 mg TDS as an antioxidant that can also affect intracellular metabolism and fatty acids transmission[25-28]. L-Carnitine (β-hydroxy-γ-trimethylaminobutyric acid) is a small water soluble molecule which essential for the normal oxidation of fats by the mitochondria and is involved in the trans esterification and excretion of acyl-CoA esters, the oxidation of branched chain a-ketoacids, and removal of potentially toxic acyl Carnitine esters from within mitochondria[27]. In the absence of L-Carnitine, the accumulation of free fatty acids in the cytoplasm produces a toxic effect on the cell, and an energy deficit arises from the unavailability of fatty acids within the mitochondria[39].

In a study in China, L-Carnitine supplements ameliorated fatty liver in type 2 diabetic mice by increasing fatty acid oxidation and decreasing the L-Carnitine/ acetyl L-Carnitine ratio in the liver and they concluded oral administration of L-Carnitine protected mitochondrial function in liver[40] and these protective effects confirmed in another study by Jun, Dae Won, et al[41].

In a study conducted by Malaguarnera et al in Italy, the NASH patients treated with L-Carnitine 2 gr daily and At the end of the study, L-Carnitine-treated patients showed significant improvements in the parameters of AST, ALT, γ-GT, total cholesterol, LDL, HDL, TG, glucose and histological scores and they concluded L-Carnitine supplementation to diet could be useful for improving liver function, glucose plasma level, lipid profile, HOMA-IR, and histological manifestations of NASH[28]. Our findings revealed a very dramatic decline in serum level of liver transaminases (AST, ALT) among intervention group (p < 0.001) that was similar to results of Malaguarnera study and could be interpreted as decreasing inflammation and accordingly fibrogenesis in liver. But we did not found any significant change in serum level of cholesterol, TG and FBS level in treated patients in comparison with placebo group (P > 0.05) (Table 2).

In a Korean study, 12 weeks of treatment with carnitine-orotate complex resulted a significantly higher rate of normalization of serum ALT level (17.9% vs 89.7%, p < 0.001) in comparison with placebo[42] that was also similar to findings of current study and they concluded that carnitine-orotate complex improves serum ALT and may improve hepatic steatosis in patients with diabetes and NAFLD. But they also revealed a significant decrease in HbA1c in the treatment group (-0.33 ± 0.82%, p = 0.007) and this decrease was in contrary to our study (p = 0.299). Accordingly another Korean study reported the Carnitine to be able to improve liver profile and peripheral blood mitochondrial DNA copy number and suggest that Carnitine activate the mitochondria, thereby contributing to the improvement of NAFLD[43].

Shakerhosseini in 2005 investigated the effects of oral L-Carnitine administration 3gr daily on fasting plasma glucose, HbA1c and lipid parameters in 18 patients with diabetes mellitus type II for a period of 12 weeks[25]. They found no significant changes in LDL-C, HDL-C, HbA1C or in total cholesterol (TC) between the two groups similar to our results and concluded L-Carnitine increases fasting triglycerides in type II diabetic patients while significantly lowers fasting plasma glucose.

The common point of almost all of the mentioned studies is the significant decline in serum level of liver transaminases secondary to treatment with L-Carnitine among patients suffered by NAFLD and based on population based follow up studies, patients with NASH and especially those with elevated liver enzymes, are at increased risk of death compared with the general population[44-46]. So this decline in serum level of liver transaminases can be interpreted as survival benefit and highlighting the therapeutic efficacy of L-Carnitine as a safe and easily accessible option for treatment of fatty liver. And base on more rapid progression of fatty liver among diabetic patients[9,18,19], it seems logic that L-Carnitine be recommended for them as a therapeutic option or at least as an additive to their medications even without any unwanted effect on the level of serum sugar.

During the current study, the sonographic follow up of patients in either group did not shown any significant changes. This matter could be explained by the short course of study (3 months) and usually sonographic changes of fatty liver necessitate longer time periods to be clinically recordable.


It seems that L-Carnitine with dose of 750 mg TDS significantly decreases the serum levels of liver transaminases among diabetic patients suffered by fatty liver and is effective in treatment of NAFLD. This supplementary medication could be a potential therapeutic approach in such patients and is worthful to be added to their therapeutic regimen. We recommend these findings to further be verified by future studies.


This article is extracted from final thesis of Dr Mahmoud Chobineh for his course of internal medicine residency. Dr Pezhman Alavinejad as the corresponding author and designer of study. Dr Mehrnoosh Zakerkish as responsible endocrinologist. Dr Eskandar Hajiani as consultant hepatologist. Dr Seyed Jalal Hashemi as consultant hepatologist. Dr Mahmoud Chobineh as cooperative colleague in outpatient clinic. Dr Elham Karimi Moghaddam cooperative colleague in writing of article.


All authors declared no potential conflicts of interest.


1Welsh JA, Karpen S, Vos MB. Increasing prevalence of nonalcoholic fatty liver disease among United States adolescents, 1988-1994 to 2007-2010. The Journal of pediatrics 2013; 162(3): 496-500. [PubMed] [DOI]

2Browning JD, Szczepaniak LS, Dobbins R, Nuremberg P, Horton JD, Cohen JC, Grundy SM, Hobbs HH. Prevalence of hepatic steatosis in an urban population in the United States: impact of ethnicity. Hepatology 2004; 40(6): 1387-1395. [PubMed] [DOI]

3Ludwig J, Viggiano TR, McGill DB, Oh BJ. Nonalcoholic steatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease. Mayo Clin Proc. 1980 Jul; 55(7): 434-438. [PubMed]

4Adams LA, Sanderson S, Lindor KD, Angulo P. The histological course of nonalcoholic fatty liver disease: a longitudinal study of 103 patients with sequential liver biopsies. Journal of hepatology 2005; 42(1): 132-138. [PubMed] [DOI]

5Jamali R, Jamali A. “Fatty Liver Disease.” Kashan: Davat (2010): 9-10.

6Neuschwander-Tetri BA, Caldwell SH. Nonalcoholic steatohepatitis: summary of an AASLD Single Topic Conference. Hepatology. 2003 May; 37(5): 1202-1219. [PubMed] [DOI]

7Bellentani S, Saccoccio G, Masutti F, Crocè LS, Brandi G, Sasso F, Cristanini G, Tiribelli C. Prevalence of and risk factors for hepatic steatosis in Northern Italy. Ann Intern Med. 2000 Jan 18; 132(2): 112-117. [PubMed]

8Sheth, Sunil G, Fredric D. Gordon, Sanjiv Chopra. “Nonalcoholic steatohepatitis.” Annals of internal medicine 1997; 126(2): 137-145.

9Bertolini L, Padovani R, Rodella S, Tessari R, Zenari L, Day C, Arcaro G. “Prevalence of nonalcoholic fatty liver disease and its association with cardiovascular disease among type 2 diabetic patients.” Diabetes care 2007; 30(5): 1212-1218. [PubMed] [DOI]

10Park HS, Han JH, Choi KM, Kim SM. “Relation between elevated serum alanine aminotransferase and metabolic syndrome in Korean adolescents.” Am J Clin Nutr. 2005 Nov; 82(5): 1046-1051. [PubMed]

11Jamali R, Khonsari M, Merat S, Khoshnia M, Jafari E, Bahram Kalhori A, Abolghasemi H, Amini S, Maghsoudlu M, Deyhim MR, Rezvan H, Pourshams A. Persistent alanine aminotransferase elevation among the general Iranian population: prevalence and causes. World J Gastroenterol. 2008 May 14; 14(18): 2867-2871. [PubMed] [DOI]

12Park SH, Jeon WK, Kim SH, Kim HJ, Park DI, Cho YK, Sung IK, Sohn CI, Keum DK, Kim BI. Prevalence and risk factors of non-alcoholic fatty liver disease among Korean adults. J Gastroenterol Hepatol. 2006 Jan; 21(1 Pt 1): 138-143. [PubMed] [DOI]

13Fan JG, Farrell GC. Epidemiology of non-alcoholic fatty liver disease in China. J Hepatol. 2009 Jan; 50(1): 204-210

14Amarapurkar D, Kamani P, Patel N, Gupte P, Kumar P, Agal S, Baijal R, Lala S, Chaudhary D, Deshpande A. Prevalence of non-alcoholic fatty liver disease: population based study. Ann Hepatol. 2007 Jul-Sep; 6(3): 161-163. [PubMed]

15Abrams GA, Kunde SS, Lazenby AJ, Clements RH. “Portal fibrosis and hepatic steatosis in morbidly obese subjects: a spectrum of nonalcoholic fatty liver disease.” Hepatology. 2004 Aug; 40(2): 475-483. [PubMed] [DOI]

16Bacon BR, Farahvash MJ, Janney CG, Neuschwander-Tetri BA. Nonalcoholic steatohepatitis: an expanded clinical entity. Gastroenterology. 1994 Oct; 107(4): 1103-1109. [PubMed]

17Bedogni G, Miglioli L, Masutti F, Tiribelli C, Marchesini G, Bellentani S. Prevalence of and risk factors for nonalcoholic fatty liver disease: the Dionysos nutrition and liver study.” Hepatology. 2005 Jul; 42(1): 44-52. [PubMed] [DOI]

18Marchesini G, Brizi M, Morselli-Labate AM, Bianchi G, Bugianesi E, McCullough AJ, Forlani G, Melchionda N. Association of nonalcoholic fatty liver disease with insulin resistance. Am J Med. 1999 Nov; 107(5): 450-455. [PubMed]

19Machado M, Cortez-Pinto H. Non-alcoholic steatohepatitis and metabolic syndrome. Curr Opin Clin Nutr Metab Care. 2006 Sep; 9(5): 637-642.[PubMed] [DOI]

20Grundy SM, Brewer HB Jr, Cleeman JI, Smith SC Jr, Lenfant C; American Heart Association; National Heart, Lung, and Blood Institute. “Definition of metabolic syndrome report of the National Heart, Lung, and Blood Institute/American Heart Association Conference on scientific issues related to definition.” Circulation. 2004 Jan 27; 109(3): 433-438. [PubMed] [DOI]

21Marchesini G, Brizi M, Bianchi G, Tomassetti S, Bugianesi E, Lenzi M, McCullough AJ, Natale S, Forlani G, Melchionda N. Nonalcoholic fatty liver disease a feature of the metabolic syndrome. Diabetes. 2001 Aug; 50(8): 1844-1850. [PubMed]

22Reid AE. “Nonalcoholic steatohepatitis.” Gastroenterology. 2001 Sep; 121(3): 710-723. [PubMed]

23Boden G, Shulman GI. “Free fatty acids in obesity and type 2 diabetes: defining their role in the development of insulin resistance and β-cell dysfunction.” Eur J Clin Invest. 2002 Jun; 32 Suppl 3: 14-23. [PubMed]

24Weyer C1, Funahashi T, Tanaka S, Hotta K, Matsuzawa Y, Pratley RE, Tataranni PA. “Hypoadiponectinemia in obesity and type 2 diabetes: close association with insulin resistance and hyperinsulinemia.” J Clin Endocrinol Metab. 2001 May; 86(5): 1930-1935. [PubMed] [DOI]

25Shakerhosseini R, Aadat N, Pordal A, Taleban F, Golestan B, Rahbar A. The effect of L-carnitine supplement on lipidemic and glycemic profile in patients with type II diabetes mellitus.” Iranian Journal of Endocrinology and Metabolism 2005; 7(2): 157-165. [Link]

26Lysiak W, Lilly K, DiLisa F, Toth PP, Bieber LL. Quantitation of the effect of L-carnitine on the levels of acid-soluble short-chain acyl-CoA and CoASH in rat heart and liver mitochondria. J Biol Chem. 1988 Jan 25; 263(3): 1151-1156. [PubMed]

27Walter JH. L-Carnitine. Archives of disease in childhood. 1996; 76(4): 475.[PubMed]

28Malaguarnera M, Gargante MP, Russo C, Antic T, Vacante M, Malaguarnera M, Avitabile T, Li Volti G, Galvano F. L-carnitine supplementation to diet: a new tool in treatment of nonalcoholic steatohepatitis—a randomized and controlled clinical trial.” Am J Gastroenterol. 2010 Jun; 105(6): 1338-1345 [PubMed] [DOI]

29Perseghin G, Lattuada G, De Cobelli F, Ragogna F, Ntali G, Esposito A, Belloni E, Canu T, Terruzzi I, Scifo P, Del Maschio A, Luzi L. “Habitual physical activity is associated with intrahepatic fat content in humans.” Diabetes Care. 2007 Mar; 30(3): 683-688. [PubMed]

30Kistler KD, Brunt EM, Clark JM, Diehl AM, Sallis JF, Schwimmer JB; NASH CRN Research Group. “Physical activity recommendations, exercise intensity, and histological severity of nonalcoholic fatty liver disease.” Am J Gastroenterol. 2011 Mar; 106(3): 460-8 [PubMed] [DOI]

31Gerber, Lynn H., Ali Weinstein, and Lisa Pawloski. “Role of exercise in optimizing the functional status of patients with nonalcoholic fatty liver disease.” Clinics in liver disease 2014; 18(1): 113-127.

32Huang MA, Greenson JK, Chao C, Anderson L, Peterman D, Jacobson J, Emick D, Lok AS, Conjeevaram HS. One-year intense nutritional counseling results in histological improvement in patients with non-alcoholic steatohepatitis: a pilot study. Am J Gastroenterol. 2005 May; 100(5): 1072-1081. [PubMed] [DOI]

33Ueno T, Sugawara H, Sujaku K, Hashimoto O, Tsuji R, Tamaki S, Torimura T, Inuzuka S, Sata M, Tanikawa K. Therapeutic effects of restricted diet and exercise in obese patients with fatty liver. J Hepatol. 1997 Jul; 27(1): 103-107. [PubMed]

34Sanyal AJ, Chalasani N, Kowdley KV, McCullough A, Diehl AM, Bass NM, Neuschwander-Tetri BA, Lavine JE, Tonascia J, Unalp A, Van Natta M, Clark J, Brunt EM, Kleiner DE, Hoofnagle JH, Robuck PR, NASH CRN. Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. N Engl J Med. 2010 May 6; 362(18): 1675-1685. [PubMed] [DOI]

35Mohammadshahi M, Farsi F, Nejad PA, Hajiani E, Zarei M, Engali KA. The coenzyme Q10 supplementation effects on lipid profile, fasting blood sugar, blood pressure and oxidative stress status among non-alcoholic fatty liver disease patients: A randomized, placebo-controlled, pilot study. Journal of Gastroenterology and Hepatology Research. 2014 Jun 21; 3(6): 1108-1113. [Link]

36Alavinejad Pezhman, Farnaz Farsi, Afshin Rezazadeh, Moosa Mahmoodi, Eskandar Hajiani, Abdol Rahim Masjedizadeh, Seyed Ali Mard, Niloofar Neisi,Hosein Hoseini, Haghighizadeh MH, Elham Karimi Moghaddam. The effects of dark chocolate consumption on lipid profile, fasting blood sugar, liver enzymes, inflammation, and antioxidant status in patients with non-alcoholic fatty liver disease: A randomized, placebo-controlled, pilot study. Journal of Gastroenterology and Hepatology Research 2015; 4(12): 1858-1864.[Link]

37Lavine JE, Schwimmer JB, Van Natta ML, Molleston JP, Murray KF, Rosenthal P, Abrams SH, Scheimann AO, Sanyal AJ, Chalasani N, Tonascia J, Ünalp A, Clark JM, Brunt EM, Kleiner DE, Hoofnagle JH, Robuck PR; Nonalcoholic Steatohepatitis Clinical Research Network. “Effect of vitamin E or metformin for treatment of nonalcoholic fatty liver disease in children and adolescents: the TONIC randomized controlled trial.” JAMA. 2011 Apr 27; 305(16): 1659-1668. [PubMed] [DOI]

38Neuschwander-Tetri BA, Loomba R, Sanyal AJ, Lavine JE, Van Natta ML, Abdelmalek MF, Chalasani N, Dasarathy S, Diehl AM, Hameed B, Kowdley KV, McCullough A, Terrault N, Clark JM, Tonascia J, Brunt EM, Kleiner DE, Doo E; NASH Clinical Research Network. Farnesoid X nuclear receptor ligand obeticholic acid for non-cirrhotic, non-alcoholic steatohepatitis (FLINT): a multicentre, randomised, placebo-controlled trial. Lancet. 2015 Mar 14; 385(9972): 956-965. [PubMed] [DOI]

39Goa Karen L, Rex N. Brogden. “L-carnitine.” Drugs 1987; 34(1): 1-24. [Link]

40Xia Y, Li Q, Zhong W, Dong J, Wang Z, Wang C. L-carnitine ameliorated fatty liver in high-calorie diet/STZ-induced type 2 diabetic mice by improving mitochondrial function. Diabetol Metab Syndr. 2011 Nov 15; 3: 31 [PubMed] [DOI]

41Jun DW, Cho WK, Jun JH, Kwon HJ, Jang KS, Kim HJ, Jeon HJ, Lee KN, Lee HL, Lee OY, Yoon BC, Choi HS, Hahm JS, Lee MH. Prevention of free fatty acid-induced hepatic lipotoxicity by carnitine via reversal of mitochondrial dysfunction. Liver Int. 2011 Oct; 31(9): 1315-1324. [PubMed] [DOI]

42Bae JC, Lee WY, Yoon KH, Park JY, Son HS, Han KA, Lee KW, Woo JT, Ju YC, Lee WJ, Cho YY, Lee MK. Improvement of Nonalcoholic Fatty Liver Disease With Carnitine-Orotate Complex in Type 2 Diabetes (CORONA): A Randomized Controlled Trial. Diabetes Care. 2015 Jul; 38(7): 1245-1252. [PubMed] [DOI]

43Lim CY, Jun DW, Jang SS, Cho WK, Chae JD, Jun JH. Effects of carnitine on peripheral blood mitochondrial DNA copy number and liver function in non-alcoholic fatty liver disease. Korean J Gastroenterol. 2010 Jun; 55(6): 384-389. [PubMed]

44Söderberg C, Stål P, Askling J, Glaumann H, Lindberg G, Marmur J, Hultcrantz R. Decreased survival of subjects with elevated liver function tests during a 28-year follow-up. Hepatology. 2010 Feb; 51(2): 595-602 [PubMed] [DOI]

45Del Ben M, Polimeni L, Baratta F, Pastori D, Angelico F. The role of nutraceuticals for the treatment of non-alcoholic fatty liver disease. Br J Clin Pharmacol. 2016 Feb 6. [PubMed] [DOI]

46Somi MH, Fatahi E, Panahi J, Havasian MR. Data from a randomized and controlled trial of LCarnitine prescription for the treatment for Non-Alcoholic Fatty Liver Disease. Bioinformation. 2014 Sep 30; 10(9): 575-579. [PubMed] [DOI]

Peer reviewers: Mônica Rodrigues de Araíjo Souza, PhD, Professor, Centro de Ciências Médicas - Universidade Federal da Paraíba - Curso de Medicina, Térreo do Hospital Universitário Lauro Wanderley (HU), João Pessoa, Brazil; Ming-Hua Zheng, MD, Associate Professor, Department of Infection and Liver Diseases, Liver Research Center, The First Affiliated Hospital of Wenzhou Medical College, No.2 Fuxue lane, Wenzhou, 325000, China..


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