Shahinul Alam, SKM Nazmul Hasan, Golam Mustafa, Mahabubul Alam, Mohammad Kamal and Nooruddin Ahmad
Non-alcoholic fatty liver disease (NAFLD) is a condition pathologically linked to the metabolic syndrome by the intervention of insulin resistance (IR), characterized by hepatic steatosis in the absence of significant alcohol use, hepatotoxic medications or other known liver diseases.[ 1 ] Globally, the prevalence of NAFLD is 25.24%.[ 2 ] In the Asia-Pacific region, the prevalence of NAFLD has increased remarkably over the years affecting up to 30% of the general population.[ 3 ] In case of NAFLD, Bangladeshi ethnicity is an independent risk
Shahinul Alam, Mohammad Jahid Hasan, Md. Abdullah Saeed Khan, Mahabubul Alam and Nazmul Hasan
Non-alcoholic fatty liver disease (NAFLD), the most prevalent chronic liver disorder worldwide, is a clinico-histopathological entity ranging from simple fat accumulation (steatosis) to non-alcoholic steatohepatitis (NASH). [ 1 , 2 ] NASH is diagnosed by the joint presence of steatosis and inflammation along with hepatocyte injury (evident as hepatocyte ballooning). [ 3 ] It is estimated that NASH occurs in 20% of patients with NAFLD, whereas in Bangladesh, it shows a higher proportion (42.4%). [ 4 , 5 ] Due to its progressive nature
Daniela Maria Hurjui, Otilia Niţă, Lidia Iuliana Graur, Dana Ştefana Popescu, Laura Mihalache, Cătălin Ilie Huţanaşu and Mariana Graur
, atherosclerosis, and aspects of insulin action. Diabetes Care 28: 2312-2319, 2005.
18. Targher G, Bertolini L, Scala L et al . Nonalcoholic hepatic steatosis and its relation to increased plasma biomarkers of inflammation and endothelial dysfunction in nondiabetic men. Role of visceral adipose tissue. Diabet Med 22: 1354-1358, 2005.
19. Savage DB, Petersen KF, Shulman GI . Disordered lipid metabolism and the pathogenesis of insulin resistance. Physiol Rev 87: 507-520, 2007.
20. Cnop M, Landchild MJ, Vidal J et al. The
Elena Caceaune, Daniela Licăroiu, O. Brădescu, N. Caceaune and C. Ionescu-Tîrgovişte
1. Angulo P . Nonalcoholic Fatty Liver Disease. The New England Journal of Medicine Vol. 346, No. 16: 1221-1231, 2002.
2. Festi D, Colecchia A, Sacco T, Bondi M, Roda E and Marchesini G. Hepatic steatosis in obese patients: clinical aspects and prognostic significance. Obesity reviews 5: 27-42, 2004.
3. Farrell GC, Larter CZ. Nonalcoholic fatty liver disease: from steatosis to cirrhosis. Hepatology 43(2 Suppl 1): S99-S112, 2006.
4. Szczepaniak LS, Nurenberg P, Leonard D
Puth Muangpaisarn, Kanisa Jampoka, Sunchai Payungporn, Naruemon Wisedopas, Chalermrat Bunchorntavakul, Pisit Tangkijvanich and Sombat Treeprasertsuk
Currently, nonalcoholic fatty liver disease (NAFLD) has become a worldwide health concern because its prevalence is rising and it is an emerging etiology of chronic liver diseases [ 1 - 3 ]. Moreover. NAFLD is closely associated with obesity metabolic syndrome, and cardiovascular diseases [ 4 ]. NAFLD can be divided into two groups: simple steatosis and nonalcoholic steatohepatitis (NASH) [ 5 ]. In particular, NASH increases the risk of death compared with the general population, and can progress to cirrhosis and hepatocellular carcinoma [ 5 , 6 ]. Importantly
Oana Irina Gavril, Lidia Iuliana Arhire, Ovidiu Mitu, Radu Sebastian Gavril, Alexandra Mastaleru, Madalina Ioana Zota, Maria-Magdalena Leon-Constantin, Teodor Vasilcu, Laura Mihalache and Florin Mitu
; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009; 120: 1640-5
17. Williamson RM, Price JF, Glancy S et al. Edinburgh Type 2 Diabetes Study Investigators. Prevalence of and risk factors for hepatic steatosis and nonalcoholic fatty liver disease in people with type 2 diabetes: The Edinburgh Type 2 Diabetes Study. Diabetes Care 2011; 34: 1139-44.
18. DaiW. : Prevalence of nonalcoholic fatty liver disease
Non-alcoholic fatty liver disease (NAFLD) is a leading cause of chronic liver disease worldwide. The disease spectrum ranges from fatty liver, non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma.
In general, the definition of NAFLD comprises evidence for fatty infiltration in liver tissue either by histology or imaging and known causes of fat accumulation must be excluded, whereas NASH is classified as steatosis and inflammation with or without fibrosis [ 1 ]. Recent meta-analyses suggest that NAFLD is a precursor of type 2
Barbara Stawiarska-Pięta, Jolanta Zalejska-Fiolka, Magdalena Wyszyńska, Anna Kleczka, Beata Janiga, Natalia Grzegorzak and Ewa Birkner
1. Berliner J.A., Heinecke W.J.: The role of oxidized lipoproteins in atherogenesis. Free Radic Biol Med 1996, 20, 707–727.
2. Brukow K.G.: Oxidized lipids: The two faces of vascular inflammation. Curr Atheroscler Rep 2006, 8, 223–231.
3. Bukol-Krawczyk K.: Nonalcoholic steatosis of the liver – to treat or not to treat? Forum Metabol Disord 2010, 1, 66–72.
4. Choe E., Min D.B.: Chemistry of deep-fat frying oils. J Food Sci 2007, 72, 77–86.
5. Cohn J.: Oxidized fat in the diet, postprandial lipaemia and cardiovascular
Muhammed Manzoor, Rajesh K. Wadhwa, Zaigham Abbas, Syed Mujahid Hasan, Nasir Hasan Luck and Muhammed Mubarak
Nonalcoholic steatohepatitis (NASH) is defined as the presence of hepatic steatosis and inflammation with hepatocyte injury (ballooning) with or without fibrosis. NASH is often a “silent” liver disease. Estimated prevalence of NASH ranges from 3% to 5% in different studies. The prevalence of NASH-related cirrhosis in the general population is not known. Herein, we report a case of a young female presented with NASH-related cirrhosis in the setting of poorly controlled celiac disease (CD) and microscopic colitis. A variety of liver abnormalities have been observed in patients with CD, but this unique constellation of the gut and liver pathologies has not been reported previously.
Maryana Kondro, Nazarii Kobyliak, Oleksandr Virchenko, Tetyana Falalyeyeva, Tetyana Beregova and Petro Bodnar
Considering the association between microflora and obesity, and the significantly higher prevalence of non-alcoholic fatty liver disease (NAFLD) in obese people, the aim of our study was to investigate the preventive effect of multiprobiotics on the monosodium glutamate (MSG) induced NAFLD model, in rats. The work was carried out on 60 rats placed into three groups: the Control group, the MSG-group and the MSG-probiotic group. The MSG-group and the MSG-probiotic group were injected with 4 mg/g of MSG subcutaneously neonatally on the 2nd-10th days of life. The MSG-probiotic rats were also treated with 140 mg/kg of multiprobiotic “Symbiter” from the 4th week of life. In the 4-month-old rats, biochemical and morphological changes in liver were assessed, and steatosis was confirmed by the NAFLD activity score (NAS). Our results reveal that the multiprobiotic lowered total NAS, the degree of steatosis and the liver lobular inflammation caused by MSG. It also brought about decreased liver total lipids and triglycerids content, as well as decreased visceral adipose tissue mass. However, there was no difference in the liver serum biochemical indicators between all experimental groups. The obtained data does suggest the efficacy of probiotics in the prevention of NAFLD.