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| 1 | From fatty liver to fibrosis:A tale of “second hit”显示文摘Although much is known about how fat accumulates in the liver,much remains unknown about how this causes sustained hepatocellular injury.The consequences of injury are recognized as nonalcoholic steatohepatitis(NASH) and progressive fibrosis.The accumulation of fat within the hepatocytes sensitizes the liver to injury from a variety of causes and the regenerative capacity of a fatty liver is impaired.An additional stressor is sometimes referred to as a 'second hit' in a paradigm that identifies the accumulation of fat as the 'first hit'.Possible candidates for the second hit include increased oxidative stress,lipid peroxidation and release of toxic products such as malondialdehyde and 4-hydroxynonenal,decreased antioxidants,adipocytokines,transforming growth factor(TGF)-β,Fas ligand,mitochondrial dysfunction,fatty acid oxidation by CYPs(CYP 2E1,4A10 and 4A14),and peroxisomes,excess iron,small intestinal bacterial overgrowth,and the generation of gut-derived toxins such as lipopolysaccharide and ethanol.Oxidative stress is one of the most popular proposed mechanisms of hepatocellular injury.Previous studies have specifically observed increased plasma and tissue levels of oxidative stress markers and lipid peroxidation products,with reduced hepatic and plasma levels of antioxidants.There is also some indirect evidence of the benefit of antioxidants such as vitamin E,S-adenosylmethionine,betaine,phlebotomy to remove iron,and N-acetylcysteine in NASH.However,a causal relationship or a pathogenic link between NASH and oxidative stress has not been established so far.A number of sources of increased reactive oxygen species production have been established in NASH that include proinflammatory cytokines such as tumor necrosis factor(TNF)-α,iron overload,overburdened and dysfunctional mitochondria,CYPs,and peroxisomes.Briefly,the pathogenesis of NASH is multifactorial and excess intracellular fatty acids,oxidant stress,ATP depletion,and mitochondrial dysfunction are important causes of hepatocellular injury in the steatotic liver. | Metin Basaranoglu Gkcen Basaranoglu Hakan Sentürk | 2013 | World Journal of Gastroenterology2013，19，8： | 28 |
| 2 | Understanding mechanisms of the pathogenesis of nonalcoholic fatty liver disease显示文摘A central issue in the understanding of the pathogenesis of nonalcoholic fatty liver disease is the problem of the underlying mechanisms which are not fully understood.In the setting of excessive central adiposity,insulin resistance is the major underlying cause of fat accumulation in hepatocytes.Because of the difficulties with human trials,several animal models have been developed for this purpose mainly characterized as follows:genetically disturbed or murine fatty liver,methionine-choline deficient diet fed or murine steatohepatitis,and high-fat or sucrose diet fed models.Although these animal models have provided useful information,none of them accurately reflect genetic,metabolic and biochemical characteristics of the human disease. | Metin Basaranoglu Serra Kayacetin Nevin Yilmaz Ertugrul Kayacetin Orhan Tarcin Abdullah Sonsuz | 2010 | World Journal of Gastroenterology2010，16，18： | 14 |
| 3 | Fructose as a key player in the development of fatty liver disease显示文摘We aimed to investigate whether increased consumption of fructose is linked to the increased prevalence of fatty liver.The prevalence of nonalcoholic steatohepatitis(NASH) is 3% and 20% in nonobese and obese subjects,respectively.Obesity is a low-grade chronic inflam-m-atory condition and obesity-related cytokines such as interleukin-6,adiponectin,leptin,and tumor necrosis factor-α may play important roles in the developm-ent of nonalcoholic fatty liver disease(NAFLD).Additionally,the prevalence of NASH associated with both cirrhosis and hepatocellular carcinom-a was reported to be high am-ong patients with type 2 diabetes with or without obesity.Our research group previously showed that consumption of fructose is associated with adverse alterations of plasma lipid profiles and metabolic changes in m-ice,the Am-erican Lifestyle-Induced Obesity Syndrom-e m-odel,which included consum-ption of a high-fructose corn syrup in amounts relevant to that consum-ed by som-e Am-ericans.The observation reinforces the concerns about the role of fructose in the obesity epidem-ic.Increased availability of fructose(e.g.,high-fructose corn syrup) increases not only abnorm-al glucose flux but also fructose m-etabolism-in the hepatocyte.Thus,the anatomic position of the liver places it in a strategic buffering position for absorbed carbohydrates and am-ino acids.Fructose was previously accepted as a beneficial dietary com-ponent because it does not stim-ulate insulin secretion.However,since insulin signaling plays an important role in central m-echanism-s of NAFLD,this property of fructose m-ay be undesirable.Fructose has a selective hepatic m-etabolism,and provokes a hepatic stress response involving activation of c-Jun N-term-inal kinases and subsequent reduced hepatic insulin signaling.As high fat diet alone produces obesity,insulin resistance,and som-e degree of fatty liver with m-inim-al inflam-m-ation and no fibrosis,the fast food diet which includes fructose and fats produces a gene expression signature of increased hepatic fibrosis,inflam-m-ation,endoplasm-ic reticulumstress and lipoapoptosis.Hepatic de novo lipogenesis(fatty acid and triglyceride synthesis) is increased in patients with NAFLD.Stable-isotope studies showed that increased de novo lipogenesis(DNL) in patients with NAFLD contributed to fat accum-ulation in the liver and the developm-ent of NAFLD.Specifically,DNL was responsible for 26% of accum-ulated hepatic triglycerides and 15%-23% of secreted very low-density lipoprotein triglycerides in patients with NAFLD com-pared to an estim-ated less than 5% DNL in healthy subjects and 10% DNL in obese people with hyperinsulinem-ia.In conclusion,understanding the underlying causes of NAFLD form-s the basis for rational preventive and treatm-ent strategies of this m-ajor form-of chronic liver disease. | Metin Basaranoglu Gokcen Basaranoglu Tevfik Sabuncu Hakan Sentürk | 2013 | World Journal of Gastroenterology2013，19，8： | 14 |
| 4 | Pathophysiology of insulin resistance and steatosis in patients with chronic viral hepatitis显示文摘Chronic hepatitis due to any cause leads to cirrhosis and end-stage liver disease.A growing body of literature has also shown that fatty liver due to overweight or obesity is a leading cause of cirrhosis.Due to the obesity epidemic,fatty liver is now a significant problem in clinical practice.Steatosis has an impact on the acceleration of liver damage in patients with chronic hepatitis due to other causes.An association between hepatitis C virus (HCV) infection,steatosis and the onset of insulin resistance has been reported.Insulin resistance is one of the leading factors for severe fibrosis in chronic HCV infections.Moreover,hyperinsulinemia has a deleterious effect on the management of chronic HCV.Response to therapy is increased by decreasing insulin resistance by weight loss or the use of thiazolidenediones or metformin.The underlying mechanisms of this complex interaction are not fully understood.A direct cytopathic effect of HCV has been suggested.The genomic structure of HCV (suggesting that some viral sequences are involved in the intracellular accumulation of triglycerides),lipid metabolism,the molecular links between the HCV core protein and lipid droplets (the core protein of HCV and its transcriptional regulatory function which induce a triglyceride accumulation in hepatocytes) and increased neolipogenesis and inhibited fatty acid degradation in mitochondria have been investigated. | Metin Basaranoglu Gkcen Basaranoglu | 2011 | World Journal of Gastroenterology2011，17，36： | 8 |
| 5 | Mallory-Denk Bodies in chronic hepatitis显示文摘Mallory-Denk Bodies(MDB) are important as investigators,suggesting MDB as an indicator of the histologic severity of chronic hepatitis,causes of which include hepatitis C,primary biliary cirrhosis(PBC),and nonalcoholic fatty liver disease(NAFLD).Matteoni et al scored MDB in patients with NAFLD as none,rare and many,and reported that MDB plays a prominent role in this classification scheme in an earlier classification system.In this study,we evaluated 258 patients with chronic hepatitis due to metabolic,autoimmune and viral etiologies.Liver biopsy samples were evaluated with hematoxylin and eosin,periodic acid-Schiff-diastase,Gordon and Sweet's reticulin,Masson's trichrome,and iron stains.Both staging and grading were performed.Additionally,MDB were evaluated and discussed for each disease.We examined patients with nonalcoholic steatohepatitis(NASH;50 patients),alcoholic hepatitis(10 patients),PBC(50 patients),Wilson disease(WD;20 patients),hepatitis B(50 patients),hepatitis C(50 pati-ents) and hepatocellular carcinoma(HCC;30 patients).Frequency of MDB was as follows;NASH:10 patients with mild in 60% and moderate in 40% and observed in every stage of the disease and frequently seen in zone 3.PBC:11 patients with mild in 10%,moderate in 70%,and cirrhosis in 20%,and frequently seen in zone 1.WD:16 patients with moderate and severe in 60% and cirrhosis in 40% and frequently seen in zone 1.Hep B:3 patients with mild in 66% and severe in 34%.Hep C:7 patients with mild in 40% and moderate in 60% and observed in every stage.HCC:3 patients with hep B in 2 patients.We found that there is no relationship between MDB and any form of chronic hepatitis regarding histologic severity such as alcoholic steatohepatitis and NAFLD and variable zone distribution by etiology. | Metin Basaranoglu Nesrin Turhan Abdullah Sonsuz Gkcen Basaranoglu | 2011 | World Journal of Gastroenterology2011，17，17： | 6 |
| 6 | Smoking and postoperative analgesia 显示文摘 | ErdenV Basaranoglu G Delatioglu H eta1 | 2005 | Ann Pharmacother2005，39，9： | 1 |
| 7 | A controlled trial of gemfibrozil in the treatment of patients with nonalcoholic steatohepatitis显示文摘 | Basaranoglu M Acbay D Sonsuz A | 1999 | Hepatol1999，31，2： | 1 |
| 8 | The fluctuation of serum levels of aminotransferase in patients with nonalcoholic steatohepatitis 显示文摘 | Ipekci SH Basaranoglu M Sonsuz A | 2003 | J Clin Gastroenterol2003，36，4： | 1 |
| 9 | Serum levels of triglyeeride and insulin resistance in patients with nonalcoholic steatohepatitis显示文摘 | Basaranoglu M | 2002 | Can J Gastroenterol2002，16，5： | 1 |
| 10 | Gall bladder sludge and acute pancreatitis induced by acute hepatitis A显示文摘 | Basaranoglu M Balci NC Klor HU | 2006 | Pancreatology2006，6，12： | 1 |
| 11 | A controlled trial of gemfibrol in the treatment of patients with nonalcoholic steatohepatitis显示文摘 | BASARANOGLU M ACBAY O SONSUZ A | 1999 | J Hepatol1999，31，： | 1 |
| 12 | Oxidant/antioxidant st at us,pa raoxonase act ivit y,a nd lipid prof ile i n plasma of ovariectomized rats under the inf luence of estrogen,estrogen combined with progesterone,and genistein显示文摘 | Agacayak E Basaranoglu S Tunc SY | 2015 | Drug Des Devel Ther2015，9，： | 1 |
| 13 | Chemotherapy-induced Hepatitis B virus reactivation in HbsAg positive cancer patients: a single center experience显示文摘 | Orhan Onder Eren Mehmet Artac Melih Cem Boruban Ozlem Yavas Ugur Arslan Metin Basaranoglu | 2009 | Medical Oncology2009，，4： | 1 |
| 14 | Recurrent cholangitis associated with bil- iary sludge and Phrygian cap anomaly diagnosed by magnetic reso- nance imaging and magnetic resonance cholangiopancreatography despite normal ultrasound and computed tomography 显示文摘 | Basaranoglu M Balci NC | 2005 | Scand J Gastroenrerol2005，40，： | 1 |
| 15 | A tree fundic diverticulum of the gall- bladder显示文摘 | Basaranoglu M Balci NC | 2006 | J Gastroenterol Hepatol2006，21，： | 1 |
| 16 | Reduction of pain on injection of propofol using mepiridine and remifentanil显示文摘 | Basaranoglu G Erden V Delatioglu H | 2005 | Eur J Anaesthesiol2005，22，11： | 1 |
| 17 | Reduction of pain on injection of propofol using meperidine and rernifen- tanil显示文摘 | Basaranoglu G Erden V Delatioglu H | 2005 | Eur J Anaesthesiol2005，22，11： | 1 |
| 18 | Reduction of pain on injec-tion of propofol:a comparison of fentanyl with remifentanil显示文摘 | Basaranoglu G Erden V Delatioglu H | 2012 | Anesthesia and Analgesia2012，33，1： | 1 |
| 19 | A controlled trial of gemfibrozil in the treatment of patient with nonalcoholic steatohepatitis显示文摘 | Basaranoglu M Acbay O Sonsuz A | 1999 | J Hepatol1999，31，： | 1 |
| 20 | The fluctuation of serum levels of aminotransferase in patients with nonalcoholic steatohepatitis 显示文摘 | Ipekci SH Basaranoglu M Sonsuz A | 2003 | J Clin Gastroenterol2003，36，4： | 1 |
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