Moreover, long-term studies of dieting indicate that the majority of individuals who dieted regain virtually all of the weight that was lost after dieting, regardless of whether they maintain their diet or exercise program.[8-10] Therefore, the maintenance of weight loss is still one of the biggest challenges of dietary interventions in patients with NAFLD. Provide 200–800 calories AZD4547 manufacturer per day, maintaining protein intake but limiting calories from both fat and carbohydrates. Must be undertaken with medical supervision to prevent adverse side-effects, such as loss

of lean muscle mass, increased risks of gout, gallbladder stone, and electrolyte imbalances. Aside from the possibility of achieving weight loss through caloric restriction (either low in carbohydrates or low in fats) as see more a treatment for NAFLD, many dietary factors (especially macronutrients) can directly influence the development of NAFLD (Table 2).[3-7, 12-27] Manipulation of dietary composition might affect the outcomes of NAFLD and associated metabolic disorders independent of weight loss.[4-6] The dietary carbohydrates are often divided into complex carbohydrate (refer to any sort of digestible saccharide present in a whole food, where fiber, vitamins, and minerals are also found), or simple carbohydrates such as monosaccharides and disaccharides

(refer to sugar, provide calories but few other nutrients, and raise blood glucose rapidly especially if processed). Dietary carbohydrate

especially sugars contribute to increased circulating insulin and triglyceride concentrations and lead to increased hepatic de novo lipogenesis and decreased hepatic insulin sensitivity 上海皓元医药股份有限公司 because of the lipogenic potential of fructose during liver metabolism.[12-16] In addition, recent genome-wide studies have identified several polymorphisms that contribute to increased liver fat accumulation, with some of these genes relating to dietary carbohydrate and sugar consumption.[7, 33] Dietary fructose consumption primarily in the form of soft drinks worldwide has increased in parallel with the increase in obesity, diabetes, and NAFLD, and some studies have suggested a direct association.[1-6] The role of fructose and sucrose in NAFLD and metabolic disorders has been thoroughly reviewed elsewhere. Low-carbohydrate diets are increasingly employed for treatment of obesity and NAFLD; they have been shown to promote weight loss, decrease intrahepatic triglyceride content, and improve metabolic parameters of patients with obesity.[4-6, 9, 34] However, the relationship between long-term maintenance on low-carbohydrate diets and systemic insulin resistance in humans remains to be elucidated. In addition, low glycemic index (GI ≤ 55) foods such as oats have been shown to increase appetite, reduce calories intake, and decrease plasma glucose and total cholesterol levels.

SPG stimulation is being evaluated for both migraine and cluster headaches.

The device is approved in Europe for chronic cluster headache, and a major study is planned in the USA for cluster patients. At this time, it is not FDA approved for cluster or migraine in the USA. Stimulating the occipital nerves, found at the back of the head, can terminate or prevent migraine and cluster. ONS for chronic migraine has been studied in 3 separate trials, but none of these studies was significantly positive. All showed some benefits in smaller segments of people with chronic migraine. PD0325901 One problem in determining whether ONS is an effective measure is the difficulty in setting up an effective placebo, which would be important for a

randomized controlled trial. At the time of this writing, there is a plan to do at least one more study on ONS for chronic migraine in both Europe Selleckchem Tipifarnib and in the USA. In Europe, one of the ONS devices has approval for use in chronic migraine. Currently, ONS is not approved by the FDA for chronic migraine patients in the USA. A small number of patients with very hard to treat and very disabling cluster headache have had a stimulator placed deep in the brain’s hypothalamus, the most risky and invasive of the surgical procedures for headache. While the results have been promising in a limited number of cases, there remains a risk of brain bleeding and even death. Because cluster headache is not a fatal illness, the recommendation is to try peripheral or noninvasive neuromodulation for these patients before resorting to DBS. No scientific studies with placebo have been performed on DBS, and the technique is not FDA approved for cluster in the USA. To find more resources, please visit the American Migraine Foundation (http://kaywa.me/ir2eb) “
“Orthostatic headache with or without associated symptoms (neck or intrascapular pain, nausea and vomiting, change in hearing, diplopia, visual

blurring, bitemporal hemianopsia, upper limb paresthesias, parkinsonism,[1] stupor, and coma[2]) is indicative of intracranial hypotension that MCE公司 can occur either after active cerebrospinal fluid (CSF) removal (eg, after a lumbar puncture) or spontaneously (spontaneous intracranial hypotension [SIH]) as a result of a spinal meningeal CSF leak.[3, 4] Spontaneous CSF leaks are attributed to the underlying fragility of the spinal meninges (sometimes associated with connective-tissue disorders) that easily tear when exposed to a mechanical factor, such as a minor trauma.[3] A trivial trauma such as coughing, pulling, pushing, and lifting is reported in a minority of the patients.[3] Diagnosis is based on clinical presentation and typical brain magnetic resonance imaging (MRI): thickening of the dura with diffuse pachymeningeal enhancement, sometimes brain sagging, subdural fluid collections, dilatation of the venous compartment with dural sinuses, and pituitary gland enlargement.

9–12

Indeed, many articles on adult stem cells have embedded somewhere in their introductions and/or discussions a distinct explanation why the adult stem cell system being studied circumvents the bioethics problem. However, with the exception of bone marrow transplants, adult stem cells, to date, still have their problems, which, similar to hESCs, have also kept them out of the clinic for use as stem cell therapies. Hence, human ingenuity has led to profound discovery that somatic cells could be induced to become pluripotent by simply adding four genes. Induced pluripotent stem cells (iPS cells) were first generated by two research teams led by Drs. Yamanaka and Thomson, respectively, who pioneered and generated stem cells PD98059 from human skin through ectopic expression of four genes (Oct3/4, Sox2, c-Myc, Natural Product Library purchase and Klf4, or Oct3/4, Sox2, Nanog, and Lin28).13–15 Since their discovery, improvements have been made in generating iPS cells including the ability to remove the inducing genes,16 the addition of only one or two genes in certain cell types,17, 18 and generation of iPS cells by chemical induction.19, 20 In each case, no matter the inductive route, human iPS cells have been shown to mimic hESCs in virtually all aspects of pluripotency and differentiation. These iPS cells are pluripotent because they can form all three germ layers. Moreover,

mouse iPS cells have been repeatedly shown to make chimeric mice, contribute to the germ line, and generate pups.21 However, to date, most of the in vitro investigations

into iPS cell differentiation have focused on mesodermal-derived cardiomyocyte and ectodermal-derived neuronal lineages—that is, until now. In this issue, two independent laboratories reveal, for the first time, complete derivation of iPS cells into endodermal-derived hepatocytes (Sullivan et al.22 and Si-Tayeb et al.23). While the elegance of each study enables them to stand alone, when taken together, they, in essence, delineate the true potential of iPS cells for the field of hepatology. The data clearly reveal that iPS cells can become fully functional liver cells. Both articles demonstrate that iPS cell–derived hepatocytes express distinct hepatocyte markers; however, and perhaps more importantly, both also show definitive MCE公司 function of their hepatocytes in vitro and in vivo. The magnitude of these investigations will probably be felt straight away because they represent a seminal advancement in current hepatocyte cell-culture technology. A constant problem experienced by many who try to culture hepatocytes is that current protocols generally revolve around the need for consistent derivation and culture of primary hepatocytes, which have the reputation for being difficult to cultivate, are generally scarce, and are usually rather heterogeneous once in culture.

9–12

Indeed, many articles on adult stem cells have embedded somewhere in their introductions and/or discussions a distinct explanation why the adult stem cell system being studied circumvents the bioethics problem. However, with the exception of bone marrow transplants, adult stem cells, to date, still have their problems, which, similar to hESCs, have also kept them out of the clinic for use as stem cell therapies. Hence, human ingenuity has led to profound discovery that somatic cells could be induced to become pluripotent by simply adding four genes. Induced pluripotent stem cells (iPS cells) were first generated by two research teams led by Drs. Yamanaka and Thomson, respectively, who pioneered and generated stem cells PI3K Inhibitor Library clinical trial from human skin through ectopic expression of four genes (Oct3/4, Sox2, c-Myc, Tyrosine Kinase Inhibitor Library molecular weight and Klf4, or Oct3/4, Sox2, Nanog, and Lin28).13–15 Since their discovery, improvements have been made in generating iPS cells including the ability to remove the inducing genes,16 the addition of only one or two genes in certain cell types,17, 18 and generation of iPS cells by chemical induction.19, 20 In each case, no matter the inductive route, human iPS cells have been shown to mimic hESCs in virtually all aspects of pluripotency and differentiation. These iPS cells are pluripotent because they can form all three germ layers. Moreover,

mouse iPS cells have been repeatedly shown to make chimeric mice, contribute to the germ line, and generate pups.21 However, to date, most of the in vitro investigations

into iPS cell differentiation have focused on mesodermal-derived cardiomyocyte and ectodermal-derived neuronal lineages—that is, until now. In this issue, two independent laboratories reveal, for the first time, complete derivation of iPS cells into endodermal-derived hepatocytes (Sullivan et al.22 and Si-Tayeb et al.23). While the elegance of each study enables them to stand alone, when taken together, they, in essence, delineate the true potential of iPS cells for the field of hepatology. The data clearly reveal that iPS cells can become fully functional liver cells. Both articles demonstrate that iPS cell–derived hepatocytes express distinct hepatocyte markers; however, and perhaps more importantly, both also show definitive MCE公司 function of their hepatocytes in vitro and in vivo. The magnitude of these investigations will probably be felt straight away because they represent a seminal advancement in current hepatocyte cell-culture technology. A constant problem experienced by many who try to culture hepatocytes is that current protocols generally revolve around the need for consistent derivation and culture of primary hepatocytes, which have the reputation for being difficult to cultivate, are generally scarce, and are usually rather heterogeneous once in culture.

APC; Presenting Author: WENYI XIE Corresponding Author: WENYI XIE Affiliations: the ninth hospital of Chongqing Objective: To INK 128 chemical structure compare the expression of COX-2 mRNA in Barrett esophagus before and after treatment, analyze the efficacy of argon plasma coagulation in combination with acid suppression in BE patients. Methods: The BE patients diagnosed with endoscopy and biopsy were randomly classified into 3 groups, group A served as control, group B treated with PPI after APC, gourp C subjected to PPI treatment.

The clinical effect was observed in the follow-up patients and endosopy examination were taken. We used quantitive real-time PCR (Taqman) to access the mRNA expression of COX-2 in Barrett esophagus before and after treatment. Total tissue RNA was extracted from Selleck GW572016 BE. COX-2 mRNA was quantitatively analyzed by monitoring

the increase in fluorescence by the binding of SYBR green to double-stranded DNA during real-time PCR (Sequence detection system, TaqMan; Applied Biosystems, CA). The copy numbers of cDNA for COX-2 were standardized to glyceraldehyde-3-phosphate dehydrogenase from the same samples. Results: 1) All the treatment can alleviate or relieve the symptoms of BE compared to group A. There were no significant differences between them. 2) Patients of group B whose BE epithelium were eradicated and replaced with squamous epithelium. The sizes of Barrett’s esophagus didn’t change significantly in group A, C by endoscopy. 3) 上海皓元医药股份有限公司 The expression of Cox-2 in groupB is similar to the level of sham-control. The expression of Cox-2 in groupC also decrease, but there was no significant differences before and after treatment. Conclusion: PPI treatment can’t eradicate BE, but they can relieve clinical symptoms and decrease the expression of Cox-2 in BE epithelium. Argon plasma coagulation combined with PPI can eradicate BE epithelium and relieve clinical symptoms and decrease the expression of Cox-2 to the normal level. It is an effective, safe and promising therapy against Barrett’s esophagus. Key Word(s): 1. Barrett’s esophagus; 2. COX-2; 3. Bcl-2; 4. APC; Presenting Author: DIANCHUN FANG Additional Authors: JUN WANG Corresponding Author: DIANCHUN FANG

Affiliations: A member of standing committee, Association of Chinese Digestive Disease Objective: To investigate the effects of bile salt exposure on expression of tight junction proteins claudin-4 in squamous epithelium of gastroesophageal reflux disease and the role of the p38 MAPK in this course. Methods: Tissue samples from 80 patients with reflux esophagitis (RE, n = 31), and Nonerosive reflux disease (NERD, n = 29) and Barrett’s esophagus (BE, n = 20) were obtained in routine upper GI endoscopy. Expression of claudin-4 in tissue samples were measured by immunohistochemical staining. Expressions of claudin-4 and p38 in esophageal squamous cells treated by bile salt were detected with reverse trancriptase polymerase chain reaction (RT-PCR) and western blot method.

8% and 100% of patients respectively, while transami-nases were within normal range in 55.6% and 83.3% of patients respectively. A significant reduction in CPT score was observed from 8.84±1.7

at baseline to 7.66±2.24, 6.67±1.68 and 6.50±1.38 at 6, 12 and 24 months, respectively (P=0.003). Vismodegib CPT was >1 0 in 36.4% of the patients at baseline, 21.8% at 6 months, 5.5% at 12 months, and in no patients thereafter. Similarly Modification for End-stage Liver Disease (MELD) score was reduced from 14.22±4.15 at baseline to 13.44±4.45 and 12.06±3.78, at 6 and 12 months, respectively (p=0.018). The mean serum creatinine changed from 0.90±0.20 at baseline to 1.00+0.20, 1.07+0.23, 1.10+0.30 and 1.10+0.23 mg/dl at 12, 24, 26 and 48 months respectively (P=0.81). None of the patients discontinued treatment due to SAEs while in 2 patients the TDF dose was reduced. Three patients died at 2 and 4 months

of follow up because of liver failure and sepsis. All had severe disease (CPT and MELD scores 10.67±1.15 and 17.33±4.04, respectively). Treatment with TDF or ENT offered a significantly better survival rate compared to LAM monotherapy (log-rank test, P=0.02). Conclusions: In patients with selleck chemicals decompensated liver disease due to CHB, long term TDF and ENT monotherapy is well tolerated and associated with an improvement in biochemical, virological and clinical parameters. In these severely ill patients, TDF or ENT monotherapy improves survival when compared to lamivudine monotherapy. However deaths may occur soon after TDF/ETV initiation in patients with severe liver disease. Disclosures: Spilios Manolakopoulos – Advisory Committees or Review Panels: NOVARTIS, ROCHE,

MSD, BMS, GILEAD; Consulting: ROCHE, GILEAD, BMS; Speaking and Teaching: MSD, GILEAD, BMS Melanie Deutsch – Consulting: MSD George V. Papatheodoridis – Advisory Committees or Review Panels: Janssen, Abbott, Boehringer, Novartis, BMS, Gilead, Roche; Consulting: Roche; Grant/Research Support: BMS, Gilead, Roche; Speaking and Teaching: Janssen, Novartis, BMS, Gilead, Roche, MSD The following people have nothing to disclose: Christos K. Triantos, Nikoletta Mathou, Maria medchemexpress Mela, Athanasia Striki, Maria Kalafateli, Georgios Kontos, Hariklia Kranidioti, Emanuel K. Manesis Objectives: To evaluate the efficacy and safety of telbivudine in preventing mother-to-child transmission (MTCT) of hepatitis B virus (HBV) in HBeAg-positive pregnant women with high viral load. Methods: We investigated the effect of telbivudine in preventing MTCT of HBV in an open-label study since 2008. A total of 232 HBeAg-positive pregnant women with HBV DNA levels≧106 IU/mL received telbivudine 600 mg daily from 24 to 33 weeks of gestation, and 153 pregnant women with the same situation who were unwilling to take antiviral drugs were served as untreated controls. Each infant of both groups was vaccinated with recombinant HBV vaccine and injected with hepatitis B immune globulin (HBIG) according to standard routine methods.

A stepwise multiple linear regression analysis was employed to identify significant predictors of the number of drug doses taken per month. Results.— No significant association was found between 5HT2A A and 1438G and C516T gene polymorphisms and MOH risk. In contrast, a higher consumption of monthly drug doses was observed

among 516T 5HT2A carriers (median 50, range 13-120) compared to 516CC patients (median 30, range 12-128) (Mann–Whitney U-test, P = .018). In the stepwise multiple regression analysis, C516T 5HT2A polymorphism Rucaparib mw (P = .018) and class of overused drug (P = .047) emerged as significant, independent predictors of the monthly drug consumption in MOH patients. Conclusions.— Although our results do not support a major role of the A-1438G and C516T polymorphic variants of the 5HT2A gene in the susceptibility of MOH, our findings support an influence of the C516T polymorphism on the number of symptomatic drug doses taken and, possibly, on the drug-seeking behavior in these patients. “
“Objective.— The objective Selleck Ruxolitinib of this study was to assess the clinical benefits of onabotulinumtoxinA (BOTOX®) treatment on the symptoms

of cervical dystonia and the frequency, severity, and associated symptoms of migraine in patients with cervical dystonia and concurrent migraine. Background.— Botulinum toxin is established as first-line treatment of cervical dystonia. Recent clinical trials have shown onabotulinumtoxinA to be an effective prophylactic therapy for patients with chronic migraine, and onabotulinumtoxinA has been approved for use in this patient population by the Food and Drug Administration. Patients with headache associated

with cervical dystonia have been identified as a specific subpopulation of patients in whom botulinum toxin treatment may be effective for controlling the symptoms of both conditions. Methods.— An open-label pilot study was conducted for 7.5 months in patients at least 18 years old with primary cervical dystonia of moderate severity (baseline rating of at least 20 on the Toronto Western Spasmodic Torticollis Rating Scale) complicated by migraine headache meeting the International Classification of Headache Disorders-II criteria for migraines with or without aura. Each patient received 2 cycles of treatment 上海皓元 at Visit 3 (baseline) and Visit 6 (Day 90). For cervical dystonia, each patient was injected with a maximum of 175 units. At the same visit, a maximum of 125 units was also injected for migraine using a fixed-site, fixed-dose injection paradigm, with additional cervical dystonia injection-site treatment to a maximum dose of 300 units. Patients were assessed following onabotulinumtoxinA injection and at follow-up on Visit 4 (Day 30), Visit 5 (Day 60), Visit 6 (Day 90), and at Visits 7, 8, and 9 (Days 120, 150, and 180). The primary outcome measures for this study were change in Toronto Western Spasmodic Torticollis Rating Scale total score for cervical dystonia and frequency of headache episodes per 28-day period.

UCMSCs are widely characterized MSCs that are easy to obtain and to expand in culture. As we previously demonstrated, UCMSCs are capable of exhibiting many of the markers and functions typical of mature hepatocytes.16 Nevertheless, we observed variability in the quality of differentiation among donors. As shown by the direct correlation between CYP3A4

activity (a surrogate marker of differentiation state) and susceptibility to viral replication, quality of differentiation seems to be a key factor influencing efficiency of infection in D-UCMSCs. CYP3A4 activity could therefore be used as a marker to predict suitability of each UCMSCs population for infection studies. The understanding of the viral life cycle has been hampered by the extremely restrictive tropism of HBV. PHHs are the preferred tissue culture model, but they are difficult to obtain, maintain in culture, and infect in vitro.11 Primary Tupaia hepatocytes selleck chemical (PTH) are an interesting alternative.12, 13 Unfortunately, it is well known that susceptibility of primary hepatocytes to HBV infection is rapidly lost during prolonged culture.11 Such a loss in susceptibility has been correlated to the dedifferentiation process to which hepatocytes rapidly undergo in vitro.30 It has been shown that transcription Olaparib research buy of HBV genes and subsequent viral replication is dependent upon the degree of differentiation

of the host cell.1 Liver-enriched transcription factors such as HNF4α, HNF1α, and HNF3β have been shown to have a central role in regulating viral promoters 上海皓元 and enhancers.2, 3 Here we show that UCMSCs express HNF4α mRNA upon differentiation, but at a much lower level than PHHs, which could account for the observed lower intracellular replication efficiency. The role of the differentiation state on cell susceptibility to HBV entry is far less understood. HBV binding and uptake seem to be the most important determinants of HBV hepatotropism. Although

many different hepatoma-derived cell lines have been demonstrated to be capable of viral replication after transfection of the viral genome,4-6 very few in vitro models, besides PHHs, permit viral uptake.12-14 D-UCMSCs susceptibility to HBV uptake therefore makes them a highly promising model. HBV binding and entry into susceptible cells is a multistep process which is poorly understood. The initial attachment of the virus to the cell membrane is believed to be mediated by heparan sulfate proteoglycans,23 and does not seem to be specific for susceptible cells.26 A more specific binding to one or multiple receptors, expressed mainly on hepatocytes, and localized on the basolateral membrane, is probably responsible for the restricted HBV host range.31 Among the many candidate receptors, ASGPR is the only one that is strictly hepatocyte-specific.

UCMSCs are widely characterized MSCs that are easy to obtain and to expand in culture. As we previously demonstrated, UCMSCs are capable of exhibiting many of the markers and functions typical of mature hepatocytes.16 Nevertheless, we observed variability in the quality of differentiation among donors. As shown by the direct correlation between CYP3A4

activity (a surrogate marker of differentiation state) and susceptibility to viral replication, quality of differentiation seems to be a key factor influencing efficiency of infection in D-UCMSCs. CYP3A4 activity could therefore be used as a marker to predict suitability of each UCMSCs population for infection studies. The understanding of the viral life cycle has been hampered by the extremely restrictive tropism of HBV. PHHs are the preferred tissue culture model, but they are difficult to obtain, maintain in culture, and infect in vitro.11 Primary Tupaia hepatocytes GSK-3 beta pathway (PTH) are an interesting alternative.12, 13 Unfortunately, it is well known that susceptibility of primary hepatocytes to HBV infection is rapidly lost during prolonged culture.11 Such a loss in susceptibility has been correlated to the dedifferentiation process to which hepatocytes rapidly undergo in vitro.30 It has been shown that transcription Sorafenib purchase of HBV genes and subsequent viral replication is dependent upon the degree of differentiation

of the host cell.1 Liver-enriched transcription factors such as HNF4α, HNF1α, and HNF3β have been shown to have a central role in regulating viral promoters MCE and enhancers.2, 3 Here we show that UCMSCs express HNF4α mRNA upon differentiation, but at a much lower level than PHHs, which could account for the observed lower intracellular replication efficiency. The role of the differentiation state on cell susceptibility to HBV entry is far less understood. HBV binding and uptake seem to be the most important determinants of HBV hepatotropism. Although

many different hepatoma-derived cell lines have been demonstrated to be capable of viral replication after transfection of the viral genome,4-6 very few in vitro models, besides PHHs, permit viral uptake.12-14 D-UCMSCs susceptibility to HBV uptake therefore makes them a highly promising model. HBV binding and entry into susceptible cells is a multistep process which is poorly understood. The initial attachment of the virus to the cell membrane is believed to be mediated by heparan sulfate proteoglycans,23 and does not seem to be specific for susceptible cells.26 A more specific binding to one or multiple receptors, expressed mainly on hepatocytes, and localized on the basolateral membrane, is probably responsible for the restricted HBV host range.31 Among the many candidate receptors, ASGPR is the only one that is strictly hepatocyte-specific.

Disclosures: Kazuaki Chayama – Consulting: Abbvie;

Grant/Research Support: Dainippon Sumitomo, Chugai, Mitsubishi Īanabe, DAIICHI SANKYO, Toray, BMS, MSD; Speaking and Teaching: Chugai, Mitsubishi Īanabe, DAIIcHl SANKYO, KYORIN, Nihon Medi-Physics, BMS, Dainippon Sumitomo, MSD, ASKA, Astellas, AstraZeneca, Eisai, Olympus, GlaxoSmithKline, ZERIA, Bayer, Minophagen, Shinyaku, Takeda, AJINOMOTO, Meiji Seika, Toray The following people have nothing to disclose: Tsunehiro Ochi, Motoi Hashiba, Masafumi Ono, Hideyuki Hyogo, Yukio Ikeda, Kensuke Munekage, Nobuto Okamoto, Shinji Iwasaki, Yuichiro Eguchi, Toshiji Saibara Background/Aims: Gallstone disease and fatty liver are both prevalent diseases in the general populations and share the same risk factors Ku-0059436 research buy such as obesity and insulin resistance. However, association between gallstone disease and ultrasonographically diagnosed fatty liver has not been completely established. The aim of this study was to characterize the relationship between gallstone

disease and fatty liver in large population. Methods: A cross-sectional study with 24, 050 health check-up subjects was conducted. Gallstone disease was defined as the presence of gallstones on abdominal sonography or previous history of cholecystectomy. Fatty liver was diagnosed on the basis of typical ultrasonographic findings. Subjects positive for hepatitis B or C virus or BIBW2992 with a history of other forms of hepatitis were excluded. Results: The mean age of the subjects was 48.7 ± 11.1 years and 54.5% were male. The prevalence of gallstone disease was 5.3% (n=1, 280). The prevalence of fatty liver increased with presence of gallstone disease (43.0% vs.31.3%, p <0.001). In the same manner, the prevalence of gallstone disease increased with presence of fatty liver (7.2% vs.4.4%, p <0.001). The gallstone disease was significantly associated with fatty liver after adjusted for age 上海皓元医药股份有限公司 and sex [odds ratio (OR) 1.50 95%

confidence interval (Cl) 1.331.69]. Multivariate regression analysis after adjustment for body mass index, waist circumference, total cholesterol, triglycerides, HDL cholesterol, HbA1 c, and systolic blood pressure showed that gallstone disease was statistically significantly associated with fatty liver (OR 1.23, 95% CI 1.06-1.42, p=0.007). These association was attenuated, however still statistically significant after adjusting for insulin resistance (OR 1.27 95% Cl 1.04-1.55, p=0.018). Conclusions: Patients with fatty liver have a high prevalence of gallstone disease. Gallstone disease is associated with fatty liver independently of known metabolic risk factors, especially insulin resistance.