玉蚕枳椇膏对醉酒及酒精肝大鼠的影响

目的 探讨玉蚕枳椇膏对醉酒及酒精肝大鼠的影响。方法 将36只SD大鼠随机分为空白对照组、模型对照组、联苯双酯阳性对照组、低剂量玉蚕枳椇膏组(2g/kg)、中剂量玉蚕枳椇膏组(4g/kg)和高剂量玉蚕枳椇膏组(8g/kg),连续给予药物35d。给予药物后间隔4h,每7天,除了空白对照组外,都给予灌胃1mL/kg牛栏山二锅头。观察大鼠体重变化、平衡木行走、醉酒和醒酒时间等,考察对大鼠醉酒的影响。利用肝重指数、肝脏形态、苏木素-伊红染色,评价对大鼠肝脏的影响。结果 与模型对照组相比,中高剂量组大鼠平衡木行走更稳定些;醉酒时间显著延长;醒酒时间显著缩短;肝细胞结构紊乱、胞质脂肪空泡化以及细胞边界模糊等均有一定的改善。结论 中高剂量玉蚕枳椇膏对醉酒及酒精肝大鼠具有一定干预作用。

电子鼻技术对哈达山白酒中掺兑酒精的鉴别

结合主成分分析法(PCA)、线性判别分析法(LDA)和方差分析法(ANOVA),通过单因素试验确定了样品测试时的较佳酒精度、装样体积和装样瓶顶空生成时间分别为1.9%vol、15 mL和30 min。并在优化参数条件下,对哈达山粮食酒和酒精酒进行鉴别。结果表明,采用主成分分析法及线性判别分析法,电子鼻技术可鉴别哈达山粮食酒与食用酒精含量分别为0.38%vol、0.76%vol、0.95%vol、1.14%vol、1.52%vol、1.90%vol的酒精酒。两种分析方法相比,线性判别分析法比主成分分析法鉴别效果更好。

呼气式酒检技术及其防醉驾应用的发展综述

根据国内外发展现状,从呼气酒检标准和气样采集方法、影响酒检结果准确性的因素、各种酒检技术优缺点、防酒驾应用的若干实用措施等方面,对呼气酒检技术及其防醉驾应用做出综述,并给出发展建议。

通过政策调整促进白酒质量的提高

中国是世界酒类消费大国,中国酿酒技术具有悠久的历史。在科学技术突飞猛进发展的今天,中国逐渐由发酵白酒朝着勾调新型白酒的方向发展,与国际制酒行业趋于一致,这无疑是酿酒工业的进步。然而中国白酒出口却困难重重。其主要原因之一是中国白酒的理化指标还没有达到发达国...

Prevention and Cure of Acute Alcohol Intoxication in Mice by Administration of Compound of Japanese Raisintree Fruit, Lobed Kudzuvine Flower Bud and Lightyellow Sophora Root

[Objective] We aimed to investigate the preventive and therapeutical effect of compound of traditional Chinese drugs （Japanese raisintree fruit, lobed kudzuvine flower bud and lightyel ow sophora root） on acute alcohol intoxication in mice. [Method] Acute alcohol intoxication was induced by administering alcohol to mice. Three different doses （low, middle and high） of compound of traditional Chinese drugs were administered to mice before and after administering alcohol respectively to investigate the preventive and therapeutical effect of drugs on acute alcohol intox-ication through doing statistical analysis about drunk mice and their sleeping time. The concentration of malondialdehyde （MDA）, reduced glutathione （GSH） and triglyc-erides （TG） in liver was also determined to investigate the protective effect of drugs on liver. [Result] The efficacy of compound of traditional Chinese drugs on acute al-cohol intoxication was dose-dependent. High-dose administration decreased the number of drunk mice significantly compared with control group; middle- and high-dose administration reduced the sleeping time of drunk mice and the concentration of MDA and TG in liver tissue; three doses al increased the concentration of GSH. [Conclusion] The compound of Japanese raisintree fruit, lobed kudzuvine flower bud and lightyel ow sophora root had preventive and therapeutical effect on hangover, and it also had certain preventive and therapeutical effect on liver damage caused by alcohol.

Does an association exist between chronic pancreatitis and liver cirrhosis in alcoholic subjects?

AIM: To study the possible association between chronic pancreatitis (CP) and liver cirrhosis (LC) of alcoholic etiology,after excluding any other causes.METHODS: One hundred and forty consecutive alcoholic patients were subdivided into three groups: CP (n = 53),LC (n = 57),and asymptomatic alcoholic (n = 30).Clinical,biochemical and morphological characteristics,Child-Pugh index,indocyanine green test,and fecal pancreatic elastase-1 test were assessed.RESULTS: In patients with cirrhosis,major clinical manifestations of CP such as pancreatic pain and steatorrhea,as well as imaging alterations of CP such as calcifications,duct dilation and pseudocysts were absent; insulin-dependent diabetes was present in 5.3% of cases,and elastase-1 test was altered in only 7%,and severely altered in none.In patients with CP,clinical characteristics of cirrhosis such as ascites,encephalopathy and gastrointestinal hemorrhage were present in one case,Child-Pugh grade > A in 5.7%,and altered indocyanine green test in 1.9% cases.In asymptomatic alcoholism,there was only a non-coincident alteration of elastase-1 test and indocyanine test in 14.8% and 10%,respectively,but other characteristics of cirrhosis or CP were absent.An inverse correlation (r = -0.746) between elastase-1 test and indocyanine test was found in alcoholic patients.CONCLUSION: There is a scarce coincidence in clinical and morphological alterations among patients with CP or LC of alcoholic etiology,but an inverse correlation between pancreatic and liver function tests.These findings support that these alcoholic diseases evolve in a different manner and have different etiopathogenesis.

Genetic polymorphism in CD14 gene, a co-receptor of TLR4 associated with non-alcoholic fatty liver disease

AIM To evaluate the pathogenic role of toll-like receptor(TLR) gene polymorphisms in patients with nonalcoholic fatty liver disease(NAFLD).METHODS Two hundred and fifty subjects(NAFLD = 200, healthy volunteers = 50) underwent polymerase chain reaction and restriction fragment length polymorphism to assess one polymorphism in the toll-like receptor 2(TLR2) gene(A753G), two polymorphisms in the TLR4 gene(TLR4 Asp299 Gly and Thr399 Ile allele), and two polymorphisms in the cluster of differentiation 14(CD14)(C-159 T and C-550T) gene, a co-receptor of TLR4. Association of TLR gene polymorphisms with NAFLD and its severity was evaluated by genetic models of association.RESULTS On both multiplicative and recessive models of gene polymorphism association, there was significant association of CD14 C(-159) T polymorphism with NAFLD; patients with TT genotype had a 2.6 fold increased risk of developing NAFLD in comparison to CC genotype. There was no association of TLR2 Arg753 Gln, TLR4 Asp299 Gly, Thr399 Ile, and CD14 C(-550) T polymorphisms with NAFLD. None of the TLR gene polymorphisms had an association with histological severity of NAFLD.CONCLUSION Patients with CD14 C(-159) T gene polymorphism, a co-receptor of TLR4, have an increased risk of NAFLD development.

Oral administration of a non-absorbable plant cellexpressed recombinant anti-TNF fusion protein induces immunomodulatory effects and alleviates nonalcoholic steatohepatitis

AIM To evaluate the immunomodulatory effect of oral administration of PRX-106 in the high-fat diet model.METHODS For 22 wk, C57BL/6 HFD-fed mice received daily oral treatments with BY-2 cells expressing recombinant antitumor necrosis factor alpha fusion protein(PRX-106). Mice were followed for serum liver enzyme and triglyceride levels, liver histology and intrahepatic and systemic FACS.RESULTS The orally administered non-absorbable PRX-106 w a s b i o l o g i c a l l y a c t i v e. A l t e r e d d i s t r i b u t i o n o f CD4+CD25+Fox P3+ between the liver and spleen and an increase in the intrasplenic-to-intrahepatic CD4+CD25+Fox P3+ ratio and a decrease in the intrasplenic-to-intrahepatic CD8+CD25+Fox P3+ ratio were observed. An increase in intrahepatic NKT cells and a decrease in the intrasplenic-to-intrahepatic NKT ratio were noted. Assessment of the CD4-to-CD8 ratios showed sequestration of CD8+ lymphocytes in the liver. These effects were associated with a decrease in serum triglyceride levels, decrease in the aspartate aminotransferase levels, serum glucose levels, and HOMA-IR score. A decrease in hepatic triglycerides content was observed in the high dose-treated mice.CONCLUSION Orally administered PRX-106 shows biological activity and exerts an immunomodulatory effect, alleviating liver damage. The data suggest that PRX-106 may provide an oral immunotherapy for nonalcoholic steatohepatitis.

Th17 involvement in nonalcoholic fatty liver disease progression to non-alcoholic steatohepatitis

The nonalcoholic fatty liver disease(NAFLD) is the hepatic manifestation of the metabolic syndrome. NAFLD encompasses a wide histological spectrum ranging from benign simple steatosis to non-alcoholic steatohepatitis(NASH). Sustained inflammation in the liver is critical in this process. Hepatic macrophages, including liver resident macropaghes(Kupffer cells), monocytes infiltrating the injured liver, as well as specific lymphocytes subsets play a pivotal role in the initiation and perpetuation of the inflammatory response, with a major deleterious impact on the progression of fatty liver to fibrosis. During the last years, Th17 cells have been involved in the development of inflammation not only in liver but also in other organs, such as adipose tissue or lung. Differentiation of a na?ve T cell into a Th17 cell leads to pro-inflammatory cytokine and chemokine production with subsequent myeloid cell recruitment to the inflamed tissue. Th17 response can be mitigated by T regulatory cells that secrete anti-inflammatory cytokines. Both T cell subsets need TGF-β for their differentiation and a characteristic plasticity in their phenotype may render them new therapeutic targets. In this review, we discuss the role of the Th17 pathway in NAFLD progression to NASH and to liver fibrosis analyzing different animal models of liver injury and human studies.

Ethanol induced mitochondria injury and permeability transition pore opening: Role of mitochondria in alcoholic liver disease

AIM: To observe changes of mitochondria and investigate the effect of ethanol on mitochondrial perme- ability transition pore (PTP), mitochondrial membrane potential (MMP, ΔΨm) and intracellular calcium concentration in hepatocytes by establishing an animal model of alcoholic liver disease (ALD). METHODS: Fourty adult male Wistar rats were randomly divided into two groups, the model group (20) was administered alcohol intragastrically plus an Oliver oil diet to establish an ALD model, and the control group (20) was given an equal amount of normal saline. The ultramicrostructural changes of mitochondria were observed under electron microscopy. Mitochondria of liver was extracted, and patency of PTP, mitochondrial membrane potential (ΔΨm), mitochondrial mass and intracellular calcium concentration of isolated hepacytes were detected by flow cytometry using rhodamine123 (Rh123), Nonyl-Acridine Orange and calcium fluorescent probe Fluo-3/AM, respectively. RESULTS: Membrane and cristae were broken or disappeared in mitochondria in different shapes under electron microscopy. Some mitochondria showed U shape or megamitochondrion. In the model group, liver mitochondria PTP was broken, and mitochondria swelled, the absorbance at 450 nm, A540 decreased (0.0136 ± 0.0025 vs 0.0321 ± 0.0013, model vs control, P < 0.01); mitochondria transmembrane potential (239.4638 ± 12.7263 vs 377.5850 ± 16.8119, P < 0.01) was lowered; mitochondrial mass (17.4350 ± 1.9880 vs 31.6738 ± 3.4930, P < 0.01); and [Ca2+]i was increased in liver cells (7.0020 ± 0.5008 vs 10.2050 ± 0.4701, P < 0.01).CONCLUSION: Chronic alcohol intake might lead to broken mitochondria PTP, decreased mitochondria membrane potential and injury, and elevated intracellular Ca2+ production. Ethanol-induced chondriosome injury may be an important mechanism of alcoholic diseases.

Changes in blood alcohol concentration and driving ability after alcohol intake

Objective: To study the relationship between the amount of consumed alcohol, blood alcohol concentration (BAC), and driving ability among a part of the population in Southwest China and to provide reference for the formulation of the legal limits for safe driving. Methods: Seventy-six randomly selected volunteer drivers each had three times of alcohol intake (100 ml each time). After each drank, BAC was measured with gas chromatograph and driving ability was evaluated. The drivers were grouped according to age, weight, alcohol tolerance and driving experience respectively and changes in BAC and driving ability were analyzed. Results: Average BAC and the percentage of drivers showing impaired driving ability in the groups increased after each intake of 100 ml alcohol. BAC in Group≤60 kg was more susceptible to alcohol than that in Group>60 kg. When each drank, alcohol had greater influence on drivers who had comparatively shorter driving experience. Conclusion: Volume of consumed alcohol, BAC and driving ability have direct associations among one another and are all under the influence of various factors including individual conditions. To set an appropriate legal BAC limit for safe driving should take an overall consideration of all factors.

Effects of ethanol on hepatic cellular replication and cell cycleprogression

Ethanol is a hepatotoxin. It appears that the liver is the target of ethanol induced toxicity primarily because it is the major site of ethanol metabolism. Metabolism of ethanol results in a number of biochemical changes that are thought to mediate the toxicity associated with ethanol abuse. These include the production of acetaldehyde and reactive oxygen species, as well as an accumulation of nicotinamide adenine dinucleotide （NADH）. These biochemical changes are associated with the accumulation of fat and mitochondrial dysfunction in the liver. If these changes are severe enough they can themselves cause hepatotoxicity, or they can sensitize the liver to more severe damage by other hepatotoxins. Whether liver damage is the result of ethanol metabolism or some other hepatotoxin, recovery of the liver from damage requires replacement of cells that have been destroyed. It is now apparent that ethanol metabolism not only causes hepatotoxicity but also impairs the replication of normal hepatocytes. This impairment has been shown to occur at both the GI/S, and the G2/M transitions of the cell cycle. These impairments may be the result of activation of the checkpoint kinases, which can mediate cell cycle arrest at both of these transitions. Conversely, because ethanol metabolism results in a number of biochemical changes, there may be a number of mechanisms by which ethanol metabolism impairs cellular replication. It is the goal of this article to review the mechanisms by which ethanol metabolism mediates impairment of hepatic replication.

Effect of a counseling-supported treatment with the Mediterranean diet and physical activity on the severity of the non-alcoholic fatty liver disease

AIM To determine the clinical effectiveness of nutritional counseling on reduction of non-alcoholic fatty liver disease(NAFLD) severity, weight loss, metabolic and anthropometric indexes and liver enzymes.METHODS Forty-six adults with NAFLD received a 6-mo clinical and a dietary intervention(based on Mediterranean diet) carried out respectively by a gastroenterologist and a nutritionist with counseling license. The counseling process consisted of monthly meeting(about 45 min each). The effect of the treatment was evaluated monitoring liver enzymes, metabolic parameters, cardiovascular risk indexes, NAFLD severity [assessed by ultrasound(US)] and related indexes. All parameters were assessed at baseline. Biochemistry was also assessed at mid-and end-interventions and US was repeated at end-intervention.RESULTS The percentage of patients with steatosis grade equal or higher than 2 was reduced from 93% to 48% and steatosis regressed in 9 patients(20%). At the end of the treatment the end-point concerning the weight(i.e., a 7% weight reduction or achievement/maintenance of normal weight) was accomplished by 25 out of 46 patients(i.e., 54.3%). As far as the liver enzymes is concerned, all three liver enzymes significantly decrease during the treatment the normalization was particularly evident for the ALT enzyme(altered values reduced from 67% down to 11%). Several parameters, i.e., BMI, waist circumference, waist-to-hip ratio, AST, ALT, GGT, HDL, serum glucose, Tot-Chol/HDL, LDL/HDL, TG/HDL, AIP, HOMA, FLI, Kotronen index, VAI, NAFLD liver fat score and LAP, showed a significant improvement(P < 0.01) between baseline and end-treatment.CONCLUSION Outcomes of this study further strengthen the hypothesis that Med Diet and more active lifestyle can be considered a safe therapeutic approach for reducing risk and severity of NAFLD and related disease states. The proposed approach may be proposed as a valid and recommended approach for improving the clinical profile of NAFLD patients.

Alcohol-induced protein hyperacetylation: Mechanisms and consequences

Although the clinical manifestations of alcoholic liver disease are well-described, little is known about the molecular basis of liver injury. Recent studies have indicated that ethanol exposure induces global protein hyperacetylationo This reversible, post- translational modification on the E-amino groups of lysine residues has been shown to modulate multiple, diverse cellular processes ranging from transcriptional activation to microtubule stability. Thus, alcohol- induced protein hyperacetylation likely leads to major physiological consequences that contribute to alcohol-induced hepatotoxicity. Lysine acetylation is controlled by the activities of two opposing enzymes, histone acetyltransferases and histone deacetylases. Currently, efforts are aimed at determining which enzymes are responsible for the increased acetylation of specific substrates. However, the greater challenge will be to determine the physiological ramifications of protein hyperacetylation and how they might contribute to the progression of liver disease. In this review, we will first list and discuss the proteins known to be hyperacetylated in the presence of ethanol. We will then describe what is known about the mechanisms leading to increased protein acetylation and how hyperacetylation may perturb hepatic function.

Alcohol consumption in patients with primary sclerosing cholangitis

AIM:To assess the alcohol drinking patterns in a cohort of primary sclerosing cholangitis(PSC) patients and the possible influence on the development of fibrosis.METHODS:Ninety-six patients with PSC were evaluated with a validated questionnaire about a patient's lifetime drinking habits:the lifetime drinking history(LDH) questionnaire.In addition,clinical status,transient elastography and biochemistry values were analysed and registered.Patients were defined as having either significant or non-significant fibrosis.Significant fibrosis was defined as either an elastography value of ≥ 17.3 kPa or the presence of clinical signs of cirrhosis.Patients were divided into two groups depending on their alcohol consumption patterns;no/low alcohol consumption(one drink or unit/d) and moderate/high alcohol consumption(≥ 1 drink or unit/d).LDH data were calculated to estimate lifetime alcohol intake(LAI),current alcohol intake,drinks per year before and after diagnosis of PSC.We also calculated the number of episodes of binge-drinking(defined as consuming ≥ 5 drinks per occasion) in total,before and after the diagnosis of PSC.RESULTS:The mean LAI was 3882 units of alcohol,giving a mean intake after onset of alcohol consumption of 2.6 units per week.Only 9% of patients consumed alcohol equal to or more than one unit per day.Current alcohol intake in patients with significant fibrosis(n = 26) was less than in patients without significant fibrosis(n = 70),as shown by lower values of phosphatidylethanol(B-PEth)(0.1 mol/L vs 0.33 mol/L,respectively,P = 0.002) and carbohydrate-deficient transferrin(CDT)(0.88% vs 1.06%,respectively,P = 0.02).Self-reported LAI was similar between the two groups.Patients with significant fibrosis reduced their alcohol intake after diagnosis from 103 to 88 units per year whereas patients without fibrosis increased their alcohol intake after PSC diagnosis from 111 to 151 units/year.There were no correlations between elastography values and intake of alcohol(units/year)(r =-0.036).CONCLUSION:PSC patients have low alcohol consumption.The lack of correlation between fibrosis and alcohol intake indicates that a low alcohol intake is safe in these patients.

Phenolic Compounds and Antiradical Efficiency of Georgian （Kakhethian） Wines

According to ancient Georgian traditional winemaking technology, the crushed grape is placed in a clay vessel （qvevri） dug in the ground, and alcoholic fermentation is carried out together with solid parts of grape cluster （stem, skin, seeds）. Quantitative content of phenolic compounds and antiradical efficiency of Kakhethian wines were studied and findings are compared to the appropriate data of the European wines. Analysis showed Kakhethian wines to considerably surpass the European wines with regard to total phenolics compounds： 1,330-2,430 mg/L （Kakhethian white wines）, 210-468 mg/L （European white wines）, 2,898-4,416 mg/L （Kakhethian red wines）, 1,630-2,340 mg/L （European red wines）. Average value of antiradical efficiency of white and red wines of Kakhethian type was found to exceed the average value of antiradical efficiency of white and red wines of European type, by 2.3 and 1.7 times, respectively. Georgian wines in the world market are submitted in an insufficient measure, and the purpose of this work is r^v~alino their naritiv~ a,nlitie~

Liver histology according to the presence of metabolic syndrome in nonalcoholic fatty liver disease cases

AIM:To investigate the histologic features of the liver in nonalcoholic fatty liver disease (NAFLD) cases according to the presence of metabolic syndrome or its individual components. METHODS:We enrolled 81 patients (40 male,41 fe-male) who were diagnosed with fatty liver by ultraso-nographic scan and fulfi lled the inclusion criteria. First anamnesis,anthropometric,clinical,laboratory and imaging features of all participants were recorded and then liver biopsy was performed after gaining consent from patients. Diagnosis of metabolic syndrome was dependent on patients having 3 or more out of 5 risk criteria defined by the WHO. Biopsy specimens were assessed according to Brunt et al's classification. RESULTS:Sixty-nine of the 81 patients had nonalco-holic steatohepatitis (NASH),11 had simple fatty liver and 1 had cirrhosis according to histologic evaluation. Comparisons were made between two groups of NASH patients,those with and without metabolic syndrome. We did not detect statistically significant differences in liver histology between NASH patients with and wit-hout metabolic syndrome. CONCLUSION:NASH can progress without metabolic risk factors or the presence of metabolic syndrome.

Effect of Propanoic Acid on Ethanol Fermentation by Saccharomyces cerevisiae in an Ethanol-Methane Coupled Fermentation Process

Propanoic acid accumulated in an ethanol-methane coupled fermentation process affects the ethanol fermentation by Saccharomyces cerevisiae. The effects of propanoic acid on ethanol production were examined in cassava mash under different pH conditions. Final ethanol concentrations increased when undissociated propanoic acid was <30.0 mmol·L-1 . Propanoic acid, however, stimulated ethanol production, as much as 7.6% under proper conditions, but ethanol fermentation was completely inhibited when undissociated acid was >53.2 mmol·L-1 . Therefore, the potential inhibitory effect of propanoic acid on ethanol fermentation may be avoided by controlling the undissociated acid concentrations through elevated medium pH. Biomass and glycerol production decreased with propanoic acid in the medium, partly contributing to increased ethanol concentration.

Hydrolysis of Banana Tree Pseudostem and Second-Generation Ethanol Production by Saccharomyces Cerevisae

The alcoholic fermentation of substrates rich in free soluble sugars is well known and has been industrially developed. However, the production of second-generation ethanol from lignocellulosic biomass, which is abundantly available worldwide, remains under development. The aim of this study was to evaluate the possibility of using the Musa cavendischii banana tree pseudostem as a substrate for alcoholic fermentation. Hydrolisis methods using dilute sulfuric acid （1% and 2% H2SO4; 15 and 30 min; 90 ℃, 100 ℃ and 120 ℃） and enzymes （pH 5.5; and 45 ℃ for 24 h reaction time） were evaluated both separately and in combination. The effect of chemical pre-treatment of the substrate using 1% and 3% m/m NaOH （120 ℃, 15 min） was verified for both methods. The highest yield coefficient of fermentable sugars from dry biomass （Yrs = 74%） was obtained using enzymatic hydrolysis and pre-treatment with 3% NaOH. Using acid hydrolysis, the maximum yield obtained was 22% （1% H2SO4, 120 ℃, 30 min）. Fermentation of the hydrolysates was satisfactory, and the maximum yield of ethanol formed per unit of substrate consumed, total productivity and efficiency values were 0.35 g, 0.90 g ethanol L^-1·h^-1 and 65.9%, respectively. This demonstrates the utility of banana tree pseudostems in second-generation ethanol production.

Sitagliptin in patients with non-alcoholic steatohepatitis: A randomized, placebo-controlled trial

AIMTo evaluate the effect of sitagliptin vs placebo on histologic and non-histologic parameters of non-alcoholic steatohepatitis (NASH).METHODSTwelve patients with biopsy-proven NASH were randomized to sitagliptin (100 mg daily) (n = 6) or placebo (n = 6) for 24 wk. The primary outcome was improvement in liver fibrosis after 24 wk. Secondary outcomes included evaluation of changes in NAFLD activity score (NAS), individual components of NAS (hepatocyte ballooning, lobular inflammation, and steatosis), glycemic control and insulin resistance [including measurements of glycated hemoglobin (HbA1C) and adipocytokines], lipid profile including free fatty acids, adipose distribution measured using magnetic resonance imaging (MRI), and thrombosis markers (platelet aggregation and plasminogen activator inhibitor 1 levels). We also sought to determine the correlation between changes in hepatic fat fraction (%) [as measured using the Iterative Decomposition of water and fat with Echo Asymmetry and Least-squares estimation (IDEAL) MRI technique] and changes in hepatic steatosis on liver biopsy.RESULTSSitagliptin was not significantly better than placebo at reducing liver fibrosis score as measured on liver biopsy (mean difference between sitagliptin and placebo arms, 0.40, P = 0.82). There were no significant improvements evident with the use of sitagliptin vs placebo for the secondary histologic outcomes of NAS total score as well as for the individual components of NAS. Compared to baseline, those patients who received sitagliptin demonstrated improved HbA1C (6.7% &#x000b1; 0.4% vs 7.9% &#x000b1; 1.0%, P = 0.02), and trended towards improved adiponectin levels (4.7 &#x000b1; 3.5 &#x003bc;g/mL vs 3.9 &#x000b1; 2.7 &#x003bc;g/mL, P = 0.06) and triglyceride levels (1.26 &#x000b1; 0.43 mmol/L vs 2.80 &#x000b1; 1.64 mmol/L, P = 0.08). However, when compared with placebo, sitagliptin did not cause a statistically significant improvement in HbA1C (mean difference, -0.7%, P = 0.19) nor triglyceride levels (mean difference -1.10 mmol/L, P = 0.19) but did trend towards improved adiponectin levels only (mean difference, 0.60 &#x003bc;g/mL, P = 0.095). No significant changes in anthropometrics, liver enzymes, other adipocytokines, lipid profile, thrombosis parameters, or adipose distribution were demonstrated. The MRI IDEAL procedure correlated well with steatosis scores obtained on liver biopsy in both groups at baseline and post-treatment, and the Spearman correlation coefficients ranged from r = 0.819 (baseline) to r = 0.878 (post-treatment), P = 0.002.CONCLUSIONSitagliptin does not improve fibrosis score or NAS after 24 wk of therapy. The MRI IDEAL technique may be useful for non-invasive measurement of hepatic steatosis.