OBJECTIVE:To investigate the effect of acupuncture of"Daimai"(GB26) on abdominal fat accumulation, lipid metabolism and hepatic oxidative stress in abdominal obese non-alcoholic fatty liver disease (NAFLD) rats.

METHODS:male SD rats were divided into 3 groups: normal diet (normal,＝8), high fat diet control (model) and acupuncture (＝8/group in the latter 2 groups). The abdominal obese NAFLD model was established by feeding the rats with high fat diet for 12 weeks. EA (2 Hz/15 Hz, 1.5 mA) was applied to bilateral GB26 for 20 min, once every other day for 8 weeks. Rats of the model group were also restrained for 20 min as those in the EA group. The body mass and abdominal circumference were measured weekly, the isolated adipose tissues around the bilateral kidney and epididymis and the fresh liver were weighed. The contents of serum cholesterol (TC), triglyceride (TG), alanine transaminase (ALT), glutamic oxaloacetic aminotransferase (AST) were detected by using an automatic biochemical analyzer. The abdominal visceral fat distribution was acquired by CT scanning. The oxidative stress indexes of the homogenated liver tissues, such as malondialdehyde (MDA) was assayed using sodium thiobarbital (TBA) method, and theactivity of total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-PX) were assayed by using hydroxylamine method and colorimetric method respectively. The histopathological changes of the liver were observed after staining with hematoxylin-eosin (HE).

RESULTS:Following modeling, the body mass and waist circumference, visceral fat weight of bilateral kidneys and testis (visceral fat weight), liver weight, serum ALT, AST, TG and TC and liver MDA contents, were significantly higher in the model group (<0.001，<0.05), while hepatic T-SOD and GSH-PX activity was considerably lower in the model group than those in the normal group (<0.001). After acupuncture intervention, the levels of all the above-mentioned indexes (modeling induced both increase and decrease) were reversed relevant to the model group (<0.05,<0.01). The results of CT scanning showed that the fat accumulation area in the abdomen was 8.67 cm18.51 cmand 13.75 cmin the normal, model and acupuncture groups, respectively, presenting a decrease after acupuncture. H．E. staining displayed that the degree of hepatic steatosis (including vague hepatic lobule boundary, disordered arrangement of hepatic cord, hepatocellular swelling, diffuse fatty degeneration, unequal-sized lipid droplets in the hepatocytes, nucleus excursion and dissolution after modeling) wasimproved after acupuncture.

CONCLUSION:Acupuncture can reduce body weight and abdominal fat accumulation in abdominal obese NAFLD rats, which may be related to its effects in inhibiting oxidative stress (lowering MDA level and increasing the activity of T-SOD and GSH-PX) and improving hepatic lipid metabolism.

BACKGROUND:Non-alcoholic fatty liver disease (NAFLD) has become one of the most prevalent chronic liver disease all over the world. The objective of this study was to evaluate the association between dietary vitamin C intake and NAFLD.

METHOD:Subjects were diagnosed with NAFLD by abdominal ultrasound examination and the consumption of alcohol was less than 40g/day for men or less than 20g/day for women. Vitamin C intake was classified into four categories according to the quartile distribution in the study population:≤74.80 mg/day, 74.81-110.15 mg/day, 110.16-146.06 mg/day, and ≥146.07 mg/day. The energy and multi-variable adjusted odds ratio (OR), as well as their corresponding 95% confidence interval (CI), were used to determine the relationship between dietary vitamin C intake and NAFLD through logistic regression.

RESULT:The present cross-sectional study included 3471 subjects. A significant inverse association between dietary vitamin C intake and NAFLD was observed in the energy-adjusted and the multivariable model. The multivariable adjusted ORs (95%CI) for NAFLD were 0.69 (95%CI: 0.54-0.89), 0.93 (95%CI: 0.72-1.20), and 0.71 (95%CI: 0.53-0.95) in the second, third and fourth dietary vitamin C intake quartiles, respectively, compared with the lowest (first) quartile. The relative odds of NAFLD was decreased by 0.71 times in the fourth quartile of dietary vitamin C intake compared with the lowest quartile. After stratifying data by sex or the status of obesity, the inverse association remained valid in the male population or non-obesity population, but not in the female population or obesity population.

CONCLUSION:There might be a moderate inverse association between dietary vitamin C intake and NAFLD in middle-aged and older adults, especially for the male population and non-obesity population.

Nonalcoholic fatty liver disease (NAFLD) is considered one of the most common and most important conditions affecting the liver, because of its increasing prevalence all over the world. It is usually associated with elevated liver enzymes and ranges from simple steatosis to liver cirrhosis. This study was conducted to compare the effects of electroacupuncture (EA) versus aerobic interval training (AIT) exercise and how they affect liver functions in people suffering from nonalcoholic fatty liver.This study was carried out on 50 female patients suffering from NAFLD with age ranging from 30 to 55 years; they were randomly divided into two equal groups: group A received (EA) stimulation at points of liver 3 (LR3), liver 14 (LR14), gall bladder 34 (GB34), and stomach 36 (ST36), whereas group B received AIT exercise. All patients in both groups A and B received 3 sessions per week for 6 weeks (receiving noninterrupted 18 sessions) in addition to their standard medications. Evaluation of all patients in both groups A and B was carried out before and after the treatment program by measuring the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglycerides (TGs), and C-reactive protein (CRP).There is a significant decrease ( < 0.05) of ALT, AST, TGs, and CRP within each group, A and B, after 6 weeks of treatment sessions. A significant difference post-treatment was found between both groups in ALT, AST, and TGs ( < 0.05). However, there was no significant difference in CRP ( > 0.05) between both groups post-treatment.It can be concluded that both EA and AIT exercise are potent modalities that improve liver functions in people with NAFLD with better effect toward EA.

The failure of Kupffer cells (KCs) to remove endotoxin is an important factor in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). In this study, the effects of exercise training on KC function were studied in terms of in vivo endotoxin clearance and inflammatory responses. Mice were allocated into rest and exercise groups. KC bead phagocytic capacity and plasma steroid hormone levels were determined following exercise training. Endotoxin and inflammatory cytokine levels in plasma were determined over time following endotoxin injection. KC bead phagocytic capacity was potentiated and clearance of exogenously-injected endotoxin was increased in the exercise group. Inflammatory cytokine (TNF-α and IL-6) levels were lower in the exercise group. We found that only DHEA was increased in the plasma of the exercise group. In an in vitro experiment, the addition of DHEA to RAW264.7 cells increased bead phagocytic capacity and attenuated endotoxin-induced inflammatory responses. These resultssuggest that exercise training modulates in vivo endotoxin clearance and inflammatory responses in association with increased DHEA production. These exercise-induced changes in KC capacity may contribute to a slowing of disease progression in NAFLD patients.

BACKGROUND & AIMS:The burden of non-alcoholic fatty liver disease (NAFLD) is increasing worldwide. We performed a meta-analysis to determine the effectiveness of exercise-based lifestyle interventions on liver-specific endpoints in populations with NAFLD and underlying metabolic disorders such as obesity, type-2 diabetes, or the metabolic syndrome.

METHODS:We searched PUBMED-MEDLINE, EMBASE, and the Cochrane Central register, through 21st October, 2015 for randomized trials of exercise-based lifestyle interventions on endpoints such as intrahepatic lipid content and blood levels of alanine and aspartate aminotransferases. Effect sizes are reported as standardized mean difference and weighted mean difference values. To investigate heterogeneity, we performed sensitivity and meta-regression analyses. Results were reported according to the PRISMA statement.

RESULTS:We analyzed data from 28 trials. Physical activity, independently from diet change, was associated with a significant reduction in intra-hepatic lipid content (standardized mean difference, -0.69; 95% confidence interval [CI], -0.90 to -0.48) and with reductions in alanine aminotransferase (weighted mean difference, -3.30 IU/l; 95% CI, 5.57 to -1.04) and aspartate aminotransferase (weighted mean difference, -4.85 IU/l; 95% CI, -8.68 to -1.02). By meta-regression, we found individuals with increasing body mass index to be increasingly more likely to benefit from the intervention (beta coefficient = -0.10; P=.037). We recorded no effect modification by variables related to the intensity of the intervention.

CONCLUSIONS:In a meta-analysis of randomized trials, we found strong evidence that physical activity reduces intrahepatic lipid content and markers of hepatocellular injury in patients with NAFLD. This effect correlated with baseline body mass index.

AIMS:Supervised exercise reduces liver fat and improves endothelial function, a surrogate of cardiovascular disease risk, in non-alcoholic fatty liver disease (NAFLD). We hypothesised that after a 16-week supervised exercise program, patients would maintain longer-term improvements in cardiorespiratory fitness, liver fat and endothelial function.

MATHERIALS AND METHODS:Ten NAFLD patients [5/5 males/females, age 51±13years, BMI 31±3 kg.m(2) (mean±s.d.)] underwent a 16-week supervised moderate-intensity exercise intervention. Biochemical markers, cardiorespiratory fitness (VO2peak), subcutaneous, visceral and liver fat (measured by magnetic resonance imaging and spectroscopy respectively) and brachial artery flow-mediated dilation (FMD) were assessed at baseline, after 16 weeks supervised training and 12-months after ending supervision.

RESULTS:Despite no significant change in body weight, there were significant improvements in VO2peak [6.5 ml.kg(-1).min(-1) (95% CI 2.8, 10.1); P=0.003], FMD [2.9% (1.5, 4.2); P=0.001], liver transaminases (P<0.05) and liver fat [-10.1% (-20.6, 0.5); P=0.048] immediately after the 16-weeks supervised training. Nevertheless, 12-months after ending supervision, VO2peak [0.9 ml.kg(-1).min(-1) (-3.3 5.1); P=0.65], FMD [-0.07% (-2.3, 2.2); P=0.95], liver transaminases (P>0.05) and liver fat [1.4% (-13.0, 15.9); P=0.83] were not significantly different from baseline.

CONCLUSIONS:Twelve months following cessation of supervision, exercise-mediated improvements in liver fat and other cardiometabolic variables had reversed with cardiorespiratory fitness at baseline levels. Maintenance of high cardiorespiratory fitness and stability of body weight are critical public health considerations for the treatment of NAFLD.International Journal of Obesity accepted article preview online, 21 July 2016. doi:10.1038/ijo.2016.123.

A two-arm randomized open labeled controlled clinical trial was conducted on 50 patients with non-alcoholic fatty liver disease (NAFLD). Participants were assigned to take either a lifestyle modification (LM), or LM +30 g/day brown milled flaxseed for 12 weeks. At the end of the study, body weight, liver enzymes, insulin resistance and hepatic fibrosis and steatosis decreased significantly in both groups (p< 0.05); however, this reduction was significantly greater in those who took flaxseed supplementation (p < 0.05). The significant mean differences were reached in hepatic markers between flaxseed and control group, respectively: ALT [-11.12 compared with -3.7 U/L; P< 0.001], AST [-8.29 compared with -4 U/L; p< 0.001], GGT [-15.7 compared with -2.62 U/L; p < 0.001], fibrosis score [-1.26 compared with -0.77 kPa; p = 0.013] and steatosis score [-47 compared with -15.45 dB/m; p = 0.022]. In conclusion, flaxseed supplementation plus lifestyle modification is more effective than lifestyle modification alone for NAFLD management.

A two-arm randomized open labeled controlled clinical trial was conducted on 50 patients with non-alcoholic fatty liver disease (NAFLD). Participants were assigned to take either a lifestyle modification (LM), or LM +30 g/day brown milled flaxseed for 12 weeks. At the end of the study, body weight, liver enzymes, insulin resistance and hepatic fibrosis and steatosis decreased significantly in both groups (p< 0.05); however, this reduction was significantly greater in those who took flaxseed supplementation (p < 0.05). The significant mean differences were reached in hepatic markers between flaxseed and control group, respectively: ALT [-11.12 compared with -3.7 U/L; P< 0.001], AST [-8.29 compared with -4 U/L; p< 0.001], GGT [-15.7 compared with -2.62 U/L; p < 0.001], fibrosis score [-1.26 compared with -0.77 kPa; p = 0.013] and steatosis score [-47 compared with -15.45 dB/m; p = 0.022]. In conclusion, flaxseed supplementation plus lifestyle modification is more effective than lifestyle modification alone for NAFLD management.

BACKGROUND:The prevalence of nonalcoholic steatohepatitis (NASH) in menopausal women is increasing, but current treatments have not been proven effective. The objective of this study was to investigate the treatment effects of genistein and running exercise in ovariectomized (OVX) rats with NASH.

METHODS:Thirty-six female Sprague-Dawley rats were divided into 6 groups, control; OVX with standard diet; OVX with high fat and high fructose (HFHF) diet for 4 weeks; OVX with HFHF and genistein treatment (16 mg/kg BW/day) for 5 weeks (OVX + HFHF+GEN); OVX with HFHF and moderate intensity exercise for 5 weeks (OVX + HFHF+EX); OVX with HFHF and combined treatments (OVX + HFHF+GEN + EX). Serum interleukin-6 (IL-6) levels, hepatic free fatty acid (FFA), hepatic glutathione (GSH), and hepatic malondialdehyde (MDA) levels were measured. Liver histology was examined to determine NASH severity.

RESULTS:OVX + HFHF group had the highest levels of hepatic FFA compared with OVX and control groups (5.92 ± 0.84 vs. 0.37 ± 0.01 vs. 0.42 ± 0.04 nmol/mg protein, respectively, p < 0.01). Serum IL-6 levels were significantly elevated in both OVX and OVX + HFHF groups as compared with controls (112.13 ± 6.50 vs. 121.47 ± 3.96 vs. 86.13 ± 2.40 pg/mL, respectively, p < 0.01). In OVX + HFHF group, hepatic MDA levels were higher, while GSH levels were lower than in OVX and control groups (MDA; 0.98 ± 0.04 vs. 0.82 ± 0.02 vs. 0.78 ± 0.03 nmol/mg protein, and GSH; 46.01 ± 0.91 vs. 55.21 ± 1.40 vs. 57.94 ± 0.32, respectively; p < 0.01 for both). Comparing with OVX + HFHF group, rats that received genistein, exercise and combined treatments demonstrated an improvement in liver histopathology, decreased levels of hepatic FFA (1.44 ± 0.21 vs. 0.45 ± 0.04 vs. 0.49 ± 0.05 nmol/mg protein, respectively, p < 0.01), serum IL-6 (82.80 ± 2.07 vs. 83.47 ± 2.81 vs. 94.13 ± 1.61 pg/mL, respectively, p < 0.01), and hepatic MDA (0.80 ± 0.03 vs. 0.76 ± 0.02 vs. 0.76 ± 0.03 nmol/mg protein, respectively, p < 0.01).

CONCLUSIONS:Genistein and moderate intensity exercise were effective in reducing the severity of NASH in OVX rats through the reduction in liver inflammation, oxidative stress and liver fat contents.

Background:In recent years, much evidence has emerged to indicate that exercise can benefit people when performed properly. This review summarizes the exercise interventions used in studies involving mice as they are related to special diseases or physiological status. To further understand the effects of exercise interventions in treating or preventing diseases, it is important to establish a template for exercise interventions that can be used in future exercise-related studies.

Methods:PubMed was used as the data resource for articles. To identify studies related to the effectiveness of exercise interventions for treating various diseases and organ functions in mice, we used the following search language: (exercise [Title] OR training [Title] OR physical activity [Title]) AND (mice [title/abstract] OR mouse [title/abstract] OR mus [title/abstract]). To limit the range of search results, we included 2 filters: one that limited publication dates to"in 10 years"and one that sorted the results as"best match". Then we grouped the commonly used exercise methods according to their similarities and differences. We then evaluated the effectiveness of the exercise interventions for their impact on diseases and organ functions in 8 different systems.

Results:A total of 331 articles were included in the analysis procedure. The articles were then segmented into 8 systems for which the exercise interventions were used in targeting and treating disorders: motor system (60 studies), metabolic system (45 studies), cardio-cerebral vascular system (58 studies), nervous system (74 studies), immune system (32 studies), respiratory system (7 studies), digestive system (1 study), and the system related to the development of cancer (54 studies). The methods of exercise interventions mainly involved the use of treadmills, voluntary wheel-running, forced wheel-running, swimming, and resistance training. It was found that regardless of the specific exercise method used, most of them demonstrated positive effects on various systemic diseases and organ functions. Most diseases were remitted with exercise regardless of the exercise method used, although some diseases showed the best remission effects when a specific method was used.

Conclusion:Our review strongly suggests that exercise intervention is a cornerstone in disease prevention and treatment in mice. Because exercise interventions in humans typically focus on chronic diseases, national fitness, and body weight loss, and typically have low intervention compliance rates, it is important to use mice models to investigate the molecular mechanisms underlying the health benefits from exercise interventions in humans.

BACKGROUND & AIMS:Dietary modification has been recommended for treatment of nonalcoholic fatty liver disease (NAFLD), although it is not clear whether improving diet quality can prevent its development. We performed a prospective study to examine the association between diet quality change and change in liver fat change. We also examined the association between genetic risk score and liver fat change in individuals with different levels of diet quality change.

METHODS:Our study included 1521 participants who attended the seventh and eighth examinations (1998-2001 and 2005-2008) of the second-generation cohort or attended the first and second examinations (2002-2005 and 2008-2011) of the third-generation cohort in the Framingham Heart Study. The self-administered semi-quantitative 126-item Harvard food frequency questionnaire was used to determine dietary intake in the year leading up to an examination. We assessed levels of liver fat using liver-phantom ratio (LPR) and computed tomography images from 2002 through 2005 and again from 2008 through 2011. LPR values are inversely related to liver fat-increased LPR indicates decreased liver fat. We examined associations of changes in 2 diet scores-the Mediterranean-style diet score (MDS) and Alternative Healthy Eating Index (AHEI)-with changes in liver fat and new-onset fatty liver. We evaluated interactions between diet score change and a weighted genetic risk score for NAFLD, determined based on multiple single nucleotide polymorphisms identified in genome-wide association studies of NAFLD. The primary outcome was change in LPR between baseline and follow-up measurement.

RESULTS:For each 1-standard deviation increase in MDS, the LPR increased (meaning liver fat decreased) by 0.57 (95% CI, 0.27-0.86; P<.001) and the odds for incident fatty liver decreased by 26% (95% CI, 10%-39%; P=.002). For each 1-standard deviation increase in AHEI, LPR increased by 0.56 (95% CI, 0.29-0.84; P<.001) and the odds for incident fatty liver decreased by 21% (95% CI, 5%-35%; P=.02). Increased diet scores were also associated with reduced odds of developing more-advanced fatty liver. Higher genetic risk scores were associated with increased liver fat accumulation in participants who had decreased MDS (P<.001) or AHEI scores (P=.001), but not in those with stable or improved diet scores (P for gene-diet interaction<.001).

CONCLUSIONS:In an analysis of participants in the Framingham Heart Study, increasing diet quality, determined based on MDS and AHEI scores, is associated with less liver fat accumulation and reduced risk for new-onset fatty liver. An improved diet is particularly important for individuals with a high genetic risk for NAFLD.

Background and objectives:Nonalcoholic steatohepatitis (NASH) is strongly associated with obesity. A weight loss of≥10% is necessary to improve NASH severity, but this goal has rarely been achieved in published studies using different diet protocols. The effect of a ketogenic, hypocaloric, commercial diet ("Ideal Protein,"IP) on body weight, metabolic markers, and liver tests in a group of NASH patients is evaluated in this study. Daily calorie intake was tailored to achieve a weight loss of≥10%.

Methods:We analyzed 38 patients with NASH who were placed on the IP diet between 2014 and 2018 and compared their outcomes with 6 control patients who declined the diet. All patients were evaluated by a trained health coach in weekly intervals throughout the study period. Clinical and laboratory data obtained before and at 6.5 months after intervention were compared using paired t-testing.

Results:The patients on the IP diet experienced a significant weight reduction (217± 8 lb. 194± 7 lb; mean ± S.E.M.), corresponding to an average weight loss of 9.7% ± 1.6%. Significant changes in systolic blood pressure (133 ± 3 mmHg. 123± 3 mmHg), triglycerides (200 ± 21 mmol/L. 132± 11 mmol/L), hemoglobin A1c (6.71% ± 0.29%. 5.74%± 0.19%), SGPT (97.3 ± 11.1 IU/L. 44.2± 5.9 IU/L), SGOT (82.4 ± 10.5 IU/L. 32.8± 5.2 IU/L), and Fib-4 scores (2.25 ± 0.23. 1.40± 0.13) were also observed (<0.05 in all cases). In the IP group, 50.5% of patients lost≥10% body weight. In contrast, no significant changes were observed in the control group. The IP diet was well tolerated, and no safety signals were noticed.

Conclusions:A ketogenic, hypocaloric resulted in striking weight loss and significant improvements in metabolic parameters and liver tests, suggesting that this approach carries promise for the dietary management of patients with NASH.

Nutritional habits modifications have shown an important impact in preventing and ameliorating metabolic alterations, such as nonalcoholic fatty liver disease (NAFLD). Among several dietary approaches that exert positive effects in NAFLD patients, the Mediterranean dietary pattern has shown notable benefits. This review explores the molecular mechanisms through which the Mediterranean diet would improve risk factors associated with metabolic syndrome and NAFLD. The main features of the Mediterranean diet acting on metabolism are represented by its whole-grain and low glycemic index cereal-based items, its fatty acid profile, and its content in phytochemical compounds. Carbohydrate-rich foods high in dietary fiber inducing low glycemic response are able to interact with glucose and insulin metabolism. Unsaturated fatty acids are associated with better hepatic lipid metabolism. Finally, phytochemical compounds, such as dietary polyphenols, are thought to ameliorate inflammation, which is considered one of the mechanisms through which NALFD may evolve into nonalcoholic steatohepatitis (NASH).

We have shown that combination treatment with decaffeinated green tea extract (GTE) and voluntary exercise (Ex) reduces obesity and insulin resistance in high-fat (HF)-fed mice to a greater extent than either treatment alone. Here, we investigated the effects of GTE-, Ex- or the combination on the development of obesity-related NAFLD. Male C57BL/6 J mice were treated for 16 weeks with HF diet (60% energy from fat), HF supplemented with 7.7 g GTE/kg, HF plus access to a voluntary running wheel, or the combination. We found that treatment of mice with the combination mitigated the development of HF-induced NAFLD to a greater extent than either treatment alone. Combination-treated mice had lower plasma alanine aminotransferase (92% lower) and hepatic lipid accumulation (80% lower) than HF-fed controls: the effect of the single treatments was less significant. Mitigation of NAFLD was associated with higher fecal lipid and nitrogen levels. Combination treated, but not singly treated mice, had higher hepatic expression of genes related to mitochondrial biogenesis (sirtuin 1 [59%]; peroxisome proliferator-activated receptorγ coactivator 1α [42%]; nuclear respiratory factor 1 [38%]; and transcription factor B1, mitochondrial [89%]) compared to the HF-fed controls. GTE-, Ex-, and the combination-treatment groups also had higher hepatic expression of genes related to cholesterol synthesis and uptake, but the combination was not better than the single treatments. Our results suggest the combination of GTE and Ex can effectively mitigate NAFLD. Future studies should determine if the combination is additive or synergistic compared to the single treatments.

Nonalcoholic fatty liver disease (NAFLD) develops in ulcerative colitis (UC) and Crohn's disease. However, there is scarce reporting on the onset of UC in patients with NAFLD. A 44-year-old man was diagnosed with UC and referred to us in 2019. His height was 166.0 cm, and body weight was 86.3 kg. The waist circumference was 93.7 cm (normal range<85) and triglyceride was 751 mg/dL. These findings, in addition to hypertension, resulted in a diagnosis of metabolic syndrome. HbA1c was normal. Ultrasonography disclosed severe fatty liver. Nonalcoholic fatty liver disease was diagnosed. He underwent 12 days of educational hospitalization for UC. A lacto-ovo-semi-vegetarian diet (1400 kcal/day), a kind of plant-based diet (PBD), was provided. He lost 4 kg, which was 4.6% of his base body weight. Triglyceride and total cholesterol decreased to the normal ranges. Transaminases andγ-glutamyl transpeptidase also decreased. His body weight decreased further after discharge. Follow-up ultrasonography indicated an improvement in hepatic enlargement. The shear wave velocity decreased from 1.11 to 0.88 m/s. His soft stool became normal stool by 2 months after discharge. Records ofhis health checkups revealed the presence of metabolic syndrome and abnormal liver function tests already in 2015. Thus, it was concluded that UC developed in a patient with NAFLD in this case. Plant-based diet has already been shown to be effective in inflammatory bowel disease (IBD). In the present case, NAFLD parameters were dramatically improved by PBD. Whether the improvement was due to weight loss per se or due to weight loss with PBD is to be clarified.

Skeletal muscle insulin resistance has been implicated in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and atherogenic dyslipidemia associated with the metabolic syndrome by altering the distribution pattern of postprandial energy storage. We conducted a study to examine this hypothesis by reversing muscle insulin resistance with a single bout of exercise and measuring hepatic de novo lipogenesis and hepatic triglyceride synthesis after a carbohydrate-rich meal. We studied 12 healthy, young, lean, insulin resistant individuals in an interventional, randomized cross-over trial. The response to the ingestion of a carbohydrate-rich meal was studied at rest and after one 45-min bout of exercise on an elliptical trainer. Hepatic de novo lipogenesis was assessed by using (2)H(2)O, and changes in glycogen and fat content in liver and muscle were measured by (13)C and (1)H magnetic resonance spectroscopy, respectively. Exercise resulted in a greater than threefold increase in postprandial net muscle glycogen synthesis (P<0.001), reflecting improved muscle insulin responsiveness, and a≈40% reduction (P<0.05) in net hepatic triglyceride synthesis. These changes in whole body energy storage were accompanied by a≈30% decrease in hepatic de novo lipogenesis (P<0.01) and were independent of changes in fasting or postprandial plasma glucose and insulin concentrations. These data demonstrate that skeletal muscle insulin resistance is an early therapeutic target for the treatment and prevention of atherogenic dyslipidemia and NAFLD in young insulin resistant individuals who are prone to develop the metabolic syndrome and type 2 diabetes.

BACKGROUND:A non-negligible percentage of patients with non-alcoholic fatty liver disease, a leading cause of hepatic progressive disorder related to insulin resistance, have no metabolic risk factors, and abnormal intestinal permeability has been suggested to be involved in the pathogenesis of the liver damage. Coeliac disease, a curable disorder characterised by inflammatory mucosal damage, may show hepatic histological features similar to steatohepatitis. Conflicting data have been reported on the prevalence of coeliac disease in non-alcoholic steatohepatitis.

AIM:To search for coeliac disease in a series of patients with non-alcoholic fatty liver disease by screening with anti-tissue transglutaminase and anti-endomysium antibodies.

PATIENTS AND METHODS:Fifty-nine consecutive patients with hypertransaminasemia and non-alcoholic fatty liver disease, 38 (64%) with steatohepatitis. Anti-endomysium antibodies were assayed by indirect immunofluorescence, IgA anti-tissue transglutaminase by ELISA. Patients who tested positive underwent HLA DQ typing and endoscopy.

RESULTS:Tissue transglutaminase antibodies were positive in six (10%) patients and anti-endomysium in two (3.4%); only two (3.4%), positive for both anti-endomysium positive and anti-transglutaminase, resulted to have coeliac disease based on histological findings. After 6 months of gluten-free diet, liver enzymes normalised.

CONCLUSIONS:The prevalence of silent coeliac disease is 3.4% in patients with non-alcoholic fatty liver. The inclusion of anti-endomysium antibodies test in studying patients with non-alcoholic fatty liver and persistent biochemical abnormalities has to be taken into account, since positivity for tissue transglutaminase antibodies, in the absence of confirmatory anti-endomysium antibodies, is not sufficient to perform diagnostic endoscopy.

BACKGROUND:Dietary habit can play a key role in the prevention and treatment of fatty liver disease (NAFLD). Although many studies have investigated the effect of Mediterranean diet on NAFLD, findings are inconsistent and there is no systematic review on this topic. Therefore, the aim of this systematic review is to summarize the effect of Mediterranean diet on serum metabolic indices and anthropometric measures among NAFLD patients.

METHODS:We searched titles, abstracts, and keywords of articles indexed in Science Direct, MEDLINE, and Google Scholar databases up to October 2018 to identify eligible RCT studies. Randomized clinical trials assessing the effects of MD on NAFLD were included.

RESULTS:The present study included 10 randomized controlled trials, which involved a total of 856 adults with NAFLD. According to the result, MD may improve anthropometric measures, lipid profile, glycemic indices, liver enzyme, and NAFLD severity indices among patients with NAFLD.

CONCLUSION:We found that MD could alleviate NAFLD severity parameters but differences between studies should be taken into account. Finally, in order to draw a firm link between MD and NAFLD, more clinical trials with adequate sample size and better methodology should be done.