Celiac Disease, Gluten-Free Diet and Metabolic Dysfunction-Associated Steatotic Liver Disease.

Celiac disease (CD) is a chronic autoimmune disorder triggered by the ingestion of gluten-containing food by genetically predisposed individuals. Hence, treatment of CD consists of permanent avoidance of wheat, rye, barley, and other gluten-containing foods. Lifelong adherence to a gluten-free diet (GFD) improves the symptoms of CD, but recent evidence suggests it is also associated with a higher risk for hepatic steatosis and the coexistence or emergence of other cardiometabolic risk factors. Moreover, a higher risk for liver steatosis is also reported by some authors as a potential extraintestinal complication of the CD itself. Recent nomenclature changes designate the association between hepatic steatosis and at least one of five cardiometabolic risk factors as metabolic dysfunction-associated steatotic liver disease (MASLD). An extended network of potentially causative factors underlying the association between MAFLD and CD, before and after dietary therapy is implemented, was recently described. The individualized treatment of these patients is less supported by evidence, with most of the current recommendations relying on empiric clinical judgment. This review focuses on the causative associations between CD and hepatic injury, either as an extraintestinal manifestation of CD or a side effect of GFD, also referring to potential therapeutic strategies for these individuals.

A Healthful Plant-Based Diet as an Alternative Dietary Approach in the Management of Metabolic Dysfunction-Associated Steatotic Liver Disease.

Plant-based diets (PBDs) are gaining attention as a sustainable and health-conscious alternative for managing various chronic conditions, including metabolic dysfunction-associated steatotic liver disease (MASLD). In the absence of pharmacological treatments, exploring the potential of lifestyle modifications to improve biochemical and pathological outcomes becomes crucial. The adoption of PBDs has demonstrated beneficial effects such as weight control, increased metabolic health and improved coexisting diseases. Nonetheless, challenges persist, including adherence difficulties, ensuring nutritional adequacy, and addressing potential deficiencies. The aim of this review is to provide a comprehensive overview of the impact of PBDs on MASLD, emphasizing the need for tailored dietary interventions with professional support to optimize their effectiveness in preventing and treating metabolic diseases.

Inflammatory markers as diagnostic and precision nutrition tools for metabolic dysfunction-associated steatotic liver disease: Results from the Fatty Liver in Obesity trial.

BACKGROUND & AIMS: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing public health concern. The disease is silent, and its diagnosis is often delayed. Inflammatory markers constitute an interesting tool to act as subrogate, non-invasive markers. This study aimed to evaluate the changes of inflammatory markers throughout a two-year dietary intervention in subjects presenting MASLD, to determine which of the markers are suitable to predict the disease, and act as a customizing tool for MASLD's dietary treatment. METHODS: Ninety-eight subjects with MASLD and forty-five controls from the Fatty Liver in Obesity (FLiO) Study were analyzed. MASLD was diagnosed and graded by ultrasound. The MASLD subjects were randomly assigned to two different dietary strategies, the American Heart Association (AHA diet) or a dietary strategy based on the Mediterranean pattern, which was specially designed for the study (FLiO diet), and then followed for two years. Hepatic status was additionally assessed through Magnetic Resonance Imaging (MRI), elastography, and determination of transaminases. RESULTS & DISCUSSION: Inflammatory markers improved throughout the intervention in the MASLD subjects and managed to reach similar levels to controls, especially at 6 and 12 months. Additionally, leptin, adiponectin, M30, and LECT2 managed to significantly diagnose the disease at all time marks of the intervention, making them candidates for subrogate non-invasive markers of the disease. Moreover, baseline chemerin, leptin, LECT2, and M65 were used to build a predictive score to achieve greater weight loss, and therefore, which strategy could be more useful for MASLD 's treatment. The predictive score was significantly able assign a specific diet to 55% of the study participants, meaning that the remaining 45% could achieve the same amount of weight loss following either diet equally. CONCLUSION: Inflammatory markers constitute a potential non-invasive tool to be used in MASLD screening and could also constitute an interesting tool for MASLD's treatment customization, being able to predict the effectiveness of a dietary strategy based on the initial inflammatory state of each subject. TRIAL REGISTRATION: www. CLINICALTRIALS: gov (NCT03183193).

Gender Differences in Liver Steatosis and Fibrosis in Overweight and Obese Patients with Metabolic Dysfunction-Associated Steatotic Liver Disease before and after 8 Weeks of Very Low-Calorie Ketogenic Diet.

Obesity and metabolic syndrome are linked to steatotic liver disease (SLD), the most common form of chronic liver disease. Lifestyle modifications and dieting are strategies that can prevent metabolic dysfunction-associated steatotic liver disease (MASLD). The very low-calorie ketogenic diet (VLCKD) is a helpful treatment for MASLD and has been recommended for people affected by obesity; we evaluated the effect of gender on steatosis and fibrosis in a cohort of 112 overweight or obese patients undergoing an eight-week treatment with a VLCKD. Differences between the genders in terms of anthropometric measures, body composition, and metabolic indicators were examined before, during, and after the nutritional intervention. At baseline, there were significant differences between men and women in terms of anthropometric parameters, blood pressure, Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), fasting insulin, hepatic markers, and lipid profile. Men had considerably higher levels of liver steatosis (measured by CAP) and liver stiffness (measured by E) under basal conditions than women. After the VLCKD, there were reductions in both genders of controlled attenuation parameter (CAP), body weight, body mass index (BMI), waist circumference, systolic and diastolic blood pressure, insulin resistance, fat mass (FM), free fat mass (FFM), and fasting blood glucose, insulin, glycated hemoglobin (HbA1c), triglycerides, total cholesterol, low-density lipoprotein (LDL) cholesterol, alanine transaminase (ALT), gamma-glutamyl transferase (γGT), and uric acid levels. Only in men, liver stiffness, aspartate aminotransferase (AST), creatinine, and C-reactive protein (CRP) levels significantly decreased. Moreover, men had significantly greater levels of liver steatosis: the male gender featured an increase of 23.96 points of the Fibroscan CAP. Men exhibited higher levels of steatosis and fibrosis than women, and these differences persist despite VLCKD. These gender-specific variations in steatosis and fibrosis levels could be caused by hormonal and metabolic factors, suggesting that different therapeutic strategies might be required depending on the gender.

Can Nutraceuticals Support the Treatment of MASLD/MASH, and thus Affect the Process of Liver Fibrosis?

Currently, metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) are considered to be the main causes of fibrosis. In turn, fibrosis may lead to the development of hepatocellular carcinoma or advanced cirrhosis, i.e., potentially life-threatening conditions. It is likely that therapy aimed at reducing the risk of developing hepatic steatosis and inflammation could be helpful in minimizing the threat/probability of organ fibrosis. In recent years, increasing attention has been paid to the influence of nutraceuticals in the prevention and treatment of liver diseases. Therefore, the aim of this review was to describe the precise role of selected ingredients such as vitamin C, beta-carotene, omega-3 fatty acids, and curcumin. It is likely that the use of these ingredients in the treatment of patients with MASLD/MASH, along with behavioral and pharmacological therapy, may have a beneficial effect on combating inflammation, reducing oxidative stress, and thereby preventing liver damage.

Short-term reduction of dietary gluten improves metabolic-dysfunction associated steatotic liver disease: A randomised, controlled proof-of-concept study.

BACKGROUND: The current management of metabolic dysfunction-associated steatotic liver disease (MASLD) relies on lifestyle intervention. Prior studies have shown that nutritional wheat amylase trypsin inhibitors (ATI) activate toll-like receptor 4 on intestinal myeloid cells to enhance intestinal and extra-intestinal inflammation, including the promotion of murine MASLD, insulin resistance and liver fibrosis. AIMS: We aimed to assess the impact of ATI (gluten)-free diet in liver as well as metabolic parameters of biopsy-proven MASLD patients. METHODS: We performed a 6-week, proof-of-concept 1:1 randomised controlled trial of an ATI-free diet. The controls followed a balanced diet recommended by the German Nutrition Society. We assessed changes in controlled attenuation parameter (CAP), body mass index (BMI) and homeostatic model assessment of insulin resistance (HOMA-IR). Patient-reported outcomes were assessed by the CLDQ-NASH questionnaire. Forty-five patients were consecutively enrolled (21 in the intervention arm and 24 in the control arm). RESULTS: Three patients from each arm discontinued the study. In the ATI-free diet group, a significant decrease in BMI (p = 0.018), CAP (p = 0.018) and HOMA-IR (p = 0.042) was observed at 6 weeks. The mean difference in CAP between the two arms at week 6 was 30.5 dB/m (p = 0.039), with a delta significantly higher in the ATI-free diet group (p = 0.043). Only an ATI-free diet could achieve a significant improvement in CLDQ-NASH domains (p value for total scoring: 0.013). CONCLUSIONS: A short-term ATI-free diet leads to significant improvements in liver and metabolic parameters, as well as patient-reported outcomes with good tolerability. A larger follow-up study is justified to corroborate these findings. CLINICAL TRIAL NUMBER: NCT04066400.

What Is the Optimal Time on a Low-Calorie Diet Prior to Laparoscopic Anti-reflux Surgery? A Prospective Case-Controlled Study.

INTRODUCTION: A very low-calorie diet (VLCD) or low-calorie diet (LCD) is often used prior to laparoscopic surgery to optimize access to the hiatus. Much debate exists in the literature regarding the required duration for a VLCD or LCD, and how to evaluate the presence of a fatty liver. The aim of our study was to determine the optimal amount of time on an LCD to achieve maximal liver volume reduction, and to assess the accuracy of the InBody 230® vs. bedside ultrasonography vs. magnetic resonance imaging (MRI) in the measurement of liver volume. METHODS: Seventeen consecutive patients undergoing laparoscopic anti-reflux surgery were recruited into the study. Each patient underwent body composition analysis with the InBody® 230, liver ultrasound, and liver MRI. Patients then began an LCD with a weekly ultrasound assessment until the day before surgery when they underwent repeat body composition analysis, liver ultrasound, and MRI. RESULTS: The mean age was 54 years (range 21, 74). Maximal liver volume loss was noted within 3 weeks for 88% of participants, with 47% achieving their maximal liver volume reduction after the first week of an LCD. The mean reduction in liver volume was 16%, 18.6%, and 19% for MRI, ultrasound, and body composition analysis, respectively. CONCLUSION: Close to 90% of patients require 3 weeks or less on an LCD to achieve maximal liver volume loss prior to laparoscopic anti-reflux surgery. Body composition analysis and bedside ultrasonography were both as accurate as the gold standard MRI in the assessment of liver volume.

Tangeretin prevents obesity by modulating systemic inflammation, fat browning, and gut microbiota in high-fat diet-induced obese C57BL/6 mice.

Obesity and associated comorbidities are closely linked to gut microbiota dysbiosis, energy balance, and chronic inflammation. Tangeretin, a key citrus polymethoxylated flavone (PMF), is abundant in citrus fruits and has preventative and therapeutic effects for numerous diseases. The current study investigated the effects and possible mechanisms of tangeretin supplementation in preventing obesity in high-fat diet (HFD)-fed mice. Treatment of HFD-fed mice with tangeretin potently ameliorated HFD-induced body weight, liver steatosis, glucose intolerance, and insulin resistance. Tangeretin mitigated systemic chronic inflammation by reducing metabolic endotoxemia and inflammation-related gene expression in HFD-fed mice. An increased number of small brown adipocytes possessing multilocular and cytoplasmic lipid droplets and upregulation of thermogenic gene expression were observed after tangeretin treatment. 16S rRNA amplicon sequencing indicated that tangeretin markedly altered the gut microbiota composition (richness and diversity) and reversed 16 operational taxonomic units (OTUs) back to levels seen in mice consuming a normal chow diet (NCD). Notably, tangeretin decreased the ratio of Firmicutes-to-Bacteroidetes and greatly enriched Bacteroides and Lactobacillus. Overall, our results suggest that long-term supplementation with citrus tangeretin ameliorates the phenotype of obesity by improving adipose thermogenesis and reducing systemic inflammation and gut microbiota dysbiosis, which provides a good basis for studying the mechanism of tangeretin's beneficial effects.

Glucagon and Liver Fat are Downregulated in Response to Very Low-calorie Diet in Patients with Obesity and Type-2 Diabetes.

BACKGROUND AND STUDY AIMS: In patients with obesity and type-2 diabetes, short-time very low-calorie diet may ameliorate hyperglycemia and hepatic steatosis. Whether this also implies the glucose-regulating hormone glucagon remains to be elucidated. This study investigated the effects of a very low-calorie diet on plasma levels of glucagon and liver fat in obese patients with type-2 diabetes. PATIENTS AND METHODS: Ten obese patients with type-2 diabetes, 6 men and 4 women, were included. At baseline, fasting plasma glucagon, insulin and glucose were determined, and liver fat and stiffness evaluated by transient elastography. The subjects were then prescribed a very low-calorie diet of maximum 800 kcal/day for 7 weeks and reexamined after 7 weeks and 12 months. RESULTS: At baseline, BMI was 42±4 kg/m2 and fasting glucose 10.6±3.4 mmol/l. All patients had hepatic steatosis. Plasma glucagon was strongly related to liver fat (r2=0.52, p=0.018). After 7 weeks of very low-calorie diet, plasma glucagon was significantly decreased by nearly 30% (p=0.004) along with reductions of BMI (p<0.0001), glucose (p=0.02), insulin (p=0.03), liver fat (p=0.007) and liver stiffness (p=0.05). At 12 months follow-up, both glucagon and liver fat increased and were not different to basal levels, despite persistent reductions of BMI (p<0.002) and glucose (p=0.008). CONCLUSION: In obese type-2 diabetic subjects, plasma glucagon and liver fat are correlated and similarly affected by a very low-calorie diet, supporting a role of hepatic steatosis in glucagon metabolism.

Protective mechanism of mung bean coat against hyperlipidemia in mice fed with a high-fat diet: insight from hepatic transcriptome analysis.

Mung bean coat (MBC) is a good source of dietary fibre and phenolic compounds with medical properties, and can alleviate metabolic diseases. In the present study, the effects of MBC on high fat diet (HFD)-induced hyperlipidemia mice were evaluated, and the underlying mechanisms of MBC against hyperlipidemia from hepatic transcriptional analysis were explored. Four groups of mice were fed a normal control diet or a HFD with or without MBC supplementation (6%, w/w) for 12 weeks. The results demonstrated that MBC supplementation could effectively alleviate HFD-induced obese symptoms, such as body weight gain and white adipose tissue accumulation. Notably, the serum lipid profiles, including total triglyceride, total cholesterol, and low-density lipoprotein cholesterol, were significantly lowered, accompanied by a significant improvement in hepatic steatosis. RNA-sequencing analysis indicated 1126 differential expression genes responding to MBC supplementation, and the PPAR signaling pathway was significantly enriched. Furthermore, MBC supplementation could significantly upregulate the transcriptional expression of lipid transformation (lipidolysis)-related genes (Cpt1b, Cyp7a1, and PPAR-α) and downregulate the transcriptional expression of lipid synthesis-related genes (Scd1, Cd36, and PPAR-γ) to protect against the HFD-induced hyperlipidemia, and they were confirmed by qRCR and western blotting validation. Taken together, the present study provides valuable information for understanding the curative effects and action mechanism of MBC in alleviating hyperlipidemia, and thus may contribute to the development and application of MBC as functional foods or dietary supplement to protect against hyperlipidemia.

Anti-inflammatory diet consumption reduced fatty liver indices.

The aim of this study was to assess the association between dietary inflammatory index (DII) and non-invasive markers of liver status in adults. This cross-sectional study was performed on 8520 adults, recruited in Ravansar Non-Communicable Diseases (RaNCD) cohort study, western Iran. The DII score was calculated based on participants' dietary intakes obtained from Food Frequency Questionnaire (FFQ). Fatty Liver Index (FLI) score was calculated by anthropometric measurements and some non-invasive markers of liver status. Linear regression models were applied to estimate the associations and adjust the possible confounding factors. A greater DII score was significantly associated with higher energy intake, body mass index (BMI), body fat mass (BFM), blood pressure, and FLI (P < 0.001). Participants with the highest DII score had a significantly higher consumption saturated fat, trans fat and red meat than those in the lowest quartile (P < 0.001). After adjustments of age and sex, participants in the highest quartile of the DII score had a greater risk of FLI (ß: 0.742, 95% CI: 0.254, 0.601). More pro-inflammatory diet in participants was associated with a higher FLI. The DII score was positively associated with non-invasive liver markers. Thus, having an anti-inflammatory diet can help balance liver enzymes, reduce obesity, and decrease fatty liver.

Preparation and characterization of soybean insoluble dietary fiber and its prebiotic effect on dyslipidemia and hepatic steatosis in high fat-fed C57BL/6J mice.

The potential benefits of insoluble dietary fiber (IDF) in the regulation of lipid metabolism have been reported in large prospective cohort studies although the molecular regulatory mechanism is still unclear. Okara is a by-product obtained during soybean processing for soy milk and soybean curd (tofu), which is rarely utilized and can be a cheap potential dietary fiber (DF) resource. In this study, the structure and physicochemical properties of insoluble dietary fiber (SIDF) extracted from okara were characterized, and the prebiotic effects on fat metabolism were investigated in vivo. The results showed that the main monosaccharides of SIDF (90.50%) identified were galactose, arabinose, xylose, rhamnose and glucose. Scanning electron microscopy (SEM), Fourier transform infrared spectroscopy (FT-IR), and X-ray diffraction (XRD) analyses suggested that SIDF had a loose and porous structure, polysaccharide functional groups, and a typical crystalline cellulose I structure. In addition, SIDF had ideal oil-adsorption capacity (OAC; 7.95 g g-1) and significantly improved cholesterol adsorption (11.14 mg g-1) at pH 7.0. In vivo, IDF supplementation reduced the serum lipid levels and inhibited hepatic fat accumulation. Additionally, SIDF administration improved hepatic steatosis by stimulating lipolysis via upregulation of PPARα, CYP4a10 and CPT1a. This is the first systematic study on the composition, structure, physicochemical properties, adsorption function and biological effects of SIDF. The above results show that SIDF could be used as an ideal functional ingredient in food processing as well as play a positive role in improving the added value of okara and promoting its comprehensive utilization.

Punicic acid ameliorates obesity and liver steatosis by regulating gut microbiota composition in mice.

This study aimed to elucidate the effect of punicic acid (PUA, cis9,trans11,cis13-18 : 3) on obesity and liver steatosis in mice induced by high-fat diet (HFD), and to explore the possible mechanism. Mice were fed with either a HFD or a control diet for 8 weeks. Half of HFD-mice received daily supplementation of PUA. Supplementation with PUA ameliorated the liver steatosis and obesity in mice fed by HFD, as demonstrated by the decreased hepatic triglyceride accumulation, body weight gain and fat weight. A HFD increased the ratio of Firmicutes to Bacteroidetes, whereas supplementation with PUA effectively restored it. PUA supplementation counteracted the upregulation in family Desulfovibrionaceae and Helicobacteraceae, and the downregulation in Muribaculaceae and Bacteroidaceae induced by HFD. Correspondingly, the family of Desulfovibrionaceae was positively related, whereas Muribaculaceae was negatively related to the amount of epididymal and perirenal fat, and the level of liver triglyceride and total cholesterol. The family Helicobacteraceae was also positively related to the amount of epididymal and perirenal fat. Moreover, PUA supplementation counteracted the increase in the population of Anaerotruncus, Faecalibaculim, Mucispirillum, and the decrease in the population of Lactobacillus, Roseburia, Oscillibacter at the genus level induced by HFD. These results demonstrated that PUA can at least in part ameliorate obesity and liver steatosis in mice induced by HFD by regulating gut microbiota composition.

AB-Kefir Reduced Body Weight and Ameliorated Inflammation in Adipose Tissue of Obese Mice Fed a High-Fat Diet, but Not a High-Sucrose Diet.

Consumption of different types of high-calorie foods leads to the development of various metabolic disorders. However, the effects of multi-strain probiotics on different types of diet-induced obesity and intestinal dysbiosis remain unclear. In this study, mice were fed a control diet, high-fat diet (HFD; 60% kcal fat and 20% kcal carbohydrate), or western diet (WD; 40% kcal fat and 43% kcal carbohydrate) and administered with multi-strain AB-Kefir containing six strains of lactic acid bacteria and a Bifidobacterium strain, at 109 CFU per mouse for 10 weeks. Results demonstrated that AB-Kefir reduced body weight gain, glucose intolerance, and hepatic steatosis with a minor influence on gut microbiota composition in HFD-fed mice, but not in WD-fed mice. In addition, AB-Kefir significantly reduced the weight and size of adipose tissues by regulating the expression of CD36, Igf1, and Pgc1 in HFD-fed mice. Although AB-Kefir did not reduce the volume of white adipose tissue, it markedly regulated CD36, Dgat1 and Mogat1 mRNA expression. Moreover, the abundance of Eubacterium_coprostanoligenes_group and Ruminiclostridium significantly correlated with changes in body weight, liver weight, and fasting glucose in test mice. Overall, this study provides important evidence to understand the interactions between probiotics, gut microbiota, and diet in obesity treatment.

Leaf powder supplementation of Senna alexandrina ameliorates oxidative stress, inflammation, and hepatic steatosis in high-fat diet-fed obese rats.

Obesity is an enduring medical issue that has raised concerns around the world. Natural plant extracts have shown therapeutic potential in preventing oxidative stress and inflammation related to obesity complications. In this study, Senna alexandrina Mill. leaves were utilized to treat high-fat diet-related metabolic disorders and non-alcoholic fatty liver diseases. Plasma biochemical assays were conducted to determine the lipid profiles and oxidative stress parameters, and the gene expression of antioxidant enzymes and inflammatory mediators was measured. Histological stained livers of high-fat diet-fed rats were observed. S. alexandrina leaf powder supplementation prevented the increase in cholesterol and triglyceride levels in high-fat diet-fed rats. Moreover, S. alexandrina leaves also reduced lipid peroxidation and nitric oxide production in these rats. Prevention of oxidative stress by S. alexandrina leaf supplementation in high-fat diet-fed rats is regulated by enhancing the antioxidant enzyme activity, followed by the restoration of corresponding gene expressions, such as NRF-2, HO-1, SOD, and CAT. Histological staining provides further evidence that S. alexandrina leaf supplementation prevents inflammatory cell infiltration, lipid droplet deposition, and fibrosis in the liver of high-fat diet-fed rats. Furthermore, this investigation revealed that S. alexandrina leaf supplementation controlled non-alcoholic fatty liver disease by modulating the expression of fat metabolizing enzymes in high-fat diet-fed rats. Therefore, S. alexandrina leaf supplementation inhibits fatty liver inflammation and fibrosis, suggesting its usefulness in treating non-alcoholic steatohepatitis. Thus, this natural leaf extract has potential in treatment of obesity related liver dysfunction.

Multidimensional Impact of Mediterranean Diet on IBD Patients.

BACKGROUND & AIMS: Malnutrition with the accumulation of fat tissue and nonalcoholic fatty liver disease (NAFLD) are conditions associated with inflammatory bowel disease (IBD). Visceral fat and NAFLD-related liver dysfunction can both worsen intestinal inflammation. Because the Mediterranean diet (Md) has been shown to ameliorate both obesity and NAFLD, the aim of this study was to analyze the impact of Md on the nutritional state, liver steatosis, clinical disease activity, and quality of life (QoL) in IBD patients. METHODS: Patients with IBD, both Crohn's disease (CD) and ulcerative colitis (UC), followed Md for 6 months. Their body mass index (BMI), body tissue composition, liver steatosis and function, serum lipid profile, clinical disease activity, and inflammatory biomarkers (C-reactive protein and fecal calprotectin) were collected at baseline (T0) and compared with those obtained after 6 months (T180) to evaluate the impact of Md. RESULTS: One hundred forty-two IBD patients, 84 UC and 58 CD, followed Md for 6 months. At T180, diet-adherent CD and UC improved BMI (UC -0.42, P = 0.002; CD -0.48, P = 0.032) and waist circumference (UC -1.25 cm, P = 0.037; CD -1.37 cm, P = 0.041). Additionally, the number of patients affected by liver steatosis of any grade was significantly reduced in both groups (UC T0 31 of 84 [36.9%] vs T180 18 of 84 [21.4%], P = 0.0016; CD T0 27 of 58 [46.6%] vs T180 18 of 58 [31.0%], P < 0.001) after dietary intervention. Finally, after 6 months of the diet, fewer UC and CD patients with stable therapy had active disease (UC T0 14 of 59 [23.7%] vs T180 4 of 59 [6.8%], P = 0.004; CD T0 9 of 51 [17.6%] vs T180 2 of 51 [3.0%], P = 0.011) and elevated inflammatory biomarkers. Mediterranean diet improved QoL in both UC and CD, but neither serum lipid profile nor liver function were modified by the diet. CONCLUSIONS: A significant reduction of malnutrition-related parameters and liver steatosis was observed in both CD and UC patients after short-term dietary intervention based on the adoption of Md, and this was associated with a spontaneous improvement of disease activity and inflammatory markers.

Eficácia e segurança de mudanças no estilo de vida na Esteatose Hepática não Alcoólica: revisão rápida de evidências / Effectiveness and safety of lifestyle modifications for Nonalcoholic Hepatic Steatosis: rapid response review of evidence

Tecnologia: Intervenção de mudança no estilo de vida (dieta, exercícios). Indicação: doença hepática gordurosa não alcoólica (DHGNA). Pergunta clínica: Intervenções de mudança no estilo de vida, comparados a nenhum tratamento ou placebo, são eficazes no tratamento de DHGNA para modificar indicadores metabólicos, reduzir mortalidade e prevenir complicações relacionadas à esteatose hepática? Métodos: Foi feito levantamento bibliográfico na base de dados PUBMED, seguindo estratégias de buscas predefinidas. As revisões sistemáticas foram avaliadas com a ferramenta "AMSTAR 2 - Assessing the Methodological Quality of Systematic Reviews version 2". Resultados: Foram selecionadas 4 revisões sistemáticas, que atendiam aos critérios de inclusão. Conclusão: As evidências disponíveis não são suficientes para confirmar ou refutar que as modificações do estilo de vida têm efeitos benéficos de longo prazo sobre a DHGNA. Protocolos com dieta mediterrânea, jejum intermitente ou exercícios aeróbicos são benéficos para reduzir parâmetros metabólicos em pessoas com DHGNA

Technology: Lifestyle change intervention (diet, exercise). Indication: Non-alcoholic fatty liver disease (NAFLD). Clinical question: Are lifestyle change interventions, compared to no treatment or placebo, effective in NAFLD treatment to modify metabolic indicators, reduce mortality and prevent complications related to hepatic steatosis? Methods: A bibliographic survey was carried out in the PUBMED database, following predefined search strategies. Systematic reviews were evaluated using the tool "AMSTAR 2 - Assessing the Methodological Quality of Systematic Reviews version 2". Results: 4 systematic reviews that met the inclusion criteria were selected. Conclusion: The available evidence is not sufficient to confirm or refute that lifestyle modifications have long-term beneficial effects on NAFLD. Protocols such as a Mediterranean diet, intermittent fasting, or aerobic exercise are beneficial in reducing metabolic parameters in people with NAFLD

Study on the new strategy and key techniques for accurate prevention and treatment of nonalcoholic steatohepatitis based on intestinal target bacteria.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) has emerged as a major health problem worldwide; according to statistics, 10% to 25% of patients with NAFLD can progress to nonalcoholic steatohepatitis (NASH). A link between the composition and metabolites of intestinal microbiota and the development of NAFLD is becoming clearer. It is believed that microbiota factors are driving forces of hepatic steatosis and inflammation. The formulated food that contains prebiotics and dietary fiber may improve NAFLD by altering the intestinal flora and its metabolites. METHODS: The study plan to recruit adult patients (18-75 years, n = 120) with NAFLD, range of alanine aminotransferase is 1.5 to 5 times upper limit of normal (ULN) or liver biopsy is confirmed as NASH. Participants will be randomly allocated into 2 groups: formulated food (n = 80) and a placebo group (n = 40) for 24 weeks. Both groups will receive lifestyle and nutritional advice. The primary endpoint is a decrease in MRS-PDFF by more than 30% from baseline at 24 weeks. The secondary endpoints include the change of anthropometric, liver function, glycolipid metabolism, and systemic inflammation at 4, 12, and 24 weeks. In addition, we consider the changes in intestinal microbiota as an exploration to assess the abundance and diversity at 24 weeks. Weeks 24 to 36 are the follow-up period of drug withdrawal. DISCUSSION: This clinical trial will provide evidence of efficacy and safety of formulated food as a potential new therapeutic agent for NAFLD patients. TRIAL REGISTRATION: The trial is registered in the China Clinical Trial Center (ChiCTR1800016178).