scholarly journals Dietary wheat amylase trypsin inhibitors promote features of murine non-alcoholic fatty liver disease

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Muhammad Ashfaq-Khan ◽  
Misbah Aslam ◽  
Muhammad Asif Qureshi ◽  
Marcel Sascha Senkowski ◽  
Shih Yen-Weng ◽  
...  
Keyword(s):  
Cell Activation ◽  
Intestinal Inflammation ◽  
Macrophage Polarization ◽  
Trypsin Inhibitors ◽  
Protein Component ◽  
Liver Fat ◽  
Major Protein ◽  
Alcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
Wheat Amylase

AbstractWe previously demonstrated that a common dietary protein component, wheat amylase trypsin inhibitors (ATI), stimulate intestinal macrophages and dendritic cells via toll like receptor 4. Activation of these intestinal myeloid cells elicits an inflammatory signal that is propagated to mesenteric lymph nodes, and that can facilitate extraintestinal inflammation. Mice were fed a well-defined high fat diet, with (HFD/ATI) or without (HFD) nutritionally irrelevant amounts of ATI. Mice on HFD/ATI developed only mild signs of intestinal inflammation and myeloid cell activation but displayed significantly higher serum triglycerides and transaminases compared to mice on HFD alone. Moreover, they showed increased visceral and liver fat, and a higher insulin resistance. ATI feeding promoted liver and adipose tissue inflammation, with M1-type macrophage polarization and infiltration, and enhanced liver fibrogenesis. Gluten, the major protein component of wheat, did not induce these pathologies. Therefore, wheat ATI ingestion in minute quantities comparable to human daily wheat consumption exacerbated features of the metabolic syndrome and non-alcoholic steatohepatitis, despite its irrelevant caloric value.

scholarly journals Beyond Body Weight-Loss: Dietary Strategies Targeting Intrahepatic Fat in NAFLD

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1316 ◽  
Author(s):  
Nicolai Worm
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Body Weight ◽  
Liver Disease ◽  
Glycogen Synthesis ◽  
Liver Fat ◽  
Meal Replacement ◽  
Alcoholic Fatty Liver ◽  
Therapeutic Concept ◽  
The Metabolic Syndrome

Non-alcoholic fatty liver disease (NAFLD) has emerged as the most prevalent liver disease in industrialized countries. It is regarded as the hepatic manifestation of the metabolic syndrome (MetS) resulting from insulin resistance. Moreover, insulin resistance impairs glycogen synthesis, postprandially diverting a substantial amount of carbohydrates to the liver and storing them there as fat. NAFLD has far-reaching metabolic consequences involving glucose and lipoprotein metabolism disorders and risk of cardiovascular disease, the leading cause of death worldwide. No pharmaceutical options are currently approved for the treatment of NAFLD. Exercise training and dietary interventions remain the cornerstone of NAFLD treatment. Current international guidelines state that the primary goal of nutritional therapy is to reduce energy intake to achieve a 7%–10% reduction in body weight. Meal replacement therapy (formula diets) results in more pronounced weight loss compared to conventional calorie-restricted diets. However, studies have shown that body mass index (BMI) or weight reduction is not obligatory for decreasing hepatic fat content or to restore normal liver function. Recent studies have achieved significant reductions in liver fat with eucaloric diets and without weight loss through macronutrient modifications. Based on this evidence, an integrative nutritional therapeutic concept was formulated that combines the most effective nutrition approaches termed “liver-fasting.” It involves the temporary use of a low calorie diet (total meal replacement with a specific high-protein, high-soluble fiber, lower-carbohydrate formula), followed by stepwise food reintroduction that implements a Mediterranean style low-carb diet as basic nutrition.

scholarly journals Metabolic Syndrome and Nonalcoholic Fatty Liver Disease

2019 ◽  
Vol 16 (1) ◽  
pp. 51-58
Author(s):  
Oana Irina Gavril ◽  
Lidia Iuliana Arhire ◽  
Ovidiu Mitu ◽  
Radu Sebastian Gavril ◽  
Alexandra Mastaleru ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Normal Liver ◽  
Liver Fat ◽  
Equal Distribution ◽  
Alcoholic Fatty Liver ◽  
Hepatic Expression ◽  
The Metabolic Syndrome

AbstractIntroduction. Non-alcoholic fatty liver disease (NAFLD) is regarded as the hepatic expression of the metabolic syndrome, both conditions presenting similar clinical features.Aim. The aim of this study was to evaluate, among diabetic subjects, the relationship between fatty liver load and the presence of metabolic syndrome criteria.Methods. An observational study was conducted on 92 subjects with type 2 diabetes. We followed anthropometric measurments, lipid profile, blood pressure and the degree of hepatic steatosis using ultrasonography.Results. The average age of the study group was 60,38 ± 10,37 years, with an approximately equal distribution by gender (48% male and 52% female). More than half of the subjects presented hypercholesterolemia, hypertriglyceridemia, and low HDL cholesterol level. Most of the patients included in the study had varying degrees of liver fat load (only 9,89% of cases of apparently normal liver on ultrasound), and met the criteria for metabolic syndrome (81,31%). It was found that the frequency of the cases with fatty liver impairment was significantly higher in subjects with metabolic syndrome (32,43% compared to 5,88% for those without metabolic syndrome, p = 0,01) and the frequency of the cases with normal liver were significantly higher in subjects without metabolic syndrome (23,53% to 6,76%, p=0,02).Conclusion. We can say that NAFLD is a risk factor for the presence of metabolic syndrome and it can be considered the hepatic expression of this syndrome.

scholarly journals Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4

2012 ◽  
Vol 209 (13) ◽  
pp. 2395-2408 ◽  
Author(s):  
Yvonne Junker ◽  
Sebastian Zeissig ◽  
Seong-Jun Kim ◽  
Donatella Barisani ◽  
Herbert Wieser ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Immune Responses ◽  
Intestinal Inflammation ◽  
Storage Proteins ◽  
Trypsin Inhibitors ◽  
Innate Immune Responses ◽  
Toll Like Receptor 4 ◽  
Wheat Amylase ◽  
Hla Dq2

Ingestion of wheat, barley, or rye triggers small intestinal inflammation in patients with celiac disease. Specifically, the storage proteins of these cereals (gluten) elicit an adaptive Th1-mediated immune response in individuals carrying HLA-DQ2 or HLA-DQ8 as major genetic predisposition. This well-defined role of adaptive immunity contrasts with an ill-defined component of innate immunity in celiac disease. We identify the α-amylase/trypsin inhibitors (ATIs) CM3 and 0.19, pest resistance molecules in wheat, as strong activators of innate immune responses in monocytes, macrophages, and dendritic cells. ATIs engage the TLR4–MD2–CD14 complex and lead to up-regulation of maturation markers and elicit release of proinflammatory cytokines in cells from celiac and nonceliac patients and in celiac patients’ biopsies. Mice deficient in TLR4 or TLR4 signaling are protected from intestinal and systemic immune responses upon oral challenge with ATIs. These findings define cereal ATIs as novel contributors to celiac disease. Moreover, ATIs may fuel inflammation and immune reactions in other intestinal and nonintestinal immune disorders.

scholarly journals Could sugar intake initiate or aggravate non-alcoholic fatty liver during aging? An integrative review

2016 ◽  
Vol 33 (02) ◽  
pp. 121-128
Author(s):  
A. Teodoro ◽  
R. Nucci ◽  
E. Gama ◽  
G. Rodrigues ◽  
A. Machado-Lima
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Liver ◽  
Selection Criteria ◽  
Integrative Review ◽  
De Novo Lipogenesis ◽  
Liver Fat ◽  
Alcoholic Fatty Liver ◽  
Sugar Intake ◽  
The Metabolic Syndrome ◽  
Pubmed Database

Abstract Introduction: Non-alcoholic fatty liver disease (NAFLD) is part of the metabolic syndrome (MS) which is a clustering of risk factors that increase the incidence of cardiovascular events and diabetes mellitus (DM). The population aging process brings with it higher prevalence of MS. The prevalence of NAFLD has increased considerably, simultaneously with the expansion of MS, ranging from 15% to 25% in the general population. In Brazil, overweight plus obesity corresponds to 40% of the adult population and the prevalence found in the elderly age group reaches 81%. Thus, the carbohydrate intake has been identified as a key factor for the development of NAFLD. Objective: The purpose of this integrative review is to assess whether the sugar consumption by adults and elders may influence in the development and progression of NAFLD in individuals with or without metabolic syndrome. Materials and methods: The integrative review search was performed on PubMed database during September 2015. The selection criteria was adults and elderly people; sugar intake, such as, glucose or fructose; liver fat or NAFLD. Our major outcome was the hepatic profile because it is related to the sugar intake. We excluded review papers and studies with animals, as well as papers that were not related to our selection criteria. Results: The studies analyzed the sugar intake on hepatic de novo lipogenesis or NAFLD. Conclusion: We conclude in the most of the articles sugar intake and NAFLD have a positive correlation. However further studies are needed to elucidate the mechanism that sugars intake, mainly fructose, leads to NAFLD, or aggravating it.

scholarly journals Dietary Wheat Amylase Trypsin Inhibitors Impact Alzheimer’s Disease Pathology in 5xFAD Model Mice

2020 ◽  
Vol 21 (17) ◽  
pp. 6288 ◽  
Author(s):  
Malena dos Santos Guilherme ◽  
Victor F. Zevallos ◽  
Aline Pesi ◽  
Nicolai M. Stoye ◽  
Vu Thu Thuy Nguyen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Therapeutic Option ◽  
Clinical Intervention ◽  
Trypsin Inhibitors ◽  
Contributing Factors ◽  
Brain Disorder ◽  
The Metabolic Syndrome ◽  
The Impact ◽  
Wheat Amylase

Wheat amylase trypsin inhibitors (ATIs) represent a common dietary protein component of gluten-containing cereals (wheat, rye, and barley). They act as toll-like receptor 4 ligands, and are largely resistant to intestinal proteases, eliciting a mild inflammatory response within the intestine after oral ingestion. Importantly, nutritional ATIs exacerbated inflammatory bowel disease and features of fatty liver disease and the metabolic syndrome in mice. For Alzheimer’s disease (AD), both inflammation and altered insulin resistance are major contributing factors, impacting onset as well as progression of this devastating brain disorder in patients. In this study, we evaluated the impact of dietary ATIs on a well-known rodent model of AD (5xFAD). We assessed metabolic, behavioral, inflammatory, and microbial changes in mice consuming different dietary regimes with and without ATIs, consumed ad libitum for eight weeks. We demonstrate that ATIs, with or without a gluten matrix, had an impact on the metabolism and gut microbiota of 5xFAD mice, aggravating pathological hallmarks of AD. If these findings can be translated to patients, an ATI-depleted diet might offer an alternative therapeutic option for AD and warrants clinical intervention studies.

scholarly journals Influence of dietary macronutrients on liver fat accumulation and metabolism

2017 ◽  
Vol 65 (8) ◽  
pp. 1102-1115 ◽  
Author(s):  
Siôn A Parry ◽  
Leanne Hodson
Keyword(s):  
Intervention Studies ◽  
Saturated Fatty Acids ◽  
Fat Content ◽  
Liver Fat ◽  
Liver Fat Content ◽  
Alcoholic Fatty Liver ◽  
Consistent Finding ◽  
Content Type ◽  
The Metabolic Syndrome ◽  
Total Fat

The liver is a principal metabolic organ within the human body and has a major role in regulating carbohydrate, fat, and protein metabolism. With increasing rates of obesity, the prevalence of non-alcoholic fatty liver disease (NAFLD) is growing. It remains unclear why NAFLD, which is now defined as the hepatic manifestation of the metabolic syndrome, develops but lifestyle factors such as diet (ie, total calorie and specific nutrient intakes), appear to play a key role. Here we review the available observational and intervention studies that have investigated the influence of dietary macronutrients on liver fat content. Findings from observational studies are conflicting with some reporting that relative to healthy controls, patients with NAFLD consume diets higher in total fat/saturated fatty acids, whilst others find they consume diets higher in carbohydrates/sugars. From the limited number of intervention studies that have been undertaken, a consistent finding is a hypercaloric diet, regardless of whether the excess calories have been provided either as fat, sugar, or both, increases liver fat content. In contrast, a hypocaloric diet decreases liver fat content. Findings from both hyper- and hypo-caloric feeding studies provide some suggestion that macronutrient composition may also play a role in regulating liver fat content and this is supported by data from isocaloric feeding studies; fatty acid composition and/or carbohydrate content/type appear to influence whether there is accrual of liver fat or not. The mechanisms by which specific macronutrients, when consumed as part of an isocaloric diet, cause a change in liver fat remain to be fully elucidated.

scholarly journals Fighting liver fat

2020 ◽  
Vol 9 (7) ◽  
pp. R173-R186
Author(s):  
David Koeckerling ◽  
Jeremy W Tomlinson ◽  
Jeremy F Cobbold
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Disease Progression ◽  
Fatty Liver Disease ◽  
Cardiometabolic Risk ◽  
Transient Elastography ◽  
Liver Fat ◽  
Alcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease is a chronic liver disease which is closely associated with components of the metabolic syndrome. Its high clinical burden results from the growing prevalence, inherent cardiometabolic risk and potential of progressing to cirrhosis. Patients with non-alcoholic fatty liver disease show variable rates of disease progression through a histological spectrum ranging from steatosis to steatohepatitis with or without fibrosis. The presence and severity of fibrosis are the most important prognostic factors in non-alcoholic fatty liver disease. This necessitates risk stratification of patients by fibrosis stage using combinations of non-invasive methods, such as composite scoring systems and/or transient elastography. A multidisciplinary approach to treatment is advised, centred on amelioration of cardiometabolic risk through lifestyle and pharmacological interventions. Despite the current lack of licensed, liver-targeted pharmacotherapy, several promising agents are undergoing late-phase clinical trials to complement standard management in patients with advanced disease. This review summarises the current concepts in diagnosis and disease progression of non-alcoholic liver disease, focusing on pragmatic approaches to risk assessment and management in both primary and secondary care settings.

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