Induction Of Non-alcoholic Fatty Liver Disease Research Articles

Therapeutic potential of Lactobacillus casei and Chlorella vulgaris in high-fat diet-induced non-alcoholic fatty liver disease (NAFLD)-associated kidney damages: a stereological study.

The non-alcoholic fatty liver disease (NAFLD) is prevalent in as many as 25% of adults who are afflicted with metabolic syndrome. Oxidative stress plays a significant role in the pathophysiology of hepatic and renal injury associated with NAFLD. Therefore, probiotics such as Lactobacillus casei (LBC) and the microalga Chlorella vulgaris (CV) may be beneficial in alleviating kidney injury related to NAFLD. This animal study utilized 30 C57BL/6 mice, which were evenly distributed into five groups: the control group, the NAFLD group, the NAFLD + CV group, the NAFLD + LBC group, and the NAFLD + CV + LBC group. A high-fat diet (HFD) was administered to induce NAFLD for six weeks. The treatments with CV and LBC were continued for an additional 35 days. Biochemical parameters, total antioxidant capacity (TAC), and the expression of kidney damage marker genes (KIM 1 and NGAL) in serum and kidney tissue were determined, respectively. A stereological analysis was conducted to observe the structural changes in kidney tissues. A liver histopathological examination confirmed the successful induction of NAFLD. Biochemical investigations revealed that the NAFLD group exhibited increased ALT and AST levels, significantly reduced in the therapy groups (p < 0.001). The gene expression levels of KIM-1 and NGAL were elevated in NAFLD but were significantly reduced by CV and LBC therapies (p < 0.001). Stereological examinations revealed reduced kidney size, volume, and tissue composition in the NAFLD group, with significant improvements observed in the treated groups (p < 0.001). This study highlights the potential therapeutic efficacy of C. vulgaris and L. casei in mitigating kidney damage caused by NAFLD. These findings provide valuable insights for developing novel treatment approaches for managing NAFLD and its associated complications.

Bisphenol A induces non-alcoholic fatty liver disease by promoting the O-GlcNAcylation of NLRP3

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease. The mechanism by which bisphenol A (BPA) promots NAFLD remains unclear. Palmitic acid (PA) and lipopolysaccharide (LPS) were used to simulate NAFLD in HepG2 cells in vitro. Total cholesterol (TC), triglyceride (TG) content, and lipid accumulation were measured to evaluate lipid metabolism. The caspase-1-stained cells and NLRP3 inflammasome-associated proteins were evaluated for pyroptosis. Western blot analysis was used to detect protein levels and co-immunoprecipitation (Co-IP) was used to detect the association between the proteins. Cycloheximide (CHX) treatment combined with western blot was performed to access protein stability. This data have shown that BPA induces lipid metabolism dysfunction and pyroptosis by upregulating O-GlcNAc transferase (OGT) level. NLRP3 directly interacts with OGT, and elevated OGT enhanced the stability of NLRP3 protein. BPA promoted OGT-mediated O-GlcNAcylation to stabilised NLRP3, thus accelerating NAFLD progress in vitro. Our study reveals that BPA, as an environmental factor, may be involved in the promotion of NAFLD, and that targeting NLRP3 and OGT may inhibit BPA’s induction of NAFLD.

6,7-Dimethoxycoumarin, Gardenoside and Rhein combination improves non-alcoholic fatty liver disease in rats

Ethnopharmacological relevanceThis study explores the potential therapeutic benefits of using a three-component DGR (composed of specific compounds) to target the NLRP3 inflammasome in the context of non-alcoholic fatty liver disease (NAFLD). Aim of the studyTo assess the impact of a three-component DGR on NAFLD, specifically examining its effects on liver lipid accumulation, inflammation, and the diversity of intestinal microbial communities. MethodsNAFLD was induced in 8-week-old Sprague Dawley rats by feeding them a high-fat emulsion diet every morning for 8 consecutive weeks. Oral administration of DGR or its constituent equivalents in the afternoon. The pharmacological effects of DGR were evaluated using H&E, ORO and ELISA methods to determine the changes in serum and liver tissue indexes of rat-models. Immunohistochemical staining and Western blot were used to assess the interaction between DGR, NLRP3 and IL-1β. ResultsThe induction of NAFLD resulted in elevated hepatic triglycerides (TG), total cholesterol (TC), and free fatty acids (FFA). However, these alterations were ameliorated upon administration of DGR. It is noteworthy that DGR exhibited superior efficacy in comparison to its constituent compounds, manifesting augmented antioxidant activity, diminished hepatic damage, and the attenuation of pro-inflammatory factors. Both DGR and its individual monomeric constituents exhibited the capacity to attenuate the activation of the NLRP3 inflammasome in the liver, leading to an amelioration of the pathological characteristics associated with NAFLD. An analysis of the intestinal flora unveiled an elevated abundance of p_Firmicutes (1.1-fold), p_Cyanobacteria (5.76-fold), and p_Verrucomicrobia (5.2-fold), accompanied by a heightened p_Firmicutes to p_Bacteroidetes ratio (5.49-fold). ConclusionsIn the non-alcoholic fatty liver disease (NAFLD) rat model, the concurrent administration of three-component DGR effectively regulated lipid deposition, suppressed liver inflammation, and restored balance in the intestinal flora, thereby improving NAFLD pathology. These findings propose a promising therapeutic strategy for NAFLD, centered on inhibiting the NLRP3 inflammasome through the use of the three-component DGR.

Changes in Lipidomics, Metabolomics, and the Gut Microbiota in CDAA-Induced NAFLD Mice after Polyene Phosphatidylcholine Treatment.

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in most parts of the world. Although there is no first-line drug approved for the treatment of NAFLD, polyene phosphatidylcholine (PPC) is used by clinicians to treat NAFLD patients. This study aimed to evaluate the efficacy of PPC on a mice model of NAFLD, and to study the PPC's mechanism of action. The mice were fed a choline-deficient, L-amino acid-defined (CDAA) diet to induce NAFLD and were subsequently treated with PPC. The treatment effects were evaluated by the liver index, histopathological examination, and routine blood chemistry analyses. Lipidomics and metabolomics analyses of 54 samples were carried out using ultraperformance liquid chromatography (UPLC) coupled to a mass spectrometer to select for changes in metabolites associated with CDAA diet-induced NAFLD and the effects of PPC treatment. The intestinal flora of mice were extracted for gene sequencing to find differences before and after the induction of NAFLD and PPC treatment. PPC significantly improved the CDAA diet-induced NAFLD condition in mice. A total of 19 metabolites including 5 polar metabolites and 14 lipids showed marked changes. In addition, significant differences in the abundance of Lactobacillus were associated with NAFLD. We inferred that the protective therapeutic effect of PPC on the liver was related to the supplement of phosphatidylcholine, lysophosphatidylcholine, and sphingomyelin (PC, LPC, and SM, resectively) and acylcarnitine metabolism. This study developed a methodology for exploring the pathogenesis of NAFLD and can be extended to other therapeutic agents for treating NAFLD.

Ellagic acid ameliorates high fructose-induced hyperuricemia and non-alcoholic fatty liver in Wistar rats: Focusing on the role of C1q/tumor necrosis factor-related protein-3 and ATP citrate lyase

AimsHigh-fructose intake (HF) represents an inducible risk factor for non-alcoholic fatty liver disease (NAFLD). Present study aimed to illustrate the effect of HF diet (HFD) on the induction of NAFLD, hyperuricemia and role of ellagic acid as modulator. Main methodsTwenty-four adult male albino rats were randomly divided into four groups (6/each). The first group received normal chow diet only while the others received 60 % HFD for 4 weeks and subdivided later into 3 groups. The first and second groups received allopurinol and ellagic acid, respectively while the third group received HFD only for extra 4 weeks. Key findingsRats fed on HFD for 8 weeks displayed body weight gain, insulin resistance (IR), hyperglycemia, dyslipidemia, hyperuricemia with increased oxidative stress and hepatic lipogenic enzymes such as ATP citrate lyase (ACL), aldolase B, and fatty acid synthase (FAS), sterol regulatory element-binding protein 1 (SERBP-1c). C1q /tumor necrosis factor-related protein −3 (CTRP3), and phosphorylated AMP-activated protein kinase (p-AMPK) however showed significant decreases. Ellagic acid or allopurinol administration significantly decreased serum lipids, uric acid, glucose, insulin levels and hepatic contents of enzymes. Malondialdehyde (MDA), FAS, aldolase B, SERBP-1c, and xanthine oxidase (XO) hepatic contents showed significant decreases along with glutathione (GSH) increase as compared to fructose group where ellagic acid was more remarkable compared with allopurinol. SignificanceOur findings indicated that ellagic acid had alleviated HFD-induced hyperuricemia, its associated NAFLD pattern as mediated through activation of CTRP3 and inhibition of ACL activities in a pattern more remarkable than allopurinol.

The protective effects of Spirulina against Nonalcoholic fatty liver disease induced by high fat diet in rats

The ultimate goal of this study is to investigate the bimolecular changes in a rat model of high fat diet induced Nonalcoholic fatty liver disease (NAFLD). Also, the lipotropic, antioxidant and anti-inflammatory effects of spirulina platensis treatment were clarify through evaluation of certain biochemical and molecular parameters in the blood and liver tissue of rats. Twenty one adult white albino rats were separated into three groups. Group I (Normal control): received no drugs and balanced diet, Group II (NAFLD- induced group): rats fed high fat diet for 8 weeks followed by normal basal ration feeding for another 8 weeks. Group III (NAFLD + spirulina): rats treated with spirulina orally at a dose of (150 mg/kg b.wt/day) for 8 weeks after induction of NAFLD. The obtained results showed a significant increase in serum total cholesterol (TC) and triacylglycerols (TAG) concentrations with significant up-regulation of liver gene expression TNF-α, IL-1β, NF-kβ, PPAR-α, ACC, FAS and SREBT-1in NAFLD- induced rats. Also, various histopathological alterations were detected in liver tissue of induced NAFLD rats. Treatment with spirulina in NAFLD-induced rats parameters measured near the normal level of rats group (G1). Also, spirulina potentially improved molecular hepatic function alterations related to NAFLD. Interestingly, histopathological findings supported that spirulina markedly attenuates harmful effects of NAFLD and protects liver tissue. We conclude that, spirulina has a great role as antioxidant, anti-obesity and anti-inflammatory via inhibition of liver lipid metabolic disturbance, steatosis and oxidative stress singling.

The influence of RS738409 I148M polymorphism of patatin-like phospholipase domain containing 3 gene on the susceptibility of non-alcoholic fatty liver disease

We aimed to elucidate the frequency of polymorphic genotypes and alleles of patatin-like phospholipase domain containing 3 rs738409 polymorphism and its possible associations with non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis in a cohort from Turkey.We enrolled 200 patients diagnosed with NAFLD and genotyped for rs738409 I148M polymorphism by real-time polymerase chain reaction, particularly by melting curve analysis. SPSS analysis software was used for statistical significance. Continuous variable values were expressed as mean ± standard deviation. Significant statistical level was chosen as p = 0.05.Our results demonstrate in a cohort from Turkey that rs738409 C > G polymorphism (I148M) of patatin-like phospholipase domain containing 3 gene is significantly able to affect individuals to have NAFLD in unadjusted regression model.Consistent with the previous studies in other populations, our study group showed a significantly higher risk of having NAFLD in unadjusted regression model but not in the adjusted model indicating that non-genetic factors such as age and sex may be responsible for the association. However, independent studies need to validate our findings with a larger group of NAFLD patients, as well as in different ethnic cohorts.

Endotoxin Producers Overgrowing in Human Gut Microbiota as the Causative Agents for Nonalcoholic Fatty Liver Disease.

Gut microbiota-derived endotoxin has been linked to human nonalcoholic fatty liver disease (NAFLD), but the specific causative agents and their molecular mechanisms remain elusive. In this study, we investigated whether bacterial strains of endotoxin-producing pathogenic species overgrowing in obese human gut can work as causative agents for NAFLD. We further assessed the role of lipopolysaccharide (LPS)-Toll-like receptor 4 (TLR4) cross talk in this pathogenicity. Nonvirulent strains of Gram-negative pathobionts were isolated from obese human gut and monoassociated with C57BL/6J germfree (GF) mice fed a high-fat diet (HFD). Deletion of waaG in the bacterial endotoxin synthetic pathway and knockout of TLR4 in GF mice were used to further study the underlying mechanism for a causal relationship between these strains and the development of NAFLD. Three endotoxin-producing strains, Enterobacter cloacae B29, Escherichia coli PY102, and Klebsiella pneumoniae A7, overgrowing in the gut of morbidly obese volunteers with severe fatty liver, induced NAFLD when monoassociated with GF mice on HFD, while HFD alone did not induce the disease in GF mice. The commensal Bacteroides thetaiotaomicron (ATCC 29148), whose endotoxin activity was markedly lower than that of Enterobacteriaceae strains, did not induce NAFLD in GF mice. B29 lost its proinflammatory properties and NAFLD-inducing capacity upon deletion of the waaG gene. Moreover, E. cloacae B29 did not induce NAFLD in TLR4-deficient GF mice. These nonvirulent endotoxin-producing strains in pathobiont species overgrowing in human gut may work as causative agents, with LPS-TLR4 cross talk as the most upstream and essential molecular event for NAFLD.IMPORTANCE Recent studies have reported a link between gut microbiota and nonalcoholic fatty liver disease (NAFLD), showing that germfree (GF) mice do not develop metabolic syndromes, including NAFLD. However, the specific bacterial species causing NAFLD, as well as their molecular cross talk with the host for driving liver disease, remain elusive. Here, we found that nonvirulent endotoxin-producing strains of pathogenic species overgrowing in obese human gut can act as causative agents for induction of NAFLD and related metabolic disorders. The cross talk between endotoxin from these specific producers and the host's TLR4 receptor is the most upstream and essential molecular event for inducing all phenotypes in NAFLD and related metabolic disorders. These nonvirulent endotoxin-producing strains of gut pathogenic species overgrowing in human gut may collectively become a predictive biomarker or serve as a novel therapeutic target for NAFLD and related metabolic disorders.

The effects of hydroalcoholic extract of spinach on prevention and treatment of some metabolic and histologic features in a rat model of nonalcoholic fatty liver disease.

This study evaluated the effects of hydroalcoholic extract of spinach (HES) on nonalcoholic fatty liver disease (NAFLD). In the prevention phase, 18 Sprague-Dawley rats were fed a high-fat diet, a high-fat diet plus 400 mg kg-1 HES, or a chow diet for 7 weeks. For the treatment phase, after the induction of NAFLD, they were fed a high-fat diet, a high-fat diet plus 400 mg kg-1 HES, a chow diet, or chow diet plus 400 mg kg-1 HES for 4 weeks (n = 6). Weight gain (P = 0.01), food intake (P < 0.01), serum glucose (P = 0.01), triglyceride (TG) (P = 0.02), low-density lipoprotein cholesterol (LDL-c) (P = 0.01), aspartate aminotransferase (AST) (P = 0.02), liver steatosis, and the nonalcoholic fatty liver disease (NAFLD) activity score (NAS) (P < 0.01) in the high-fat group were statistically higher than in the other groups at the end of the prevention phase. Feeding spinach extract to rats on a high-fat diet decreased serum glucose (P = 0.01), total cholesterol (TCh) (P < 0.01), AST (P = 0.01), alkaline phosphatase (ALP) (P < 0.01), and liver steatosis (P < 0.01) in the treatment phase. Overall, spinach extract showed beneficial effects in the prevention and treatment of NAFLD. © 2019 Society of Chemical Industry.

Nonalcoholic Fatty Liver Disease Induced by High-Fat Diet in C57bl/6 Models

Researchers have a range of animal models in which to study Nonalcoholic fatty liver disease (NAFLD). Induction of NAFLD by a high-fat diet in the C57BL/6 strain is the most widely used among mice. In this study, we review works that performed NAFLD induction by a high-fat diet using the C57BL/6 strain, focusing on experiments on the effects of lipid ingestion. Studies are initially distinguished into researches in which mice received lipids by oral gavage and studies in which lipid was added to the diet, and each of these designs has peculiarities that must be considered. Oral gavage can be stressful for animals and needs trained handlers but allows accurate control of the dose administered. The addition of oils to the diet can prevent stress caused to mice by gavage, but possible changes in the consistency, taste, and smell of the diet should be considered. Regarding the experimental design, some variables, such as animal sex, treatment time, and diet-related variables, appear to have a definite pattern. However, no pattern was found regarding the number of animals per group, age at the beginning of the experiment, time of adaptation, the substance used as a vehicle, and substance used as a control.

Preparation and Evaluation of Functional Foods for Prevention of Non-alcoholic Fatty Liver Disease.

Non-alcoholic fatty liver disease (NAFLD) is a public health problem presenting one of the most important common forms of liver diseases worldwide. This study was carried out to investigate the protective effect of two functional foods in form of bread containing purslane seeds meal and garden cress seeds against NAFLD. High fat and high cholesterol diet were used for induction of NAFLD in rats for 6 weeks. Plasma lipid profile (total cholesterol, triglycerides, high density lipoprotein-cholesterol and low-density lipoprotein-cholesterol, hepatic lipid profile (total fat, cholesterol, triglycerides), malondialdehyde (MDA), as well as liver (AST, ALT, total and direct bilirubin) and kidney (creatinine and urea) functions were assessed. Histological examination of liver tissue was carried out. Results revealed that significant elevation in plasma and liver lipid profiles, MDA, liver enzymes (AST and ALT), bilirubin (total and direct) and kidney function (creatinine and urea) were observed in NAFLD control compared to normal control. Feeding rats on diet containing functional food I and II (purslane and garden cress bread, respectively) showed significant improvement in all the studied parameters with remarkable effect regards to functional food I (purslane bread). Purslane bread and garden cress bread as functional foods prepared in the present study prevent weight gain, improve plasma lipid profile and prevent hepatic lipid accumulation effectively in NAFLD model in rats. Also decreased lipid peroxidation, improve liver and kidney functions and possess hypoglycemic effect. Purslane bread was superior in the prevention of hepatic lipid accumulation.

Inhibiting poly ADP-ribosylation increases fatty acid oxidation and protects against fatty liver disease

To date, no pharmacological therapy has been approved for non-alcoholic fatty liver disease (NAFLD). The aim of the present study was to evaluate the therapeutic potential of poly ADP-ribose polymerase (PARP) inhibitors in mouse models of NAFLD. As poly ADP-ribosylation (PARylation) of proteins by PARPs consumes nicotinamide adenine dinucleotide (NAD+), we hypothesized that overactivation of PARPs drives NAD+ depletion in NAFLD. Therefore, we assessed the effectiveness of PARP inhibition to replenish NAD+ and activate NAD+-dependent sirtuins, hence improving hepatic fatty acid oxidation. To do this, we examined the preventive and therapeutic benefits of the PARP inhibitor (PARPi), olaparib, in different models of NAFLD. The induction of NAFLD in C57BL/6J mice using a high-fat high-sucrose (HFHS)-diet increased PARylation of proteins by PARPs. As such, increased PARylation was associated with reduced NAD+ levels and mitochondrial function and content, which was concurrent with elevated hepatic lipid content. HFHS diet supplemented with PARPi reversed NAFLD through repletion of NAD+, increasing mitochondrial biogenesis and β-oxidation in liver. Furthermore, PARPi reduced reactive oxygen species, endoplasmic reticulum stress and fibrosis. The benefits of PARPi treatment were confirmed in mice fed with a methionine- and choline-deficient diet and in mice with lipopolysaccharide-induced hepatitis; PARP activation was attenuated and the development of hepatic injury was delayed in both models. Using Sirt1hep-/- mice, the beneficial effects of a PARPi-supplemented HFHS diet were found to be Sirt1-dependent. Our study provides a novel and practical pharmacological approach for treating NAFLD, fueling optimism for potential clinical studies. Non-alcoholic fatty liver disease (NAFLD) is now considered to be the most common liver disease in the Western world and has no approved pharmacological therapy. PARP inhibitors given as a treatment in two different mouse models of NAFLD confer a protection against its development. PARP inhibitors may therefore represent a novel and practical pharmacological approach for treating NAFLD.

Type 3 diabetes with links to NAFLD and Other Chronic Diseases in the Western World

In the year 2015 it is now estimated that 30% of the Western World will now progress to non alcoholic fatty liver disease (NAFLD) and by the year 2050 if NAFLD remains untreated in the Western world the prevalence of the disease may rise to 40% of the global population. Type 3 diabetes and circadian rhythm disturbances may be involved in the induction of NAFLD that may promote insulin resistance and various chronic diseases such as cardiovascular disease, pancreatic disease, kidney disease and neurodegenerative disease. Multiple risk factors that induce Type 3 diabetes and NAFLD include stress, magnesium deficiency, bacterial lipopolysaccharide contamination, drug induced toxicity, xenobiotic levels, unhealthy diet/lifestyle factors and defective thermoregulation. Early diagnosis of Type 3 diabetes by multiple assessment techniques such as proteomics, genomics and lipidomics may allow reversal or stabilization of NAFLD that may progress slowly from simple non-alcoholic steatosis to non-alcoholic steatohepatitis and to hepatic fibrosis/cirrhosis of liver and hepatoma. Analysis of plasma constituents such as heat shock proteins (60,70, 90), amyloid beta, adiponectin, fibroblast growth factor 21, ceramide, sphingosine1-phosphate, vasoactive intestinal peptide, thrombospondin 1, acute phase reactants may indicate progression of Type 3 diabetes and NAFLD and these results may not be consistent with normal plasma glucose and cholesterol levels. Early nutritional interventions with temperature regulation are required to reverse premature brain disease in diabetes (Type 3/Type2) that is connected to the rapid metabolism of heat shock proteins and amyloid beta oligomers that determine the severity of insulin resistance and NAFLD in individuals in the Western World.

Aging Increases Susceptibility to High Fat Diet-Induced Metabolic Syndrome in C57BL/6 Mice: Improvement in Glycemic and Lipid Profile after Antioxidant Therapy.

Nonalcoholic fatty liver disease (NAFLD) has been considered a novel component of the metabolic syndrome (MetS), with the oxidative stress participating in its progression. This study aimed to evaluate the metabolic profile in young and old mice with MetS, and the effects of apocynin and tempol on glycemic and lipid parameters. Young and old C57BL/6 mice with high fat diet- (HFD-) induced MetS received apocynin and tempol 50 mg·kg−1/day in their drinking water for 10 weeks. After HFD, the young group showed elevated fasting glucose, worsened lipid profile in plasma, steatosis, and hepatic lipid peroxidation. Nevertheless, the old group presented significant increase in fasting insulin levels, insulin resistance, plasma and hepatic lipid peroxidation, and pronounced steatosis. The hepatic superoxide dismutase and catalase activity did not differ between the groups. Tempol and apocynin seemed to prevent hepatic lipid deposition in both groups. Furthermore, apocynin improved glucose tolerance and insulin sensitivity in old mice. In summary, old mice are more susceptible to HFD-induced metabolic changes than their young counterparts. Also, the antioxidant therapy improved insulin sensitivity and glucose tolerance, and in addition, apocynin seemed to prevent the HFD-induced hepatic fat deposition, suggesting an important role of oxidative stress in the induction of NAFLD.

Histological study on the effect of metformin on high-fat-diet-induced liver injury in adult male albino rats

Introduction Changes in lifestyle and food habits increase the prevalence of nonalcoholic fatty liver disease (NAFLD). It is a chronic condition that has no or few symptoms. It may be accompanied by inflammation and insulin resistance. Moreover, it is closely linked to diabetes. Metformin is an antidiabetic agent that can improve insulin resistance. The aim of this study The study was conducted to investigate the effect of metformin on liver injury induced by a high-fat diet. Materials and methods The study lasted for 12 weeks. Thirty-six adult male albino rats were used and divided into four groups. Group I was the control group. Group II rats received metformin. Group III rats were fed a high-fat diet for induction of NAFLD. Group IV rats were fed a high-fat diet for induction of NAFLD and then administered metformin orally in the last 4 weeks of the study. Liver specimens were processed for light and electron microscopic examination. Moreover, liver weight index was determined, and biochemical, morphometric, and statistical studies were performed. Results Induction of NAFLD (group III) resulted in severe insulin resistance. Hepatocytes showed macrovesicular and microvesicular steatosis, ballooning, and lobular inflammation. The number of positive cells and the reaction for tumor necrosis factor-α in group III apparently increased as compared with group IV. Lipid droplets, loss of mitochondrial cristae, and dispersion of rER were detected in group III. Metformin improved insulin resistance, and liver histological changes were fewer than those in group III. Conclusion Metformin can greatly improve liver histological changes associated with a model of NAFLD.

Induction of NAFLD with Increased Risk of Obesity and Chronic Diseases in Developed Countries

The susceptibility of individuals to obesity has been reported in many developed countries with predisposition of humans to obesity associated with high calorie diets and unhealthy lifestyles. Obesity may closely be involved in cell suicide in various organ diseases with the importance of accelerated aging that requires early intervention with drug therapy to prevent diseases such as non alcoholic fatty liver disease (NAFLD) that has increased in children and reached to approx. 40% of the global population. Obesity is induced by various diets and lifestyle factors such as stress, anxiety and depression which are important to consider with the global increase in obesity and are possibly linked to the rise in individuals with brain disorders that involve neurodegeneration. Xenobiotics such as the endocrine disruptor chemicals that have increased in the environment in various developed countries lead to various chronic endocrine diseases as populations divert towards unhealthy diets and lifestyles with induction of NAFLD and obesity. The amount and nature of food intake that improves and increases liver lipid and xenobiotic metabolism in obese individuals have become important to decrease the risk for increased adiposity in man. High fibre or protein diets that contain leucine may improve liver glucose, lipid and xenobiotic metabolism and require further investigation with xenobiotics such as endocrine disruptors involved in appetite dysregulation and metabolic disorders in developed countries. The use of anti-obese drugs that reduce food intake and improve hypercholesterolemia and cardiovascular disease has been assessed in obesity with drug therapy closely involved either in the prevention or induction of NAFLD and obesity in man.

Causes of Peripheral Blood Cytopenias in Patients with Liver Cirrhosis Portal Hypertension and Clinical Significances

The susceptibility of individuals to obesity has been reported in many developed countries with predisposition of humans to obesity associated with high calorie diets and unhealthy lifestyles. Obesity may closely be involved in cell suicide in various organ diseases with the importance of accelerated aging that requires early intervention with drug therapy to prevent diseases such as non alcoholic fatty liver disease (NAFLD) that has increased in children and reached to approx. 40% of the global population. Obesity is induced by various diets and lifestyle factors such as stress, anxiety and depression which are important to consider with the global increase in obesity and are possibly linked to the rise in individuals with brain disorders that involve neurodegeneration. Xenobiotics such as the endocrine disruptor chemicals that have increased in the environment in various developed countries lead to various chronic endocrine diseases as populations divert towards unhealthy diets and lifestyles with induction of NAFLD and obesity. The amount and nature of food intake that improves and increases liver lipid and xenobiotic metabolism in obese individuals have become important to decrease the risk for increased adiposity in man. High fibre or protein diets that contain leucine may improve liver glucose, lipid and xenobiotic metabolism and require further investigation with xenobiotics such as endocrine disruptors involved in appetite dysregulation and metabolic disorders in developed countries. The use of anti-obese drugs that reduce food intake and improve hypercholesterolemia and cardiovascular disease has been assessed in obesity with drug therapy closely involved either in the prevention or induction of NAFLD and obesity in man.