scholarly journals Obesity and Inflammation: Epidemiology, Risk Factors, and Markers of Inflammation

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Heriberto Rodríguez-Hernández ◽  
Luis E. Simental-Mendía ◽  
Gabriela Rodríguez-Ramírez ◽  
Miguel A. Reyes-Romero
Keyword(s):  
Chronic Diseases ◽  
Acute Phase ◽  
Public Health Problem ◽  
Low Grade ◽  
Alcoholic Fatty Liver ◽  
Protein Levels ◽  
Markers Of Inflammation ◽  
Immune System Activation ◽  
System Activation ◽  
Alcoholic Fatty Liver Disease

Obesity is a public health problem that has reached epidemic proportions with an increasing worldwide prevalence. The global emergence of obesity increases the risk of developing chronic metabolic disorders. Thus, it is an economic issue that increased the costs of the comorbidities associated. Moreover, in recent years, it has been demonstrated that obesity is associated with chronic systemic inflammation, this status is conditioned by the innate immune system activation in adipose tissue that promotes an increase in the production and release of pro-inflammatory cytokines that contribute to the triggering of the systemic acute-phase response which is characterized by elevation of acute-phase protein levels. On this regard, low-grade chronic inflammation is a characteristic of various chronic diseases such as metabolic syndrome, cardiovascular disease, diabetes, hypertension, non-alcoholic fatty liver disease, and some cancers, among others, which are also characterized by obesity condition. Thus, a growing body of evidence supports the important role that is played by the inflammatory response in obesity condition and the pathogenesis of chronic diseases related.

scholarly journals Insulin resistance and liver histopathology in metabolically unhealthy subjects do not correlate with the hepatic abundance of NLRP3 inflammasome nor circulating IL-1β levels

2021 ◽  
Vol 9 (1) ◽  
pp. e001975
Author(s):  
Nicolas Quezada ◽  
Ilse Valencia ◽  
Javiera Torres ◽  
Gregorio Maturana ◽  
Jaime Cerda ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Liver Damage ◽  
Nlrp3 Inflammasome ◽  
Low Grade ◽  
Model Assessment ◽  
Alcoholic Fatty Liver ◽  
Protein Levels ◽  
Liver Histopathology ◽  
Inflammatory Status

IntroductionSystemic chronic low-grade inflammation has been linked to insulin resistance (IR) and non-alcoholic steatohepatitis (NASH). NOD-like receptor protein 3 (NLRP3) inflammasome and its final product, interleukin (IL)-1β, exert detrimental effects on insulin sensitivity and promote liver inflammation in murine models. Evidence linking hepatic NLRP3 inflammasome, systemic IR and NASH has been scarcely explored in humans. Herein, we correlated the hepatic abundance of NLRP3 inflammasome components and IR and NASH in humans.Research design and methodsMetabolically healthy (MH) (n=11) and metabolically unhealthy (MUH) (metabolic syndrome, n=21, and type 2 diabetes, n=14) subjects were recruited. Insulin sensitivity (homeostatic model assessment of IR (HOMA-IR) and Oral Glucose Sensitivity (OGIS120)), glycemic (glycated hemoglobin), and lipid parameters were determined by standard methods. Plasma cytokines were quantified by Magpix. Hepatic NLRP3 inflammasome components were determined at the mRNA and protein levels by reverse transcription–quantitative PCR and western blot, respectively. Liver damage was assessed by histological analysis (Non-alcoholic Fatty Liver Disease Activity Score (NAS) and Steatosis, Inflammatory Activity, and Fibrosis (SAF) scores). IR and liver histopathology were correlated with NLRP3 inflammasome components as well as with liver and plasma IL-1β levels.ResultsBody Mass Index, waist circumference, and arterial hypertension frequency were significantly higher in MUH subjects. These patients also had increased high-sensitivity C reactive protein levels compared with MH subjects. No differences in the plasma levels of IL-1β nor the hepatic content of Nlrp3, apoptosis-associated speck-like (Asc), Caspase-1, and IL-1β were detected between MUH and MH individuals. MUH subjects had significantly higher NAS and SAF scores, indicating more severe liver damage. However, histological severity did not correlate with the hepatic content of NLRP3 inflammasome components nor IL-1β levels.ConclusionOur results suggest that NLRP3 inflammasome activation is linked neither to IR nor to the inflammatory status of the liver in MUH patients.

Diet containing dehulled adlay ameliorates hepatic steatosis, inflammation and insulin resistance in rats with non-alcoholic fatty liver disease

2021 ◽  
pp. 1-25
Author(s):  
Wan-Ju Yeh ◽  
Jung Ko ◽  
Wei-Yi Cheng ◽  
Hsin-Yi Yang
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Liver Weight ◽  
Vital Role ◽  
High Dose ◽  
Alcoholic Fatty Liver ◽  
Protein Levels ◽  
Alcoholic Fatty Liver Disease

Abstract Dietary modification plays a vital role in the treatment of non-alcoholic liver diseases. We investigated the effects of the consumption of different amount of dehulled adlay, which has hypolipidemic and anti-inflammatory properties, on non-alcoholic fatty liver disease (NAFLD). We fed rats a high-fat-high-fructose liquid diet for 16 weeks to induce NAFLD. The rats were divided into three groups fed the NAFLD diet only (NN) or a diet containing 44.9 g/L or 89.8 g/L of dehulled adlay (group NA and NB, respectively). After 8 weeks, the NA & NB group had lower C-reactive protein levels and improvement in insulin resistance. In addition, the NB group had lower liver weight and hepatic triglyceride and cholesterol concentrations than did the NN group. Compared with the NN group, the high-dose NB group had improved steatosis, lower hepatic TNF-α, IL-1β and IL-6 levels, and lower adipose leptin levels. Our results suggest that a diet containing dehulled adlay can ameliorate NAFLD progression by decreasing of insulin resistance, steatosis and inflammation.

Sinapine reduces non-alcoholic fatty liver disease in mice by modulating the composition of the gut microbiota

2019 ◽  
Vol 10 (6) ◽  
pp. 3637-3649 ◽  
Author(s):  
Youdong Li ◽  
Jinwei Li ◽  
Qingfeng Su ◽  
Yuanfa Liu
Keyword(s):  
Liver Disease ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Chronic Inflammation ◽  
Fatty Liver Disease ◽  
Low Grade ◽  
Alcoholic Fatty Liver ◽  
Intestinal Dysbiosis ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is associated with low-grade chronic inflammation and intestinal dysbiosis.

scholarly journals Non-alcoholic fatty liver disease and cardiovascular disease: assessing the evidence for causality

Diabetologia ◽  
2019 ◽  
Vol 63 (2) ◽  
pp. 253-260 ◽  
Author(s):  
Martijn C. G. J. Brouwers ◽  
Nynke Simons ◽  
Coen D. A. Stehouwer ◽  
Aaron Isaacs
Keyword(s):  
Cardiovascular Disease ◽  
Liver Disease ◽  
Fatty Liver Disease ◽  
Plasma Lipids ◽  
Low Grade ◽  
Alcoholic Fatty Liver ◽  
Important Mediator ◽  
Low Grade Inflammation ◽  
The Relationship ◽  
Alcoholic Fatty Liver Disease

Abstract Non-alcoholic fatty liver disease (NAFLD) is highly prevalent among individuals with type 2 diabetes. Although epidemiological studies have shown that NAFLD is associated with cardiovascular disease (CVD), it remains unknown whether NAFLD is an active contributor or an innocent bystander. Plasma lipids, low-grade inflammation, impaired fibrinolysis and hepatokines are potential mediators of the relationship between NAFLD and CVD. The Mendelian randomisation approach can help to make causal inferences. Studies that used common variants in PNPLA3, TM6SF2 and GCKR as instruments to investigate the relationship between NAFLD and coronary artery disease (CAD) have reported contrasting results. Variants in PNPLA3 and TM6SF2 were found to protect against CAD, whereas variants in GCKR were positively associated with CAD. Since all three genes have been associated with non-alcoholic steatohepatitis, the second stage of NAFLD, the question of whether low-grade inflammation is an important mediator of the relationship between NAFLD and CAD arises. In contrast, the differential effects of these genes on plasma lipids (i.e. lipid-lowering for PNPLA3 and TM6SF2, and lipid-raising for GCKR) strongly suggest that plasma lipids account for their differential effects on CAD risk. This concept has recently been confirmed in an extended set of 12 NAFLD susceptibility genes. From these studies it appears that plasma lipids are an important mediator between NAFLD and CVD risk. These findings have important clinical implications, particularly for the design of anti-NAFLD drugs that also affect lipid metabolism.

scholarly journals 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) dysregulates hepatic one carbon metabolism during the progression of steatosis to steatohepatitis with fibrosis in mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Russell R. Fling ◽  
Claire M. Doskey ◽  
Kelly A. Fader ◽  
Rance Nault ◽  
Tim R. Zacharewski
Keyword(s):  
Gene Expression ◽  
Carbon Metabolism ◽  
Fatty Liver Disease ◽  
Bolus Dose ◽  
Alcoholic Fatty Liver ◽  
Homocysteic Acid ◽  
Protein Levels ◽  
One Carbon Metabolism ◽  
Dose Dependent ◽  
Alcoholic Fatty Liver Disease

Abstract 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a persistent environmental contaminant, induces steatosis that can progress to steatohepatitis with fibrosis, pathologies that parallel stages in the development of non-alcoholic fatty liver disease (NAFLD). Coincidently, one carbon metabolism (OCM) gene expression and metabolites are often altered during NAFLD progression. In this study, the time- and dose-dependent effects of TCDD were examined on hepatic OCM in mice. Despite AhR ChIP-seq enrichment at 2 h, OCM gene expression was not changed within 72 h following a bolus dose of TCDD. Dose-dependent repression of methionine adenosyltransferase 1A (Mat1a), adenosylhomocysteinase (Achy) and betaine-homocysteine S-methyltransferase (Bhmt) mRNA and protein levels following repeated treatments were greater at 28 days compared to 8 days. Accordingly, levels of methionine, betaine, and homocysteic acid were dose-dependently increased, while S-adenosylmethionine, S-adenosylhomocysteine, and cystathionine exhibited non-monotonic dose-dependent responses consistent with regulation by OCM intermediates and repression of glycine N-methyltransferase (Gnmt). However, the dose-dependent effects on SAM-dependent metabolism of polyamines and creatine could not be directly attributed to alterations in SAM levels. Collectively, these results demonstrate persistent AhR activation disrupts hepatic OCM metabolism at the transcript, protein and metabolite levels within context of TCDD-elicited progression of steatosis to steatohepatitis with fibrosis.

scholarly journals From sugar to liver fat and public health: systems biology driven studies in understanding non-alcoholic fatty liver disease pathogenesis

2019 ◽  
Vol 78 (3) ◽  
pp. 290-304 ◽  
Author(s):  
J. Bernadette Moore
Keyword(s):  
Public Health ◽  
Liver Disease ◽  
Systems Biology ◽  
Fatty Liver ◽  
Chronic Diseases ◽  
Fatty Liver Disease ◽  
Health Concern ◽  
Alcoholic Fatty Liver ◽  
Genome Scale ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is now a major public health concern with an estimated prevalence of 25–30% of adults in many countries. Strongly associated with obesity and the metabolic syndrome, the pathogenesis of NAFLD is dependent on complex interactions between genetic and environmental factors that are not completely understood. Weight loss through diet and lifestyle modification underpins clinical management; however, the roles of individual dietary nutrients (e.g. saturated and n-3 fatty acids; fructose, vitamin D, vitamin E) in the pathogenesis or treatment of NAFLD are only partially understood. Systems biology offers valuable interdisciplinary methods that are arguably ideal for application to the studying of chronic diseases such as NAFLD, and the roles of nutrition and diet in their molecular pathogenesis. Although present in silico models are incomplete, computational tools are rapidly evolving and human metabolism can now be simulated at the genome scale. This paper will review NAFLD and its pathogenesis, including the roles of genetics and nutrition in the development and progression of disease. In addition, the paper introduces the concept of systems biology and reviews recent work utilising genome-scale metabolic networks and developing multi-scale models of liver metabolism relevant to NAFLD. A future is envisioned where individual genetic, proteomic and metabolomic information can be integrated computationally with clinical data, yielding mechanistic insight into the pathogenesis of chronic diseases such as NAFLD, and informing personalised nutrition and stratified medicine approaches for improving prognosis.

scholarly journals Reply to: “C-reactive protein levels in non-alcoholic fatty liver disease”

2012 ◽  
Vol 56 (2) ◽  
pp. 508-510
Author(s):  
Tine Jess ◽  
Esther Zimmermann ◽  
Rodolphe Anty ◽  
Joan Tordjman ◽  
An Verrijken ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
C Reactive Protein ◽  
Alcoholic Fatty Liver ◽  
Protein Levels ◽  
Reactive Protein ◽  
Alcoholic Fatty Liver Disease

Metabolic disturbances in non-alcoholic fatty liver disease

2009 ◽  
Vol 116 (7) ◽  
pp. 539-564 ◽  
Author(s):  
Christopher D. Byrne ◽  
Rasaq Olufadi ◽  
Kimberley D. Bruce ◽  
Felino R. Cagampang ◽  
Mohamed H. Ahmed
Keyword(s):  
Public Health ◽  
Liver Disease ◽  
Fatty Liver ◽  
Health Problem ◽  
Fatty Liver Disease ◽  
Public Health Problem ◽  
Alcoholic Fatty Liver ◽  
Increased Risk ◽  
Alcoholic Fatty Liver Disease ◽  
Over Time

NAFLD (non-alcoholic fatty liver disease) refers to a wide spectrum of liver damage, ranging from simple steatosis to NASH (non-alcoholic steatohepatitis), advanced fibrosis and cirrhosis. NAFLD is strongly associated with insulin resistance and is defined by accumulation of liver fat >5% per liver weight in the presence of <10 g of daily alcohol consumption. The exact prevalence of NAFLD is uncertain because of the absence of simple non-invasive diagnostic tests to facilitate an estimate of prevalence. In certain subgroups of patients, such as those with Type 2 diabetes, the prevalence of NAFLD, defined by ultrasound, may be as high as 70%. NASH is an important subgroup within the spectrum of NAFLD that progresses over time with worsening fibrosis and cirrhosis, and is associated with increased risk for cardiovascular disease. It is, therefore, important to understand the pathogenesis of NASH and, in particular, to develop strategies for interventions to treat this condition. Currently, the ‘gold standard’ for the diagnosis of NASH is liver biopsy, and the need to undertake a biopsy has impeded research in subjects in this field. Limited results suggest that the prevalence of NASH could be as high as 11% in the general population, suggesting there is a worsening future public health problem in this field of medicine. With a burgeoning epidemic of diabetes in an aging population, it is likely that the prevalence of NASH will continue to increase over time as both factors are important risk factors for liver fibrosis. The purpose of this review is to: (i) briefly discuss the epidemiology of NAFLD to describe the magnitude of the future potential public health problem; and (ii) to discuss extra- and intra-hepatic mechanisms contributing to the pathogenesis of NAFLD, a better understanding of which may help in the development of novel treatments for this condition.

Sign in / Sign up

Export Citation Format

Share Document