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Metabolic syndrome and risk factors for non-alcoholic fatty liver disease
Souza, M?nica Rodrigues de Araújo;Diniz, Margareth de Fátima Formiga de Melo;Medeiros-Filho, José Eymard Moraes de;Araújo, Maria Salete Trigueiro de;
Arquivos de Gastroenterologia , 2012, DOI: 10.1590/S0004-28032012000100015
Abstract: context: non-alcoholic fatty liver disease (nafld), hepatic manifestation of metabolic syndrome, has been considered the most common liver disease nowadays, which is also the most frequent cause of elevated transaminases and cryptogenic cirrhosis. the greatest input of fatty acids into the liver and consequent increased beta-oxidation contribute to the formation of free radicals, release of inflammatory cytokines and varying degrees of hepatocytic aggression, whose histological expression may vary from steatosis (hs) to non-alcoholic steatohepatitis (nash). the differentiation of these forms is required by the potential risk of progression to cirrhosis and development of hepatocellular carcinoma. objective: to review the literature about the major risk factors for nafld in the context of metabolic syndrome, focusing on underlying mechanisms and prevention. method: pubmed, medline and scielo data basis analysis was performed to identify studies describing the link between risk factors for metabolic syndrome and nafld. a combination of descriptors was used, non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, metabolic syndrome and risk factors. at the end, 96 clinical and experimental studies, cohorts, meta-analysis and systematic reviews of great impact and scientific relevance to the topic, were selected. results: the final analysis of all these data, pointed out the central obesity, type 2 diabetes, dyslipidemia and hypertension as the best risk factors related to nafld. however, other factors were highlighted, such as gender differences, ethnicity, genetic factors and the role of innate immunity system. how these additional factors may be involved in the installation, progression and disease prognosis is discussed. conclusion: risk factors for nafld in the context of metabolic syndrome expands the prospects to 1) recognize patients with metabolic syndrome at high risk for nafld, 2) elucidate pathways common to other co-morbidities, 3) determine risk
Non-alcoholic fatty liver disease and metabolic syndrome in obese children  [cached]
Mehmet Emre Atabek
World Journal of Gastroenterology , 2011, DOI: 10.3748/wjg.v17.i39.4445
Abstract: I read with great interest the article of Fu et al who investigated whether non-alcoholic fatty liver disease (NAFLD) is an early mediator for prediction of metabolic syndrome, and whether liver B-ultrasound could be used for its diagnosis, in a study involving 861 obese children (6-16 years old). In this study, it was reported that NAFLD is not only a liver disease, but also an early mediator that reflects metabolic disorder, and that liver B-ultrasound can be a useful tool for metabolic syndrome (MS) screening. The authors reported that NAFLD and MS were present in 68.18% and 25.67% of obese children, respectively. Moreover, they observed that the prevalence of MS in NAFLD children was 37.64%, which was much higher than that in the non-NAFLD group. Criteria analogous to those of the Adult Treatment Panel III definition for MS were used for children in this study. The reported prevalence data on MS in the young has varied markedly, in large part because of disagreement among the variously proposed definitions of MS. Therefore, in my opinion, a study aiming to assess the association between MS components and NAFLD in obese children has to take into account a simple, easy-to-apply clinical definition proposed by the international diabetes federation for MS. Interpretation of the results of the Fu et al study are limited by another major caveat: that the diagnosis or exclusion of NAFLD was based on liver enzymes and ultrasound imaging, but was not confirmed by liver biopsy. Indeed, it is known that liver enzymes may be within the reference interval in up to 70% of patients with diagnosed NAFLD and that the full histopathological spectrum of NAFLD may be present in patients with normal liver enzymes, which therefore cannot be reliably used to exclude the presence of NAFLD.
Fructose and NAFLD: metabolic implications and models of induction in rats
Castro, Gabriela S. F.;Cardoso, Jo?o F. R.;Vannucchi, Helio;Zucoloto, Sérgio;Jord?o, Alceu Afonso;
Acta Cirurgica Brasileira , 2011, DOI: 10.1590/S0102-86502011000800009
Abstract: purpose: the increase in fructose consumption is paralleled by a higher incidence of obesity worldwide. this monosaccharide is linked to metabolic syndrome, being associated with hypertriglyceridemia, hypertension, insulin resistance and diabetes mellitus. it is metabolized principally in the liver, where it can be converted into fatty acids, which are stored in the form of triglycerides leading to nafld. several models of nafld use diets high in simple carbohydrates. thus, this study aimed to describe the major metabolic changes caused by excessive consumption of fructose in humans and animals and to present liver abnormalities resulting from high intakes of fructose in different periods of consumption and experimental designs in wistar rats. methods: two groups of rats were fasted for 48 hours and reefed for 24 or 48 hours with a diet containing 63% fructose. another group of rats was fed an diet with 63% fructose for 90 days. results: refeeding for 24 hours caused accumulation of large amounts of fat, compromising 100% of the hepatocytes. the amount of liver fat in animals refed for 48 hours decreased, remaining mostly in zone 2 (medium-zonal). in liver plates of wistar rats fed 63% fructose for 45, 60 and 90 days it's possible to see that there is an increase in hepatocytes with fat accumulation according to the increased time; hepatic steatosis, however, is mild, compromising about 20% of the hepatocytes. conclusions: fructose is highly lipogenic, however the induction of chronic models in nafld requires long periods of treatment. the acute supply for 24 or 48 hours, fasted rats can cause big changes, liver steatosis with macrovesicular in all lobular zones.
Obesity in children and adolescents: the relation between metabolic syndrome and non-alcoholic fatty-liver disease
Duarte, Maria Amélia Soares de Melo;Silva, Giselia Alves Pontes da;
Revista Brasileira de Saúde Materno Infantil , 2010, DOI: 10.1590/S1519-38292010000200004
Abstract: this article aims to review clinical and diagnostic aspects of non-alcoholic fatty liver disease associated with obesity and its relation to metabolic syndrome in children and adolescents. an on-line search was carried out of original articles in the medical literature analysis and retrieval system online (medline), literatura latino-americana e do caribe em ciências da saúde (lilacs) and scientific eletronic library online (scielo) databases, using the following key words: "hepatic steatosis", "nonalcoholic fatty liver diseases", "overweight", "obesity", "children", "adolescents", "ultrasound" and "metabolic syndrome" in english and portuguese. two hundred and seventy-five articles were initially selected, all published between 1993 and 2008. after reading this was narrowed down to 67. the literature consulted revealed no consensus regarding the need to screen for metabolic syndrome and non-alcoholic fatty liver disease, especially in obese children and adolescents and those who have excess fat in the abdominal region. an ultrasound examination of the liver is typically used for screening and, in the case of children who present alterations in aminotransferases in addition to fatty infiltration of the liver, a strict clinical follow-up and a liver biopsy are recommended if these symptoms do not disappear on treatment.
Non-alcoholic fatty liver disease and the metabolic syndrome: An update  [cached]
R Scott Rector, John P Thyfault, Yongzhong Wei, Jamal A Ibdah
World Journal of Gastroenterology , 2008,
Abstract: Sedentary lifestyle and poor dietary choices are leading to a weight gain epidemic in westernized countries, subsequently increasing the risk for developing the metabolic syndrome and nonalcoholic fatty liver disease (NAFLD). NAFLD is estimated to affect approximate 30% of the general US population and is considered the hepatic manifestation of the metabolic syndrome. Recent findings linking the components of the metabolic syndrome with NAFLD and the progression to nonalcoholic steatohepatitis (NASH) will be reviewed; in particular, the role of visceral adipose tissue, insulin resistance, and adipocytokines in the exacerbation of these conditions. While no therapy has been proven effective for treating NAFLD/NASH, common recommendations will be discussed.
Fructose and cardiometabolic disorders: the controversy will, and must, continue
Wiernsperger, Nicolas;Geloen, Alain;Rapin, Jean-Robert;
Clinics , 2010, DOI: 10.1590/S1807-59322010000700013
Abstract: the present review updates the current knowledge on the question of whether high fructose consumption is harmful or not and details new findings which further pushes this old debate. due to large differences in its metabolic handling when compared to glucose, fructose was indeed suggested to be beneficial for the diet of diabetic patients. however its growing industrial use as a sweetener, especially in soft drinks, has focused attention on its potential harmfulness, possibly leading to dyslipidemia, obesity, insulin resistance/metabolic syndrome and even diabetes. many new data have been generated over the last years, confirming the lipogenic effect of fructose as well as risks of vascular dysfunction and hypertension. fructose exerts various direct effects in the liver, affecting both hepatocytes and kupffer cells and resulting in non-alcoholic steatotic hepatitis, a well known precursor of the metabolic syndrome. hepatic metabolic abnormalities underlie indirect peripheral metabolic and vascular disturbances, for which uric acid is possibly the culprit. nevertheless major caveats exist (species, gender, source of fructose, study protocols) which are detailed in this review and presently prevent any firm conclusion. new studies taking into account these confounding factors should be undertaken in order to ascertain whether or not high fructose diet is harmful.
Non-alcoholic fatty liver disease: An early mediator predicting metabolic syndrome in obese children?
Jun-Fen Fu,Hong-Bo Shi,Li-Rui Liu,Ping Jiang
World Journal of Gastroenterology , 2011,
Abstract: AIM: To investigate if non-alcoholic fatty liver disease (NAFLD) is an early mediator for prediction of metabolic syndrome, and if liver B-ultrasound can be used for its diagnosis.METHODS: We classified 861 obese children (6-16 years old) into three subgroups: group 0 (normal liver in ultrasound and normal transaminases); group 1 (fatty liver in ultrasound and normal transaminases); and group 2 (fatty liver in ultrasound and elevated transaminases). We measured the body mass index, waist and hip circumference, blood pressure, fasting blood glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), whole-body insulin sensitivity index (WBISI), lipid profile and transaminases in all the participants. The risk of developing metabolic syndrome (MS) was assessed according to the degree of liver fatty infiltration based on the B-ultrasound examination.RESULTS: Among the 861 obese children, 587 (68.18%) were classified as having NAFLD, and 221 (25.67%) as having MS. The prevalence of MS in NAFLD children (groups 1 and 2) was 37.64% (221/587), which was much higher than that in non-NAFLD group (group 0, 12.04%) (P < 0.01). There were significantly higher incidences concerning every component of MS in group 2 compared with group 0 (P < 0.05). The incidence of NAFLD in MS patients was 84.61% (187/221), which was significantly higher than that of hypertension (57.46%, 127/221) and glucose metabolic anomalies (22.62%, 50/221), and almost equal to the prevalence of dyslipidemia (89.14%, 197/221). Based on the B-ultrasound scales, the presence of moderate and severe liver fatty infiltration carried a high risk of hypertension [odds ratio (OR): 2.18, 95% confidence interval (95% CI): 1.27-3.75], dyslipidemia (OR: 7.99, 95% CI: 4.34-14.73), impaired fasting glucose (OR: 3.65, 95% CI: 1.04-12.85), and whole MS (OR: 3.77; 95% CI: 1.90-7.47, P < 0.01). The state of insulin resistance (calculated by HOMA-IR and WBISI) deteriorated as the degree of fatty infiltration increased.CONCLUSION: NAFLD is not only a liver disease, but also an early mediator that reflects metabolic disorder, and liver B-ultrasound can be a useful tool for MS screening.
Exercise counteracts fatty liver disease in rats fed on fructose-rich diet
José D Botezelli, Rodrigo F Mora, Rodrigo A Dalia, Leandro P Moura, Lucieli T Cambri, Ana C Ghezzi, Fabrício A Voltarelli, Maria AR Mello
Lipids in Health and Disease , 2010, DOI: 10.1186/1476-511x-9-116
Abstract: We separated 48 Wistar rats into two groups according to diet: a control group (balanced diet AIN-93 G) and a fructose-rich diet group (60% fructose). The animals were tested for maximal lactate-steady state (MLSS) in order to identify the aerobic/anaerobic metabolic transition during swimming exercises at 28 and 90 days of age. One third of the animals of each group were submitted to swimming training at an intensity equivalent to the individual MLSS for 1 hours/day, 5 days/week from 28 to 120 days (early protocol). Another third were submitted to the training from 90 to 120 days (late protocol), and the others remained sedentary. The main assays performed included an insulin tolerance test (ITT) and tests of serum alanine aminotransferase [ALT] and aspartate aminotransferase [AST] activities, serum triglyceride concentrations [TG] and liver total lipid concentrations.The fructose-fed rats showed decreased insulin sensitivity, and the late-exercise training protocol counteracted this alteration. There was no difference between the groups in levels of serum ALT, whereas AST and liver lipids increased in the fructose-fed sedentary group when compared with the other groups. Serum triglycerides concentrations were higher in the fructose-fed trained groups when compared with the corresponding control group.The late-training protocol was effective in restoring insulin sensitivity to acceptable standards. Considering the markers here evaluated, both training protocols were successful in preventing the emergence of non-alcoholic fatty liver status disease.Metabolic syndrome, also known as syndrome X or insulin resistance syndrome, encompasses a spectrum of disorders, one of the most important of which is impaired glucose tolerance. These disorders include insulin resistance (with or without type 2 diabetes mellitus), hypertension, obesity, dyslipidemia and endothelial dysfunction [1]. The World Health Organization offers a definition of metabolic syndrome that includes any
Role of Innate Immune Response in Non-Alcoholic Fatty Liver Disease: Metabolic Complications and Therapeutic Tools  [PDF]
Rosaria Meli,Giuseppina Mattace Raso,Antonio Calignano
Frontiers in Immunology , 2014, DOI: 10.3389/fimmu.2014.00177
Abstract: Non-alcoholic fatty liver disease (NAFLD) is currently the most common liver disease worldwide, both in adults and children. It is characterized by an aberrant lipid storage in hepatocytes, named hepatic steatosis. Simple steatosis remains a benign process in most affected patients, while some of them develop superimposed necroinflammatory activity with a non-specific inflammatory infiltrate and a progression to non-alcoholic steatohepatitis with or without fibrosis. Deep similarity and interconnections between innate immune cells and those of liver parenchyma have been highlighted and showed to play a key role in the development of chronic liver disease. The liver can be considered as an “immune organ” because it hosts non-lymphoid cells, such as macrophage Kupffer cells, stellate and dendritic cells, and lymphoid cells. Many of these cells are components of the classic innate immune system, enabling the liver to play a major role in response to pathogens. Although the liver provides a “tolerogenic” environment, aberrant activation of innate immune signaling may trigger “harmful” inflammation that contributes to tissue injury, fibrosis, and carcinogenesis. Pathogen recognition receptors, such as toll-like receptors and nucleotide oligomerization domain-like receptors, are responsible for the recognition of immunogenic signals, and represent the major conduit for sensing hepatic and non-hepatic noxious stimuli. A pivotal role in liver inflammation is also played by cytokines, which can initiate or have a part in immune response, triggering hepatic intracellular signaling pathways. The sum of inflammatory signals and deranged substrate handling induce most of the metabolic alteration traits: insulin resistance, obesity, diabetes, hyperlipidemia, and their compounded combined effects. In this review, we discuss the relevant role of innate immune cell activation in relation to NAFLD, the metabolic complications associated to this pathology, and the possible pharmacological tools.
Non-alcoholic fatty liver disease and metabolic syndrome in Brazilian middle-aged and older adults
Karnikowski, Mauro;Córdova, Cláudio;Oliveira, Ricardo Jacó de;Karnikowski, Marg? Gomes de Oliveira;Nóbrega, Otávio de Tolêdo;
Sao Paulo Medical Journal , 2007, DOI: 10.1590/S1516-31802007000600006
Abstract: context and objectives: non-alcoholic fatty liver disease (nafld) is a complex clinicopathological entity characterized by diffuse or focal fat accumulation in the hepatic parenchyma of patients who deny abusive alcohol consumption. this study aimed to assess idiopathic nafld in community-dwelling, middle-aged and older adults living in the brazilian federal district. associations between nafld and components of metabolic syndrome and the whole syndrome were investigated. design and settings: this was a cross-sectional study on 139 subjects aged 55 years or older. methods: nafld was diagnosed by means of clinical procedures, to exclude subjects with signs of liver disorders, abusive alcohol consumption and influence from hepatotoxic drugs. phenotypes were graded based on ultrasound examination. metabolic syndrome was defined using the ncep atp iii criteria. laboratory tests were performed to assist clinical examinations and define the syndrome. results nafld was present in 35.2% of the subjects. taken together, the two most intense phenotypes correlated with increased serum fasting glucose, triglyceride and vldl cholesterol levels. metabolic syndrome was diagnosed in 25.9% of the sample. in addition to associating nafld with specific traits of metabolic syndrome, non-parametric analysis confirmed the existence of a relationship (p < 0.05) between the steatotic manifestation and the syndromic condition. conclusion: compared with the literature, this study reveals greater frequency of idiopathic nafld among brazilian middle-aged and older adults than is described elsewhere. the findings also suggest that impaired glycemic metabolism coupled with increased fat delivery and/or sustained endogenous biosynthesis is the most likely physiopathogenic mechanisms underlying the onset of nafld in this population.
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