scholarly journals Rationale and Design of RNAFH Study: Effect of Rosuvastatin (10 mg/d) on Nonalcoholic Fatty Liver in Metabolic Syndrome Patients without Overt Diabetes Evaluated by 1H-Magnetic Resonance Spectroscopy

2016 ◽  
Vol 2016 ◽  
pp. 1-6
Author(s):  
Fan Ping ◽  
Xuan Wang ◽  
Jing Yang ◽  
Mei-cen Zhou ◽  
Wei Li ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Renal Function ◽  
Liver Disease ◽  
Glucose Metabolism ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Overt Diabetes ◽  
Lipid Parameters

Objective. The RNAFH study (effect of rosuvastatin on nonalcoholic fatty liver disease in metabolic syndrome patients without overt diabetes evaluated by 1H-MRS) is a prospective randomized, single-center, open-label trail designed to assess the effect of rosuvastatin on the intrahepatocellular lipid (IHCL) level of nonalcoholic fatty liver disease (NAFLD). Methods. 40 NAFLD patients meeting inclusion and exclusion criteria with metabolic syndrome (MS) but without overt diabetes mellitus will be included. Patients will be randomized to 52-week treatment with either rosuvastatin (10 mg/d) or blank control. The primary end point is IHCL evaluated by 1H-MRS, which was considered to be the most accurate noninvasive method for the evaluation of NAFLD. Secondary end points include homeostasis model assessment of insulin resistance (HOMA-IR) index on behalf of insulin resistance level and lipid parameters. Safety indicators will be monitored such as liver function, renal function, muscle stability, and glucose metabolism. The aims of the present study are noteworthy in respect that (1) IHCL is a quantitative indicator for evaluating the degree of fatty liver disease and 1H-MRS is a noninvasive technique to provide this specific index precisely, (2) meanwhile the HOMA-IR index and lipid parameters will be monitored, and (3) the safety of rosuvastatin treatment for 52 weeks will be evaluated including glucose metabolism, muscle stability, liver function, and renal function.

scholarly journals Insulin Resistance, the Metabolic Syndrome, and Nonalcoholic Fatty Liver Disease

2005 ◽  
Vol 90 (3) ◽  
pp. 1578-1582 ◽  
Author(s):  
F. Angelico ◽  
M. Del Ben ◽  
R. Conti ◽  
S. Francioso ◽  
K. Feole ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Oral Glucose ◽  
Nonalcoholic Fatty Liver ◽  
Insulin Resistant ◽  
The Metabolic Syndrome

Background/Aims: An association of nonalcoholic fatty liver disease with the insulin-resistant metabolic syndrome has been suggested. The aim of the study was to assess the association of fatty liver to different degrees of insulin resistance and secretion. Methods and Results: The study was performed in 308 alcohol- and virus-negative consecutive patients attending a metabolic clinic, who underwent a complete clinical and biochemical work-up including oral glucose tolerance test and routine liver ultrasonography. Steatosis was graded as absent/mild, moderate, and severe. In nondiabetic subjects, a progressive (P < 0.05) increase in mean homeostasis model of insulin resistance was recorded from the group without steatosis to the groups with mild/moderate and severe steatosis. Severe steatosis was associated with the clustering of the five clinical and biochemical features proposed for the clinical diagnosis of the metabolic syndrome. Subjects with the metabolic syndrome with a more pronounced insulin resistance had a higher prevalence of severe steatosis (P < 0.01) compared with those with homeostasis model of insulin resistance below the median. Conclusions: The findings stress the heterogeneous presentation of patients with the metabolic syndrome when the diagnosis is based on the broad Adult Treatment Panel III clinical criteria and demonstrate that those who are more insulin resistant have a higher prevalence of severe steatosis.

scholarly journals Role of the endocrine system in the pathogenesis of non-alcoholic fatty liver disease

2009 ◽  
Vol 150 (48) ◽  
pp. 2173-2181 ◽  
Author(s):  
Krisztina Hagymási ◽  
Péter Reismann ◽  
Károly Rácz ◽  
Zsolt Tulassay
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Endocrine System ◽  
Hormone Deficiency ◽  
Alcoholic Fatty Liver ◽  
Nonalcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

The most frequent liver disorder in metabolic syndrome is the nonalcoholic fatty liver disease. Its pathogenesis is a complex, multifactorial process, characterized by insulin resistance and involvement of the endocrine system. Hypothyroidism may lead to nonalcoholic steatohepatitis via hyperlipidemia and obesity. Adult patients with growth hormone deficiency have a metabolic syndrome-like phenotype with obesity and many characteristic metabolic alterations. The chronic activation of the hypothalamic-pituitary-adrenal axis results in metabolic syndrome as well. Cushing’s syndrome has also features of metabolic syndrome. Mild elevation of transaminase activities is commonly seen in patients with adrenal failure. Non-alcoholic steatosis is twice as common in postmenopusal as in premenopausal women and hormonal replacement therapy decreases the risk of steatosis. Insulin resistance, diabetes mellitus type 2, sleeping apnoe syndrome, cardiovascular disorders and non-alcoholic fatty liver disease are more frequent in polycystic ovary syndrome. Hypoandrogenism in males and hyperandrogenism in females may lead to fatty liver via obesity and insulin resistance. Adipokines (leptin, acylation stimulating protein, adiponectin) have a potential role in the pathogenesis of nonalcoholic fatty liver. The alterations of endocrine system must be considered in the background of cryptogenic liver diseases. The endocrine perspective may help the therapeutic approaches in the future.

scholarly journals Nonalcoholic Fatty Liver Disease Relationship with Metabolic Syndrome in Class III Obesity Individuals

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
A. Cordeiro ◽  
S. E. Pereira ◽  
C. J. Saboya ◽  
A. Ramalho
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Blood Pressure Measurement ◽  
Model Assessment ◽  
Class Iii ◽  
Nonalcoholic Fatty Liver

Introduction. Obesity is represented mainly by abdominal obesity and insulin resistance (IR), both present in most individuals diagnosed with metabolic syndrome (MS). IR is the key risk factor in the pathogenesis of nonalcoholic fatty liver disease (NAFLD).Objective. To relate NAFLD to MS in class III obese individuals.Methodology. A descriptive cross-sectional study with class III obese individuals, aged ≥ 20–60 years. Blood pressure measurement, weight, height, body mass index (BMI), waist circumference (WC) and blood glucose, insulin, high-density lipoprotein cholesterol (HDL-c), and triglycerides data were obtained. HOMA-IR (homeostatic model assessment insulin resistance) calculation was carried out with a cutoff value of 2.71 for IR evaluation. The diagnosis of NAFLD was performed by liver biopsy and the diagnosis of MS was performed in accordance with the National Cholesterol Education Program/Adult Treatment Panel III (NCEPATP III).Results. Of the 50 individuals evaluated, 86% were women and BMI means were 45.4 ± 3.6 Kg/m2. The overall individuals had NAFLD, 70% steatosis, and 30% steatohepatitis. The diagnosis of MS occurred in 56% but showed no significant association with NAFLD (P=0.254). Triglycerides (178 ± 65.5 mg/dL) and insulin (28.2 ± 22.6 mcU/mL) mean values were significantly higher in steatohepatitis (P=0.002andP=0.042, resp.) compared to individuals with steatosis. IR was confirmed in 76% and showed a relationship with NAFLD severity.Conclusion. NAFLD was not related to MS; however, MS components, evaluated in isolation, as well as IR, were related to the presence and severity of NAFLD.

scholarly journals Intrauterine Growth Retardation and Nonalcoholic Fatty Liver Disease in Children

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Anna Alisi ◽  
Nadia Panera ◽  
Carlo Agostoni ◽  
Valerio Nobili
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Growth Retardation ◽  
Fatty Liver Disease ◽  
Intrauterine Growth Retardation ◽  
Nonalcoholic Fatty Liver ◽  
Intrauterine Growth

Intrauterine growth retardation (IUGR), the most important cause of perinatal mortality and morbidity, is defined as a foetal growth less than normal for the population, often used as synonym of small for gestational age (SGA). Studies demonstrated the relationships between metabolic syndrome (MS) and birthweight. This study suggested that, in children, adolescents, and adults born SGA, insulin resistance could lead to other metabolic disorders: type 2 diabetes (DM2), dyslipidemia, and nonalcoholic fatty liver disease (NAFLD). NAFLD may evolve to nonalcoholic steatohepatitis (NASH), and it is related to the development of MS. Lifestyle intervention, physical activity, and weight reduction represent the mainstay of NAFLD therapy. In particular, a catch-up growth reduction could decrease the risk to develop MS and NAFLD. In this paper, we outline clinical and experimental evidences of the association between IUGR, metabolic syndrome, insulin resistance, and NAFLD and discuss on a possible management to avoid the risk of MS in adulthood.

scholarly journals Obese Children with Metabolic Syndrome Have 3 Times Higher Risk to Have Nonalcoholic Fatty Liver Disease Compared with Those without Metabolic Syndrome

2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
Dimitrios Papandreou ◽  
Mirey Karavetian ◽  
Zacharoula Karabouta ◽  
Eleni Andreou
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Serum Insulin ◽  
Density Lipoprotein ◽  
Obese Children ◽  
Nonalcoholic Fatty Liver

Background. The aim of this study was to investigate the relationship between metabolic syndrome (MS) and nonalcoholic fatty liver disease (NAFLD) in obese children. One hundred and twenty-five subjects aged 11-12 years old participated in the study.Methods. Anthropometric and biochemical indices were measured, including lipid and liver profile, blood glucose, serum insulin, and liver ultrasound.Results. Forty-four children (58.6%) were found to have MS. Insulin resistance was present in 78 (62.4%) children. Patients with MS were more likely to have NAFLD (P<0.001). Children with NAFLD had significantly higher body mass index, waist circumference, triglycerides, fasting insulin, and lower high-density lipoprotein compared to patients with normal livers (P<0.001). Insulin resistance was significantly higher in children with NAFLD (P<0.001). Obese children presenting with MS were 3.01 (2.87–3.57,P<0.002) times more likely to develop NAFLD compared to those without metabolic syndrome after adjustment of cofounders.Conclusions. Obese children with MS have a higher risk of developing NAFLD. Weight management and early prevention should be the first line of treatment to prevent any possible health issues later on.

scholarly journals Panhypopituitarism due to Absence of the Pituitary Stalk: A Rare Aetiology of Liver Cirrhosis

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Marta Gonzalez Rozas ◽  
Lidia Hernanz Roman ◽  
Diego Gonzalez Gonzalez ◽  
José Luis Pérez-Castrillón
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Cirrhosis ◽  
Liver Disease ◽  
Fatty Liver ◽  
Liver Damage ◽  
Fatty Liver Disease ◽  
Unknown Aetiology ◽  
Nonalcoholic Fatty Liver ◽  
Pituitary Dysfunction

Studies have established a relationship between hypothalamic-pituitary dysfunction and the onset of liver damage, which may occasionally progress to cirrhosis. Patients with hypopituitarism can develop a metabolic syndrome-like phenotype. Insulin resistance is the main pathophysiological axis of metabolic syndrome and is the causal factor in the development of nonalcoholic fatty liver disease (NAFLD). We present the case of a young patient with liver cirrhosis of unknown aetiology that was finally attributed to panhypopituitarism.

scholarly journals The Relationship between Nonalcoholic Fatty Liver Disease and Colorectal Cancer: The Future Challenges and Outcomes of the Metabolic Syndrome

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Said O. Muhidin ◽  
Ahmed A. Magan ◽  
Khalid A. Osman ◽  
Shareef Syed ◽  
Mohamed H. Ahmed
Keyword(s):  
Colorectal Cancer ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Growth Factor ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Increased Risk

Nonalcoholic fatty liver disease (NAFLD) is closely related to insulin resistance, metabolic syndrome, obesity, type 2 diabetes, and dyslipidaemia. Obesity and metabolic syndrome are associated with an increased cancer risk, and recent evidence demonstrated an association between NAFLD and colorectal cancer (CRC). The mechanism of how NAFLD can be associated with increased risk of CRC is not fully understood; however, NAFLD represents a condition of profound insulin resistance and a proinflammatory state. Insulin and insulin-like growth factors may promote the development of CRC through their proliferative and antiapoptotic effects. Patients with NAFLD have reduced expression of adiponectin, an adipokine with anti-inflammatory effects. Importantly, hypoadiponectinemia is associated with an increased risk of CRC. Decreased levels of adiponectin lead to increased insulin levels due to marked insulin resistance and in turn increased insulin growth factor-1 (IGF-1). Insulin binds to IGF-1 receptors and plays an important role in cell proliferation, apoptosis, and increased production of vascular endothelial growth factor, an angiogenic factor that supports cancer growth. Further studies are needed to establish (i) the pathophysiology of NAFLD with colorectal cancer, (ii) the benefit of early screening of CRC in NAFLD patients, and (iii) the impact of treatment of NAFLD in the modulation of the risk of colorectal cancer.

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