A. Obesity is defined as a medical condition of excess body fat has accumulated overtime, while overweight is a condition of excess body weight relatively to the height. According to the Body Mass Index(BMI), a BMI between 25 to 29.9 is considered over weight, while a BMI of over 30 is an indication of obesity. According to the statistic, 68% of American population are either overweight or obese.
B. How to calculate your BMI index
BMI= weight (kg)/ height (m2)
C. Non-alcoholic Fatty Liver Disease is defined as a condition of the fatty liver diseases as a result of accumulated of fat in the liver, not caused by abusive alcohol consumption. According to the study of "Nonalcoholic Fatty Liver Disease An Underrecognized Cause of Cryptogenic Cirrhosis" by Jeanne M. Clark, MD, MPH, Anna Mae Diehl, MD, posted in The Journals of the American Medical Association, researchers indicated in abstract that Cryptogenic cirrhosis is a common cause of liver-related morbidity and mortality in the United States. Nonalcoholic fatty liver disease (NAFLD) is now recognized as the most common cause of cryptogenic cirrhosis.
D. How Obesity associates with Non-alcoholic Fatty Liver Disease
1, In atudy of "A new risk factor for the development of non-alcoholic fatty liver disease: HLA complex genes" by Celıkbılek M, Selçuk H, Yilmaz U., posted in PubMed, researchers indicated that To reduce the influence of possible confounding factors, we excluded diseases known to be associated with non-alcoholic fatty liver disease like obesity, diabetes mellitus, coronary artery disease, hyperlipidemia, and metabolic syndrome. Non-alcoholic fatty liver disease was diagnosed in 66 individuals (33 male, median age: 53.8 [range, 32-77 years]) by means of ultrasonography data, and 50 individuals, whose ultrasonography data did not show hepatosteatosis, comprised the control group (20 male, median age: 44.6 [range, 26-71 years]). Results: Human leukocyte antigen-B65 (28.8% vs 0%, p<0.001) and DQ5 (40.7% vs 16.1%, p<0.05) were found to be expressed significantly more in non-alcoholic fatty liver disease compared with controls. Serum alanine aminotransferase (27.1 IU/L vs 20 IU/L, p<0.05) was significantly higher in the study group. Conclusions: Our preliminary study suggests that human leukocyte antigen plays a role in the pathogenesis of non-alcoholic fatty liver disease; however, more studies are needed to clarify these data.
2. In a study of "Non-alcoholic steatohepatitis in children" by Nanda K., posted in PubMed, researchers indicated that Obesity has emerged as a significant new health problem in the pediatric population. Non-alcoholic steatohepatitis (NASH),..., A system of grading depending on degree of steatosis and/or inflammation and staging depending on the extent of fibrosis has also been proposed. Although there is no consensus for the treatment for NASH, effort needs to be made to prevent development of fibrosis, which results in cirrhosis and portal hypertension. Slow, consistent weight loss has been shown to be effective in childhood NAFLD, based on improvement of serum aminotransferases or liver sonogram. A low glycemic index diet has been shown to be more effective than a low fat diet in lowering BMI.
3. According to the study of "[Non-alcoholic fatty liver disease--new view]" [Article in Polish], by Raszeja-Wyszomirska J, Lawniczak M, Marlicz W, Miezyńska-Kurtycz J, Milkiewicz P., posted in PubMed, researchers found that The most important therapeutic measure is increasing insulin sensitivity by an attempt to change a lifestyle mostly by dieting and physical activity in order to loose weight. The most used agent is metformin, the others are under controlled trials or their effectiveness is low. NASH is not a common indication for liver transplantation because of the older age distribution of patients and high prevalence of comorbidity, related to metabolic syndrome. Recurence of NASH in the grafted liver is also a relatively frequent complication.
4. In a study of "Serotonin-receptor-3-antagonists improve obesity-associated fatty liver disease in mice" by Haub S, Ritze Y, Ladel I, Saum K, Hubert A, Spruss A, Trautwein C, Bischoff SC., posted in PubMed, researchers found that Palonosetron had similar effects as tropisetron regarding the reduction of liver fat and other parameters. Conclusions: Tropisetron and palonosetron are effective in attenuating NAFLD in a genetic mouse model of obesity. The effect likely involves the intestinal nervous system, resulting in a reduction of endotoxin influx into the liver and subsequently of liver inflammation and fat accumulation.
5. According to the study of "Increased intestinal permeability in obese mice: new evidence in the pathogenesis of nonalcoholic steatohepatitis" by Brun P, Castagliuolo I, Di Leo V, Buda A, Pinzani M, Palù G, Martines D., posted in PubMed, researchers found that HSCs isolated from ob/ob and db/db mice showed higher membrane CD14 mRNA levels and more pronounced lipopolysaccharide-induced proinflammatory and fibrogenic responses than HSCs from lean animals. In conclusion, genetically obese mice display enhanced intestinal permeability leading to increased portal endotoxemia that makes HSCs more sensitive to bacterial endotoxins. We suggest that in metabolic syndrome, patients may likewise have a greater intestinal mucosa permeability and increased lipopolysaccharide levels in portal blood that can contribute to the liver inflammatory damage.
6. in the abstract of study of "Animal models of steatohepatitis" by Koteish A, Mae Diehl A., posted in PubMed, researchers indicated that Animal models of hepatic steatosis and steatohepatitis have improved our understanding of the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Three models, genetically obese ob/ob mice, lipoatrophic mice and normal rats fed choline-deficient, methionine-restricted diets, have been particularly informative. All support the multiple 'hit' hypothesis for NAFLD pathogenesis that suggests that fatty livers are unusually vulnerable to oxidants and develop steatohepatitis when secondary insults generate sufficient oxidants to cause liver cell death and inflammation.
7. Etc.
E. Treatments of Obesity and Non-alcoholic Fatty Liver Disease
1. In a study of"Review article: the metabolic syndrome and non-alcoholic fatty liver disease" by Loria P, Lonardo A, Carulli L, Verrone AM, Ricchi M, Lombardini S, Rudilosso A, Ballestri S, Carulli N., posted in PubMed, researchers stated that Metabolic syndrome represents a common risk factor for premature cardiovascular disease and cancer whose core cluster includes diabetes, hypertension, dyslipidaemia and obesity..... and concluded that Studies are needed to highlight the grey areas in this topic. Issues to be addressed include: diagnostic criteria for metabolic syndrome; nomenclature of non-alcoholic fatty liver disease; enlargement of the clinical spectrum and characterization of the prognosis of insulin resistance-related diseases; evaluation of the most specific clinical predictors of metabolic syndrome/non-alcoholic fatty liver disease and assessment of their variability over the time; characterization of the importance of new risk factors for metabolic syndrome with regard to the development and progression of non-alcoholic fatty liver disease.
2. According to the study of "Non-alcoholic fatty liver disease: further expression of the metabolic syndrome" by Tarantino G, Saldalamacchia G, Conca P, Arena A., posted in PubMed, researchers filed in abstract that Non-alcoholic fatty liver disease has been associated with metabolic disorders, including central obesity, dyslipidemia, hypertension and hyperglycemia. Metabolic syndrome, obesity, and insulin resistance are major risk factors in the pathogenesis of non-alcoholic fatty liver disease. Non-alcoholic fatty liver disease refers to a wide spectrum of liver damage, ranging from simple steatosis to non-alcoholic steatohepatitis, advanced fibrosis and cirrhosis.
3. According to the study of "Non-alcoholic steatohepatitis: an overview" by Shifflet A, Wu GY., posted in PubMed, researchers filed in abstract that Non-alcoholic fatty liver disease (NAFLD) includes a broad spectrum of fat-induced liver injury, ranging from mild steatosis to cirrhosis and liver failure. The presence of obesity and insulin resistance is strongly associated with non-alcoholic fatty liver and a greater risk of advanced disease. We present here a review of the mechanisms involved in the pathogenesis of NAFLD, advances in the diagnosis, and options for treatment.
4. Etc.
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