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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonalcoholic fatty liver disease (NAFLD), one of the most common forms of chronic liver disease, is closely associated with obesity and insulin resistance. Recent studies suggest that apelin, a newly described adipokine, is associated with hyperinsulinemia and inflammation. The aim of the study was to investigate plasma apelin concentrations in biopsy-proven NAFLD patients who had no metabolic confounders and also to search for the association of apelin with adiponectin, body mass index (BMI), and insulin sensitivity. Fifty male patients with NAFLD and 30 healthy male controls were enrolled. Apelin was measured along with BMI, lipids, glucose, insulin, adiponectin, and homeostasis model assessment (HOMA) of insulin resistance indexes. Plasma apelin levels were significantly higher and adiponectin levels were lower in NAFLD patients when compared with the controls (P < .001 and P = .013, respectively). In multivariate analysis adjusted for BMI and HOMA indexes, the differences in apelin and adiponectin disappeared in the 2 groups (P = .3 and P = .1, respectively). In addition, apelin levels were positively correlated with BMI (r = 0.29, P = .05) and HOMA indexes (r = 0.4, P = .008) in subjects with NAFLD. The results of this preliminary study suggest that plasma apelin levels are not altered in nondiabetic and normotensive male subjects with NAFLD.
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PMID:Plasma apelin levels in subjects with nonalcoholic fatty liver disease. 2004 53

Nonalcoholic fatty liver disease (NAFLD) is recognized as the leading cause of chronic liver disease in adults and children. NAFLD encompasses a spectrum of liver injuries ranging from steatosis to steatohepatitis with or without fibrosis. Fibrosis may progress to cirrhosis and complications including hepatocellular carcinoma. Histologic findings represent the complexity of pathophysiology. NAFLD is closely associated with obesity and is most closely linked with insulin resistance; the current Western diet, high in saturated fats and fructose, plays a significant role. There are several mechanisms by which excess triglycerides are acquired and accumulate in hepatocytes. Formation of steatotic droplets may be disordered in NAFLD. Visceral adipose tissue dysfunction in obesity and insulin resistance results in aberrant cytokine expression; many cytokines have a role in liver injury in NAFLD. Cellular stress and immune reactions, as well as the endocannabinoid system, have been implicated in animal models and in some human studies.
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PMID:Nonalcoholic fatty liver disease: pathology and pathogenesis. 2007 19

Obesity is associated with a spectrum of chronic liver disease. Because obesity increases the risk for advanced forms of liver disease (ie, cirrhosis and liver cancer), the obesity epidemic is emerging as a major factor underlying the burden of liver disease in the United States and many other countries. This article reviews mechanisms that mediate the pathogenesis of obesity-related liver disease, summarizes clinical evidence that demonstrates obesity-related liver disease can be life-threatening, and discusses whether or not treatments for obesity or related comorbidities impact liver disease outcomes.
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PMID:Hepatic complications of obesity. 2020 79

With rising obesity rates, nonalcoholic fatty liver disease is predicted to become the main cause of chronic liver disease in the next decades. Rising obesity prevalence is attributed to changes in dietary habits with increased consumption of palatable junk foods, but maternal malnutrition also contributes to obesity in progeny. This study examines whether a maternal junk food diet predisposes offspring to nonalcoholic fatty liver disease. The 144 rat offspring were fed either a balanced chow diet alone or with palatable junk foods rich in energy, fat, sugar, and/or salt during gestation, lactation, and/or after weaning up to the end of adolescence. Offspring fed junk food throughout the study exhibited exacerbated hepatic steatosis, hepatocyte ballooning, and oxidative stress response compared with offspring given free access to junk food after weaning only. These offspring also displayed sex differences in their hepatic molecular metabolic adaptation to diet-induced obesity with increased expression of genes associated with insulin sensitivity, de novo lipogenesis, lipid oxidation, and antiinflammatory properties in males, whereas the gene expression profile in females was indicative of hepatic insulin resistance. Hepatic inflammation and fibrosis were not detected indicating that offspring had not developed severe steatohepatitis by the end of adolescence. Hepatic steatosis and increased oxidative stress response also occurred in offspring born to junk food-fed mothers switched to a balanced chow diet from weaning, highlighting a degree of irreversibility. This study shows that a maternal junk food diet in pregnancy and lactation contributes to the development of nonalcoholic fatty liver disease in offspring.
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PMID:A maternal "junk food" diet in pregnancy and lactation promotes nonalcoholic Fatty liver disease in rat offspring. 2020 31

Nonalcoholic steatohepatitis (NASH) may account for many cases of cryptogenic cirrhosis. If so, then steatosis might recur after liver transplantation. Two thousand fifty-two patients underwent primary liver transplantation for chronic liver disease between 1986 and 2004. Serial liver biopsy samples were assessed for steatosis and fibrosis. Two hundred fifty-seven patients (12%) had a pretransplant diagnosis of cryptogenic cirrhosis (239) or NASH (18). Fatty liver developed in 31% and was more common when the pretransplant diagnosis was NASH (45% at 5 years versus 23% for cryptogenic cirrhosis, P = 0.007). NASH developed in only 4% and occurred exclusively when steatosis had already occurred. Steatosis after liver transplantation was associated with the baseline body weight and body mass index by univariate analyses, but no pretransplant or posttransplant characteristic independently predicted steatosis after liver transplantation because obesity was so common in all groups. Five percent and 10% developed bridging fibrosis or cirrhosis after 5 and 10 years, respectively, and this was more common after NASH (31%) than in those who developed steatosis alone (6%) or had no fat (3%, P = 0.002). One-, 5-, and 10-year survival was the same in patients who underwent transplantation for cryptogenic cirrhosis or NASH (86%, 71%, and 56%) and in patients who underwent transplantation for other indications (86%, 71%, and 53%; not significant), but death was more often due to cardiovascular disease and less likely from recurrent liver disease. In conclusion, fatty liver is common after liver transplantation for cryptogenic cirrhosis or NASH but is twice as common in the latter group; this suggests that some cryptogenic cirrhosis, but perhaps not all, is caused by NASH. Posttransplant NASH is unusual, and steatosis appears to be a prerequisite. Advanced fibrosis is uncommon, and survival is the same as that of patients who undergo transplantation for other causes.
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PMID:Nonalcoholic fatty liver disease after liver transplantation for cryptogenic cirrhosis or nonalcoholic fatty liver disease. 2037 52

The Baby Boomer generation is composed of 78 million Americans who are just beginning to reach their retirement years. Most Boomers have at least one chronic health problem, and these significantly increase the expense of providing medical care. Liver disease is the 12th most common cause of death in the United States, representing a relatively small portion of overall healthcare costs compared with cardiovascular disease and malignancy. Nonetheless, hepatitis C and fatty liver disease are more common in the Boomers and may play a more dominant role as they age. As a consequence, primary liver cancer is likely to become more prevalent. As with most chronic illnesses, prevention rather than disease management is likely to have the greatest impact. For those already afflicted by chronic liver disease, recognition and treatment can reduce the incidence of late complications, as was clearly demonstrated with chronic hepatitis B and C. Perhaps obesity is the greatest threat to our future health, and fatty liver disease, although likely preventable, will probably become the disease that fills the waiting rooms of future hepatologists.
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PMID:The healthcare burden imposed by liver disease in aging Baby Boomers. 2042 78

Hepatocellular carcinoma (HCC) is a common and deadly malignancy that is increasing in incidence in developed countries. The emergence of hepatitis C virus (HCV) accounts for about half of this increase in HCC, although the etiology of HCC in 15%-50% of new HCC cases remains unclear. The most common form of chronic liver disease in developed countries is nonalcoholic fatty liver disease (NAFLD), which encompasses a broad spectrum of histopathology. The prevalence of NAFLD, including the more aggressive nonalcoholic steatohepatitis (NASH), is increasing with the growing epidemics of diabetes and obesity. NASH can progress to cirrhosis and its related complications. Growing evidence suggests that NASH accounts for a large proportion of idiopathic or cryptogenic cirrhosis, which is associated with the typical risk factors for NASH. HCC is a rare, although important complication of NAFLD. Diabetes and obesity have been established as independent risk factors for the development of HCC. New evidence also suggests that hepatic iron deposition increases the risk of HCC in NASH-derived cirrhosis. Multiple case reports and case reviews of HCC in the setting of NASH support the associations of diabetes and obesity with the risk of HCC, as well as suggest age and advanced fibrosis as significant risks. Insulin resistance and its subsequent inflammatory cascade that is associated with the development of NASH appear to play a significant role in the carcinogenesis of HCC. The complications of NASH, including cirrhosis and HCC, are expected to increase with the growing epidemic of diabetes and obesity.
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PMID:Nonalcoholic fatty liver disease and hepatocellular carcinoma: a weighty connection. 2043 59

Lifestyle diseases characterize those diseases whose occurrence is primarily based on the daily habits of people and are a result of an inappropriate relationship of people with their environment. The main factors contributing to lifestyle diseases include bad food habits, physical inactivity, wrong body posture, and disturbed biological clock. A report, jointly prepared by the World Health Organization (WHO) and the World Economic Forum, says India will incur an accumulated loss of $236.6 billion by 2015 on account of unhealthy lifestyles and faulty diet. According to the report, 60% of all deaths worldwide in 2005 (35 million) resulted from noncommunicable diseases and accounted for 44% of premature deaths. What's worse, around 80% of these deaths will occur in low and middle-income countries like India which are also crippled by an ever increasing burden of infectious diseases, poor maternal and perinatal conditions and nutritional deficiencies. According to a survey conducted by the Associated Chamber of Commerce and Industry (ASSOC-HAM), 68% of working women in the age bracket of 21-52 years were found to be afflicted with lifestyle ailments such as obesity, depression, chronic backache, diabetes and hypertension. The study 'Preventive Healthcare and Corporate Female Workforce' also said that long hours and working under strict deadlines cause up to 75% of working women to suffer from depression or general anxiety disorder, compared to women with lesser levels of psychological demand at work. The study cited scientific evidence that healthy diet and adequate physical activity - at least 30 minutes of moderate activity at least five days a week - helped prevent NCDs. In India, 10% of adults suffer from hypertension while the country is home to 25-30 million diabetics. Three out of every 1,000 people suffer a stroke. The number of deaths due to heart attack is projected to increase from 1.2 million to 2 million in 2010. The diet [or lifestyle] of different populations might partly determine their rates of cancer, and the basis for this hypothesis was strengthened by results of studies showing that people who migrate from one country to another generally acquire the cancer rates of the new host country, suggesting that environmental [or lifestyle factors] rather than genetic factors are the key determinants of the international variation in cancer rates. Some of the common diseases encountered because of occupational lifestyle are Alzheimer's disease, arteriosclerosis, cancer, chronic liver disease/cirrhosis, chronic obstructive pulmonary disease (COPD), diabetes, hypertension, heart disease, nephritis/CRF, and stroke. Occupational lifestyle diseases include those caused by the factors present in the vicinity like heat, sound, dust, fumes, smoke, cold, and other pollutants. These factors are responsible for allergy, respiratory and hearing problems, and heat or cold shock. So, A healthy lifestyle must be adopted to combat these diseases with a proper balanced diet, physical activity and by giving due respect to biological clock. Kids spending too much time slouched in front of the TV or PCs, should be encourage to find a physical sport or activity they enjoy. Fun exercises should be encouraged into family outings. A pizza-and-video evening should be replaced for a hike and picnic. Kids who do participate in sport, especially at a high competitive level, can find the pressure to succeed very stressful. To decrease the ailments caused by occupational postures, one should avoid long sitting hours and should take frequent breaks for stretching or for other works involving physical movements.
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PMID:Occupational lifestyle diseases: An emerging issue. 2044 27

Over the last few years, the paradigm in hepatology has changed from focusing on a single liver disease to considering concurrent diseases, in particular obesity and related metabolic factors. Obesity has reached epidemic proportions globally and is associated with insulin resistance, steatosis and a low-grade systemic inflammatory state. These metabolic factors have a synergistic role in the natural history and treatment outcomes related to chronic liver disease. This is characterized best in chronic hepatitis C where steatosis and insulin resistance are caused by viral and metabolic effects. Non-alcoholic fatty liver disease and related metabolic abnormalities also exacerbate other diseases, such as alcoholic liver disease and haemochromatosis. In addition, there is growing evidence linking obesity and type 2 diabetes with hepatocellular carcinoma in subjects with chronic viral hepatitis. The pathogenesis of co-morbid disease may be related to increased oxidative stress, inflammatory injury and cell death, along with altered hepatocyte regeneration and repair. Hyperinsulinaemia and other metabolic factors may also have a direct role in the progression of liver injury. Data indicate that weight reduction improves steatosis and inflammation in patients with chronic hepatitis C. This has important clinical and therapeutic implications and suggests that obesity should be actively addressed in the management of patients with other chronic liver diseases.
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PMID:Metabolic factors and non-alcoholic fatty liver disease as co-factors in other liver diseases. 2046 Sep 9

Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease associated with insulin resistance, oxidative stress, and inflammation. Evidence indicates that chromium has a role in the regulation of glucose and lipid metabolism and may improve insulin sensitivity. In this study, we report that chromium supplementation has a beneficial effect against NAFLD. We found that KK/HlJ mice developed obesity and progressed to NAFLD after feeding with high-fat diet for 8weeks. High-fat-fed KK/HlJ mice showed hepatocyte injury and hepatic triglyceride accumulation, which was accompanied by insulin resistance, oxidative stress, and inflammation. Chromium supplementation prevented progression of NAFLD and the beneficial effects were accompanied by reduction of hepatic triglyceride accumulation, elevation of hepatic lipid catabolic enzyme, improvement of glucose and lipid metabolism, suppression of inflammation as well as resolution of oxidative stress, probably through enhancement of insulin signaling. Our findings suggest that chromium could serve as a hepatoprotective agent against NAFLD.
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PMID:Chromium attenuates high-fat diet-induced nonalcoholic fatty liver disease in KK/HlJ mice. 2051 51


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