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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The surgical treatment of obesity can have adverse effects on bone, but there are few published data on the effects of vertical-banded gastroplasty. Serial measurements of bone mineral density at the lumbar spine and three upper femoral sites, using dual-energy X-ray absorptiometry, and also of biochemical indices of bone and mineral metabolism at intervals up to 2 years after operation were performed in 18 patients with morbid obesity who had vertical-banded gastroplasty. Bone mineral density measurements were also made in age- and sex-matched non-obese controls. Bone density before operation was significantly greater in the obese than in the controls (P < 0.02 at all sites). The obese patients lost weight rapidly after vertical-banded gastroplasty (mean weight loss 29 kg at 1 year, P < 0.001). This was accompanied by a measurable loss of bone density from the trochanter and Ward's triangle sites in the upper femur (P < 0.05), but not from the lumbar spine. Bone density values remained stable over 14 months in the controls. Hydroxyproline excretion increased significantly (P < 0.005), indicating an increase in bone resorption. Alkaline phosphatase levels decreased significantly (P < 0.001), but this probably represents the reversal of hepatic steatosis. There was no evidence of hyperparathyroidism or vitamin D deficiency. In conclusion, vertical-banded gastroplasty causes modest bone density loss from femoral sites, but not the lumbar spine. The difficulties of assessing bone density changes in the obese are discussed.
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PMID:Effects of vertical-banded gastroplasty on bone and mineral metabolism in obese patients. 894 76

We determined the utility of fast gradient echo techniques (modified Dixon method) in the assessment of hepatic fat content. Fast spoiled gradient echo was performed on bovine liver/corn oil homogenates with known fat fractions (FFE) to assess the accuracy of fat quantitation (FFMRI). The pulse sequence was manipulated via alterations in TE (echo time), TR (repetition time), and alpha (flip angle). In vivo studies were then performed using breath-holding maneuvers on normal adult volunteers and subjects at risk to develop hepatic steatosis, with cystic fibrosis or morbid obesity. At out-of-phase, TE, TR, and alpha were 2.1 ms, 7.3 ms, and 30-50 degrees and in-phase TE, TR, and alpha were 4.2 ms, 9.3 ms, and 30-50 degrees; FFMRI correlated well with FFE. An elevated fat fraction was observed in a high percentage of subjects with cystic fibrosis and morbid obesity. Fast gradient echo techniques were used successfully in the assessment of hepatic steatosis. The reduced acquisition times permitted in vivo analysis on adults and children using breath hold maneuvers.
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PMID:Introduction of fast MR imaging in the assessment of hepatic steatosis. 920 75

Sixty to ninety percent of obese subjects show histological abnormalities of the liver. The hepatic lesion can be classified into one of the four following groups: steatosis, steatohepatitis, fibrosis and cirrhosis. The incidence of cirrhosis among patients with fatty liver changes ranges from 1.5% to 8%. The now abandoned surgery procedures performed for the treatment of morbid obesity (jejunoileal bypass) had left a negative experience: the onset of acute hepatic failure in subjects with no previous hepatic disease or the development of cirrhosis within one year of the bypass. Very low formula diets leading to precipitous weight loss in morbidly obese people induce metabolic changes similar to those observed after jejunoileal bypass. We report the case of a morbidly obese patient who had lost 40 kg of weight during the 6 months previous to his hospitalization. He came with signs of hepatic failure. He worsened rapidly and died in a month-time. The hepatic tissue obtained post-mortem showed a non alcoholic steatohepatitic cirrhosis.
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PMID:[Steatohepatic cirrhosis in a morbidly obese patient]. 1059 3

Previous studies suggest that hepatic cytochrome P450 2E1 (CYP2E1) activity is increased in individuals with chronic alcoholism, nonalcoholic steatohepatitis (NASH), and morbid obesity, and may contribute to liver disease. We studied 16 morbidly obese subjects with varying degrees of hepatic steatosis and 16 normal-weight controls. Obese subjects were evaluated at baseline, 6 weeks, and 1 year after gastroplasty, a procedure that leads to weight loss. Hepatic CYP2E1 activity was assessed by determination of the clearance of chlorzoxazone (CLZ), an in vivo CYP2E1-selective probe. Liver biopsy tissue was obtained during surgery for histopathology. Both the total and unbound oral CLZ clearance (Cl(u)/F) was elevated approximately threefold in morbidly obese subjects compared with controls (P <.001). The Cl(u)/F was significantly higher among subjects with steatosis involving >50% of hepatocytes, compared with those with steatosis in < or =50% of hepatocytes (P =.02). At postoperative week 6 and year 1, the median body mass index (BMI) of subjects who underwent gastroplasty decreased by 11% and 33%, total oral CLZ clearance declined by 16% (P <.01) and 46% (P <.05), and Cl(u)/F decreased by 18% (P <.05) and 35% (P =.16), respectively. Moreover, those subjects with a year 1 BMI <30 kg/m(2) exhibited a median Cl(u)/F that was 63% lower (P =.02) than the respective clearance for all other subjects. In conclusion, hepatic CYP2E1 activity is up-regulated in morbidly obese subjects. A positive association between the degree of steatosis and CYP2E1 activity preoperatively and between the extent of obesity and CYP2E1 activity postoperatively, suggests that CYP2E1 induction is related to or caused by hepatic pathology that results from morbid obesity.
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PMID:CYP2E1 activity before and after weight loss in morbidly obese subjects with nonalcoholic fatty liver disease. 1288 87

Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease (NAFLD) that can lead to hepatic fibrosis and cirrhosis. Portal fibrosis in the absence of NASH, called isolated portal fibrosis (IPF), has received less attention and has not been classified as a spectrum of NAFLD. The aims of this study were to determine the prevalence of IPF in subjects undergoing gastric bypass surgery, to identify biochemical variables associated with IPF, and to assess the metabolic syndrome as defined by the AdultTreatment Panel III criteria. We analyzed liver biopsies from 195 morbidly obese subjects after excluding all other causes of liver disease. The prevalence of fatty liver (FL) only, IPF, and NASH was 30.3%, 33.3%, and 36.4%, respectively. Several biochemical parameters significantly trended across the 3 groups, with IPF falling between FL and NASH. Hyperglycemia was the only metabolic parameter associated with NASH (OR, 5.4; 95% CI, 2.4-12; P < .0001) and IPF (OR, 2.8; 95% CI, 1.2-6.5; P = .01). Subjects with diabetes had the greatest risk for NASH (OR, 8; 95% CI, 3.3-19.7; P < .0001) and IPF (OR, 4.3; 95% CI, 1.6-11.6; P = .003). The metabolic syndrome was identified in 78.5% of subjects, and a significant trend for the number of metabolic criteria was observed across the spectrum of FL, IPF, and NASH. In conclusion, a significant subset of morbidly obese individuals has portal fibrosis in the absence of NASH that is associated with glycemic dysregulation. Therefore, IPF should be considered a spectrum of NAFLD that may prelude NASH in morbid obesity.
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PMID:Portal fibrosis and hepatic steatosis in morbidly obese subjects: A spectrum of nonalcoholic fatty liver disease. 1536 53

Despite major advances in understanding monogenic causes of morbid obesity, the complex genetic and environmental etiology of idiopathic metabolic syndrome remains poorly understood. One hypothesis suggests that similarities between the metabolic disease of plasma glucocorticoid excess (Cushing's syndrome) and idiopathic metabolic syndrome results from increased glucocorticoid reamplification within adipose tissue by 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1). Indeed, 11beta-HSD-1 is now a major therapeutic target. Because much supporting evidence for a role of adipose 11beta-HSD-1 comes from transgenic or obese rodents with single-gene mutations, we investigated whether the predicted traits of metabolic syndrome and glucocorticoid metabolism were coassociated in a unique polygenic model of obesity developed by long-term selection for divergent fat mass (Fat and Lean mice with 23 vs. 4% fat as body weight, respectively). Fat mice exhibited an insulin-resistant metabolic syndrome including fatty liver and hypertension. Unexpectedly, Fat mice had a marked intra-adipose (11beta-HSD-1) and plasma glucocorticoid deficiency but higher liver glucocorticoid action. Furthermore, metabolic disease was exacerbated only in Fat mice when challenged with exogenous glucocorticoids or a high-fat diet. Our data suggest that idiopathic metabolic syndrome might associate with such a novel pattern of glucocorticoid action and sensitivity in humans, with implications for tissue-specific therapeutic targeting of 11beta-HSD-1.
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PMID:A polygenic model of the metabolic syndrome with reduced circulating and intra-adipose glucocorticoid action. 1630 51

As a key metabolic organ, the liver is central to the imbalance of high-caloric diets, and particularly dietary fat consumption, in the industrialized countries and their association with the increasing prevalence of morbid obesity. By interacting with the intestinal tract and adipose tissue, the liver plays a key role in various aspects of lipid metabolism. Increasing activation of transcription factors, such as carbohydrate responsive element binding protein (ChREBP), sterol response element binding protein-1c (SREBP-1c), or forkhead box 01 (Fox01), may contribute to fatty acid synthesis. Their translocation occurs via fatty acid transporters such as fatty acid transport proteins (FATP), fatty acid translocase (FAT/CD36), caveolin-1 and fatty acid binding protein (FABP) . Eventually, the accumulation of fat in the form of lipid droplets within the hepatocytes results in hepatic steatosis which, indeed, is a hallmark of liver diseases such as non-alcoholic fatty liver disease, alcoholic fatty liver, acute fatty liver in pregnancy, and hepatitis C. In contrast, lipid accumulation within hepatocytes during liver regeneration is essential. It is thus now becoming clear that steatosis is not only a mere consequence of metabolic imbalance, but that it is also a result of discrete alterations in the beta-oxidation, transport mechanisms, and signaling pathways involved in the synthesis, systemic traffic modalities, and cellular effects of fatty acids. Such a novel insight offers potential options for improved treatment.
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PMID:Lipid metabolism in the liver. 1723 19

The objective of the present study was to identify the factors which contribute to the appearance and/or aggravation of Vitamin A Deficiency (VAD) in individuals with morbid obesity in the pre- and postoperative stages of Roux-en-Y gastric bypass (RYGBP). Bibliography searches were done in the data-bases of Medline and Lilacs, published in the last 35 years, priorizing the studies which assessed VAD through serum levels of retinol. The principal factors identified as contributors to VAD were oxidative stress, deficiency of other nutrients, lipid malabsorption in the postoperative stage, insufficient intake of lipids and food sources of Vitamin A, and presence of nonalcoholic fatty liver disease. The investigation of the nutritional status of Vitamin A in those individuals may foment intervention strategies easily incorporated in already established routine procedures, aiming to reduce VAD rates, which will reflect upon those individuals' quality of life.
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PMID:Nutritional status of vitamin A in morbid obesity before and after Roux-en-Y gastric bypass. 1789 59

Intestinal shunting procedures followed by gastrointestinal bypass surgery have been used as therapeutic modalities in the treatment of morbid obesity since the mid 1950s. Enthusiasm reached its peak in the early 1960s with the introduction of the jejunoileal bypass, however began to wane as various complications were identified in the remote postoperative period and later. Finally, the jejunoileal bypass was abandoned in the 1980s. Apart from renal disorders, it frequently resulted in abnormal liver function and liver failure which are attributed to fatty infiltration. We report a 56-year-old woman, who underwent jejunoileal bypass surgery 23 years ago. She was admitted to our ICU because of hepatic encephalopathy IV, caused by upper gastrointestinal bleeding. Beside hepatic encephalopathy there were signs of severe liver failure (INR 2.8, cholesterol 32 mg/dl, ICG PDR 5%). Liver biopsy showed fatty infiltration and cirrhosis. Excluding other causes of liver disease, severe fatty liver disease following jejunoileal bypass surgery was diagnosed. The very late onset of severe liver disease emphasizes the importance of lifelong follow-up of these patients.
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PMID:[Steatohepatitis and cirrhosis: first manifestation 23 years after jejunoileal bypass surgery]. 1815 8

The prevalence of obesity and the number of surgeries for morbid obesity are increasing worldwide. Conservative therapy is largely ineffective in producing maintenance of weight loss in morbidly obese patients, and surgery is therefore increasingly considered as the only available option for these patients. Until approximately 15 years ago, many patients and physicians regarded bariatric surgery as dangerous because it required a large laparotomy and was associated with a relatively high risk of complications. Since laparoscopic techniques have become available, however, the number of patients referred for surgery has been increasing steadily. The principles of standard procedures are independent of access, whether open or laparoscopic. The pathophysiologic mechanisms are restriction, malabsorption, or a combination of both. New findings in the field of endocrine and humoral regulations have shown that surgical procedures can induce complex changes in the regulation of enterohormones. These mechanisms are the basis for metabolic effects, especially in cases of diabetes mellitus type 2. Obesity surgery is known to be the most effective and longest-lasting treatment for morbid obesity and many related conditions, but mounting evidence now suggests that it may also be among the most effective treatments for metabolic diseases and conditions such as type 2 diabetes, hypertension, high cholesterol, nonalcoholic fatty liver disease, and obstructive sleep apnea. Surgery for severe obesity goes far beyond weight loss; benefits include improved quality of life and extended life expectancy.
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PMID:[Obesity - principles of surgical therapy]. 1875 40


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