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

Hyperuricaemia was present in 18 out of 73 men with untreated mild hypertension and was related significantly to alcohol intake, serum aspartate transaminase activity, and obesity. In the whole group the mean serum urate concentration correlated highly significantly with alcohol intake and activities of serum aspartate and alanine transferases but not with ponderal index, serum creatinine concentration, age, or blood pressure. Hypertension and hyperuricaemia are related at least in part through their common association with frequent alcohol use. A serum urate concentration exceeding 0.5 mmol/l (8--4 mg/100 ml) in a man with untreated hypertension is highly suggestive of heavy alcohol consumption. There was no evidence that hyperuricaemia had a deleterious effect on renal function.
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PMID:Hyperuricaemia in hypertension: role of alcohol. 43 9

An increased aspartate transaminase in the liver of dietary (post-cafeteria) obese rats was found. It was consistent with the functionality of the malate-aspartate shuttle, that could be responsible for enhancement of metabolic efficiency. The muscle and intestine of obese rats showed a greater capacity for alanine and glutamine synthesis than the controls. Furthermore, enterocyte adaptations in the obese rats indicated higher capabilities for the intake of nitrogen than in the controls. In conclusion, the pattern of amino-acid enzyme activities reflected adaptations to keep from amino nitrogen depletion in dietary obesity which were compatible with an enhancement of the metabolic efficiency.
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PMID:Dietary obesity shows adaptations of amino-acid metabolism on enzyme activities to save amino nitrogen. 168 27

We found that 17 out of 60 (28.3 percent) obese, otherwise healthy volunteers had elevated serum alanine aminotransferase (ALAT), aspartate aminotransferase (ASAT) or alkaline phosphatase (AP) at least once in the course of a 12 week clinical trial. ALAT was the most commonly elevated serum aminotransferase occurring in 16 out of the 17 participants. Its range of elevation, as a percentage of the upper limit of normal (ULN) at screening was 102-164 percent (mean +/- s.d.; 127 percent +/- 18.4). Three participants had slight elevations of AP (112 percent, 113 percent, 119 percent of ULN). One participant had a minor elevation of ASAT (107 percent of ULN at screening). Of the 17 participants with elevated aminotransferases and AP, six were randomized to placebo, seven were treated with the low dose and four with the high dose of the new medication. Study participants having elevated enzymes had higher ideal body weight (IBW) than the group with normal values at screening (162 +/- 10 percent IBW, 152 +/- 11 percent IBW respectively), and at week 8 (152 +/- 3 percent IBW, 146 +/- 2 percent respectively) (P less than 0.05). The corresponding body mass index (BMI) values are 36.8 +/- 2.8 for the participants with elevated liver enzymes vs 34.2 +/- 2.6 (P less than 0.001) for the participants with normal values at screening and 34.9 +/- 3.1 and 32.8 +/- 2.8 (P = 0.02) respectively at week 8. Males (46 percent) were more likely than females (21 percent) to have elevated aminotransferases. We found no evidence for hepatic disease during the study period. Slightly elevated and fluctuating serum aminotransferases and alkaline phosphatase concentrations are a more frequent finding in healthy obese populations than previously established. In studies of anti-obesity agents investigators should broaden the entry criteria since elevated aminotransferase levels rarely interfere with the safe conduct of clinical trials in obesity.
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PMID:Elevated serum liver enzymes in obesity: a dilemma during clinical trials. 179 21

Alcohol abuse is usually regarded as the most likely cause of elevated serum liver enzyme values in those attending for well population screening, but we have found increased body weight to be an important contributing factor. We have measured serum levels of alanine amino-transferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transferase (GGT) in approximately 21,000 men attending for routine health screening, and related these to behavioural factors such as alcohol consumption, cigarette smoking, exercise level and obesity. The levels of all three enzymes were positively correlated with levels of alcohol consumption. Decreasing levels of physical activity were associated with increases in mean ALT and GGT levels. Cigarette smoking showed only a weak effect on ALT and AST, which became non-significant after multivariate statistical analysis, but increasing consumption of cigarettes was associated with increased mean levels of GGT. In contrast, all three enzymes showed marked increases in mean levels with increasing body mass index (BMI). The effect of obesity was particularly important in the case of ALT: the prevalence of increased ALT values in obese subjects (BMI greater than or equal to 31 kg/m2) was more than eight times that in those with normal weight (BMI less than or equal to 25 kg/m2), even after allowing for the confounding effect of alcohol consumption. This study is concerned solely with male subjects, but we hope to extend the analysis to females in the near future.
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PMID:Effect of body mass and other factors on serum liver enzyme levels in men attending for well population screening. 257 11

Ultrasonic and laboratory studies were performed in 816 white-collar workers over 35 years old who received health examination. Prevalence of fatty liver diagnosed by ultrasonography was 17.9% in all subjects and was maximum (24.4%) in males 45-49 years of age. Obesity index and body mass index were higher in fatty liver than in normal controls. Serum levels of glutamate pyruvate transaminase (GPT), cholinesterase, glutamate oxaloacetate transaminase (GOT), gamma-glutamyl transpeptidase (gamma-GTP), triglyceride, total cholesterol, uric acid, HbA1c and glucose were significantly higher, and a serum level of HDL-cholesterol was significantly lower in males with fatty liver than in controls with obesity. Prevalence of abnormal laboratory findings in fatty liver was also shown, and prevalence of fatty liver was prominently high in males with severe obesity or with mild elevation of GPT. A major cause of fatty liver was considered as obesity. In conclusion, fatty liver was a common cause of liver dysfunction and was closely related to risk factors for atherosclerosis especially in white-collar workers.
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PMID:[Ultrasonic and laboratory studies on fatty liver in white-collar workers]. 764 60

We retrospectively examined the issues that concern parents of obese children to determine the most effective means of motivating them to seek treatment for obesity in their children. Children with an obesity index > or = 40%, aged six to 12 years, were screened in Kagoshima City in 1992. Parents were notified if their children needed an evaluation that included a family history and measurements of the blood pressure, total cholesterol, high density lipoprotein (HDL)-cholesterol, atherogenic index (ASI), triglycerides, aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Parents were informed of the results of the evaluation and invited to attend a lecture on the treatment of obesity in children. A total of 378 obese children were evaluated. However, the parents of only 39 children attended the lecture. Children whose parents attended had higher mean total levels of cholesterol (190 +/- 25 vs 175 +/- 28, P < 0.01) and ASI values (3.2 +/- 0.9 vs 2.7 +/- 0.9, P < 0.02) than those whose parents did not attend. There were no significant differences in other factors. Only 4.2% of parents whose children showed no abnormal values, except for obesity, attended the lecture, compared with 20.3% (P < 0.01) or 16.9% (P < 0.05) of parents whose children had abnormal levels of cholesterol or abnormal ASI. Parents may be more concerned about hypercholesterolemia or arteriosclerosis than obesity per se. We should perhaps use the total cholesterol or ASI values, not just the severity of obesity, to motivate parents to enter their children into treatment programs for obesity.
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PMID:What are parents of obese children concerned about in their children? 782 49

Plasminogen activator inhibitor type-1 (PAI-1) is a key determinant of the fibrinolytic capacity. Its activity correlates with most of the characteristic features of insulin resistance syndrome, i.e. obesity, high blood pressure and hyperlipidemia. We measured plasma PAI-1 antigen levels in 131 asymptomatic men (aged 44.2 +/- 11 years) who had been referred for hyperlipidemia. Those taking medication and those with a secondary hyperlipidemia were excluded. We confirmed the correlation between PAI-1 levels and the following variables: body mass index, blood pressure, triglyceride concentration, and blood glucose and insulin levels before and after an oral glucose tolerance test. We also found a significant and independent correlation between PAI-1 and the concentration of the hepatic enzymes glutamyl transferase, alanine aminotransferase and aspartate aminotransferase. Mild liver abnormalities (presumably steatosis) may thus be one of the factors accounting for high plasma PAI-1 levels in hyperlipidemic patients.
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PMID:Relation between plasminogen activator inhibitor-1 and hepatic enzyme concentrations in hyperlipidemic patients. 785 96

The objective was to determine the effects of persistent obesity on amino acid enzymes in white (WAT) and brown (BAT) adipose tissues. Dietary obesity was induced by feeding a cafeteria diet ad libitum for 3 months, then it was removed and the obese animals received the same diet as controls for 5 months. Dietary-induced obesity was persistent as obese rats showed a stable, higher body weight than controls (26%). Key enzymes of alpha-amino nitrogen metabolism were studied and results showed reduced activities in obese rats: glutamine synthetase (45%), AMP deaminase (52%), alanine aminotransferase (66%) and glutamate dehydrogenase (68%) in BAT, whereas WAT of obese animals only showed lower aspartate aminotransferase activity (47%) with respect to the controls. We can conclude that these adaptations in amino acid metabolism were exclusively dependent on the obese status as they were observed in an obesity model in which obese rats eat the same diet as controls.
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PMID:Brown and white adipose tissue adaptive enzymatic changes on amino acid metabolism in persistent dietary-obese rats. 791 90

There is strong evidence that genetic factors contribute to the development of obesity in humans as well as laboratory animals. Another important factor leading to obesity is an increase in energy intake. However, it is difficult to make normal rats obese by controlling daily food intake. There is no report of normal adult male Wistar rats becoming obese and diabetic on a high-fat diet. The aim of the present study was, therefore, to make normal adult Wistar rats obese by infusing high fat and hypercaloric diet through the cannula without disturbing the free movement and to investigate the influence of an increase in the caloric intake on body weight and glucose metabolism. High-fat hypercaloric diet (360 kcal/kg body wt./day; H group) or control diet (180 kcal/kg body wt./day; C group) was continuously infused into the stomach of normal adult male Wistar rats weighing approximately 300 g through gastric cannulas for 27 days. On day 28 after a 24-h fasting, serum concentrations of aspartate aminotransferase, alanine aminotransferase, total cholesterol, triglyceride, phospholipid, and free fatty acids (FFA) were determined, and intragastric glucose loading test (2 g/kg body wt.) was performed. The average weekly body weight gain in the H group was twice as much as that of the C group (40.0 +/- 2.4 vs. 19.4 +/- 1.9 g/week, P < 0.001). Serum levels of triglyceride, phospholipid, total cholesterol, and FFA were significantly elevated in the H group compared to those in the C group. Liver weight in the H group was significantly higher than that in the C group and showed steatosis. Pancreas weight (-13%) as well as protein (-12%), amylase (-53%) and trypsin content (-26%) were all reduced, whereas pancreatic DNA content was significantly increased in the H group compared to those in the C group. Serum glucose and insulin concentrations before and after glucose loading in the H group were significantly higher than those in the C group. Moreover, the insulin response relative to glucose response in the H group was significantly high compared to that in the C group, indicating the presence of insulin resistance. These results indicate that feeding of high-fat hypercaloric diet makes normal Wistar male adult rat obese associated with hyperlipidemia, hyperinsulinemia, and glucose intolerance.
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PMID:High-fat hypercaloric diet induces obesity, glucose intolerance and hyperlipidemia in normal adult male Wistar rat. 879 99

This study was aimed at finding out whether weight reduction alone can improve liver function in obese patients with fatty liver. We did a longitudinal, clinical intervention study on weight reduction by behavior modification, diet and exercise. The study subjects were 25 patients referred to an obesity clinic in whom obesity is the sole factor causing abnormal liver function and fatty liver. Patients were weighed about one year later. We compared the degree of improvement in hepatic function between Group I that showed weight reduction and Group II that showed no-weight reduction. Group I (13) showed dramatic improvement in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, nearly all down to within normal levels. AST showed statistically significant improvement from 74 +/- 36 IU/l to 25 +/- 7 IU/l. ALT also showed statistically significant improvement from 109 +/- 67 IU/l to 30 +/- 14 IU/l. Group II (12) showed higher AST and ALT levels on follow-up visit than initial visit. AST showed statistically significant elevation from 43 +/- 11 IU/l to 59 +/- 23 IU/l. ALT also showed statistically significant elevation from 64 +/- 21 IU/l to 97 +/- 33 IU/l. If we can rule the other causes of hepatic abnormalities in obese patients with fatty liver, we suggest these patients would benefit by weight reduction.
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PMID:Effect of weight control on hepatic abnormalities in obese patients with fatty liver. 892 25


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