Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The exact role of serum pseudocholinesterase (PSCE) is not known. Its main role probably consists in the degradation of butyril-choline, an intermediate of lipid metabolism. Decreased values have been described in liver cirrhosis as an index of diminished proteosynthetic function. An increased activity of this enzyme was reported in obesity, diabetes mellitus, nephrosis, hyperthyroidism and in hyperlipemic subjects without obesity. A significant correlation was found between serum cholesterol, triglycerides and PSCE, as an expression of lipid metabolism. In view of assessing the possible change of this enzyme during fattening, the authors investigated PSCE activity during fattening in pigs (the same breed). The results indicate a statistically significant increase of PSCE during fattening, from 30.4 +/- 1.7 to 43.6 +/- 1.7 (p less than 0.001). These results together with those reported in a previous paper concerning blood lipids and cholesterol, show a positive correlation between these parameters and PSCE during fattening in pigs, which might be due to an adaptative increase of the hepatic synthesis of this enzyme in response to the increased lipid metabolism.
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PMID:Serum pseudocholinesterase activity during experimental fattening. 94 98

We have evaluated the effect of acute administration of pyridostigmine bromide, a cholinesterase inhibitor, on the GHRH-induced GH rise in 11 obese children and in 8 age-matched controls. The GH response to GHRH (hpGRF 1-40, 1 microgram/kg iv), evaluated both as maximum GH peak and as integrated area under the curve, was significantly lower in the obese children than in the controls. Pretreatment with pyridostigmine bromide (60 mg orally 60 min before the GHRH injection) significantly increased both baseline GH levels and the GH response to GHRH in all the obese subjects, so that their mean baseline GH, peak GH levels and integrated area under the curve after pyridostigmine bromide plus GHRH were similar to those of the control children after GHRH. Also in control children pyridostigmine bromide increased (though not significantly) baseline GH levels. and caused a significant augmentation of the GH response to GHRH. Mean peak GH levels and mean integrated area under the curve after pyridostigmine bromide plus GHRH were significantly higher in the controls than in the obese children given the same treatment. Mean baseline Sm-C levels were significantly higher in the obese than in control children. These data show that enhancement of cholinergic neurotransmission, likely in the hypothalamus, counteracts the blunted GH response to GHRH present in the obese children, and that in simple obesity the potential of the pituitary to make a secretory response to a direct GH secretagogue is preserved.
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PMID:Pyridostigmine counteracts the blunted growth hormone response to growth hormone-releasing hormone of obese children. 249 49

Time and feeding influences on cholesterol, triglyceride, glucose and insulin levels, and serum cholinesterase activity were assessed in a genetically-hyperlipidemic hyperphagic obese rat model, and compared with its lean litter-mate. Following a 28-day acclimation to a 12-hr light/dark cycle, blood samples were obtained every 2 hr from rats via tail bleed for a 24-hr period. Synchronization with other animal studies was established by endogenous serum cortisol levels [acrophase 18-20 hr after light onset (HALO) in both groups]. Triglycerides cholesterol, insulin and glucose levels were significantly elevated in obese versus lean rats. Obese rats were observed to feed throughout the 24-hr cycle, whereas lean litter-mates ate only during the dark cycle. No circadian rhythmicity was found in glucose levels with either rat group. Insulin levels were not correlated. Although triglyceride levels peaks at 13 HALO in lean rats, no pattern was observed in obese rats. Cholesterol levels were unchanged with time in either group. Cholinesterase activity followed a circadian rhythm in the lean, but not obese, rats with an acrophase estimated at 8 HALO. In contrast to previous reports, enzyme activity was not correlated with triglyceride levels in either rat group. Circadian similarities in insulin levels between rat groups suggest changes in insulin metabolism and/or secretion which are likely to be independent of feeding or activity. Conversely, triglyceride levels remained elevated throughout the 24-hr period in obese rats, whereas significant increases were observed in lean rats during the dark active cycle. These data suggest that triglyceride levels, and not insulin and cholesterol levels, are most likely dependent on feeding patterns.
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PMID:Circadian assessment of lipids in the hyperphagic obese rat compared with lean litter-mates. 268 Jan 23

Two groups, 16 nonalcoholic steatohepatitis patients (group I) and 22 alcoholic hepatitis patients (group II) classified according to the presence or absence of drinking and their histological characteristics, were compared on the basis of clinical, biochemical, and liver biopsy findings. The frequencies of female patients (p less than 0.01), obesity (p less than 0.001), and maturity-onset diabetes (p less than 0.005) were significantly greater in group I than in group II. The serum glutamic pyruvic transminase (p less than 0.05) and gamma-glutamyltranspeptidase (p less than 0.05) contents were significantly greater in group II than in group I. The cholinesterase content (p less than 0.05) was significantly less in group II. Significant differences were found in the grades of nuclear vacuolation (p less than 0.001, Fisher's exact probability test), periportal pericellular fibrosis, proliferation of bile ductules, and changes in the shape of the portal tracts (p less than 0.001, Wilcoxon's rank-sum test). Zonal necrosis in group I was seen in only severe steatohepatitis. These clinical and biochemical findings were found to be useful in differentiating nonalcoholic steatohepatitis from alcoholic hepatitis. Liver biopsy was of limited value at best in separating the two conditions.
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PMID:Comparison between nonalcoholic steatohepatitis and alcoholic hepatitis. 360 26

Pseudocholinesterase activity is significantly higher in liver and serum, but lower in adipose tissue of genetically obese, diabetic and gold thioglucose treated mice. Similar enzyme changes were also observed in lean mice on a high carbohydrate diet. A marked reduction (40%) in PChE activity occurred in the liver of genetically diabetic mice when starved for 24 h. These observations suggest that pseudocholinesterase induction in the liver and repression in the adipose tissue is affected by excessive caloric intake in obesity. This provides a model to study the biological function of PChE in health and disease.
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PMID:Pseudocholinesterase in obesity: hypercaloric diet induced changes in experimental obese mice. 731 92

Obesity is often associated with coronary heart disease and metabolic disorders. In this study, the relationship between obesity and metabolic disorders and between obesity and fatty liver by ultrasonography was investigated in 307 university students (18-20 years old, men: 196, women; 111). The correlation between Body Mass Index (BMI) and the thickness of subcutaneous fat (ST) was significant between BMI and the ratio between waist and hip circumference (WHR) was more significant in male students (r = 0.838, p < 0.001) than in female students (r = 0.639, p< 0.001). The incidence of fatty liver was significantly higher in male obese students (68.6%) than in female obese students (27.3%). After adjustment for BMI, ST, WHR and sigma glucose, the mean values for serum transaminase, cholinesterase, total cholesterol, uric acid, fasting plasma insulin and sigma insulin were significantly higher in male obese students with fatty liver than in male obese students without fatty liver. The present study suggested that male obese students with fatty liver are more likely to have metabolic disorders than male obese students without fatty liver.
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PMID:[Fatty liver and obesity in university students]. 747 66

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

Serum pseudocholinesterase (PChE) was discovered in 1932. Since this protein mimics many of the catalytic properties of acetylcholinesterase, it has traditionally been referred to as PChE, even though its true biological function is unknown. Serum PChE is synthesized in the liver and secreted into the circulation as a sialated glycoprotein. Although no convincing evidence of biological function exists, a significant number of obese and diabetic patients have elevated levels of PChE. The same phenomenon is found in experimental animal models of obesity, diabetes and hyperlipoproteinemia. Streptozotocin-induced diabetic mice showed increased serum PChE activity concomitant with increased serum triacylglycerol and PChE activity declined with treatment. Iso-OMPA, a nontoxic inhibitor of serum PChE, reduced serum and liver triacylglycerols and serum VLDL in streptozotocin-induced rodent diabetes. These findings suggest that PChE may have a role in VLDL metabolism.
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PMID:Serum pseudocholinesterase and very-low-density lipoprotein metabolism. 793 19

Obesity is an excess of body fat frequently resulting in a significant impairment of health. Body index derived from body weight and height is widely available in Japan. However, body index cannot express the fat deposition in the body. Screening for early obesity was studied using a combination of body index and bioelectrical impedance for detecting fat deposition. Three hundred twenty-nine male subjects with normal body index participated in this study. Blood pressure, uric acid, total cholesterol, high density lipoprotein cholesterol, triglyceride, GOT, GPT, gamma-GTP, choline esterase and glucose tolerance after a 75-gram glucose load were measured. The following results were obtained. 1. Among 321 subjects with normal body index, 95 subjects had body fat exceeding 23% as measured by bioelectrical impedance. 2. By matched-pair comparison in the subjects whose body mass indices were within +/- 10% fasting plasma glucose, triglyceride, GOT, GPT, gamma-GTP and choline esterase were significantly higher and high density lipoprotein cholesterol was significantly lower in subjects with fat deposition over 23% than in the 92 matched controls with body fat less than 23%. In conclusion, bioelectrical impedance appears to be useful for detecting early stages of obesity in subjects with normal body index.
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PMID:[Early detection of obesity in male adults using a combination of body index and bioelectrical impedance method]. 826 Jul 42

Accuracy in measurement of plasma free fatty acids (FFA), and therefore prevention of the in vitro lipolysis, is a crucial step to understand the physiologic role of plasma FFA and their relationships in the pathogenesis of important metabolic disorders such as central obesity, insulin resistance, and diabetes mellitus. As lipoprotein triglyceride-fatty acids are elevated in these states, in vitro lipolysis of triglycerides may artifactually increase FFA. Plasma FFA were measured in subjects before and after heparin administration, under different experimental conditions affecting the in vitro activity of lipoprotein lipase (LPL) and hepatic lipase (HL). Paraoxon, a cholinesterase inhibitor neurotoxin known to block plasma lipolytic activity, and preextraction timing and temperature of collection were tested. Paraoxon was required to prevent triglyceride hydrolysis in: a) preheparin plasma allowed to stand at room temperature (21 degrees C) for 2 h, before being frozen at -20 degrees C (FFA = 1817 +/- 291 vs. 698 +/- 66 microEq/l, P < 0.005, mean +/- SEM, without and with paraoxon, respectively); and b) in postheparin plasma immediately stored at -20 degrees C (FFA = 2682 +/- 357 vs. 1299 +/- 150 microEq/l, P < 0.005, without and with paraoxon, respectively). No difference in the FFA level was found in preheparin plasma collected either with or without paraoxon when: a) the samples were placed in ice and immediately assayed; b) the specimens were immediately frozen at -70 degrees C and assayed 60 days later.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of techniques to obtain plasma for measurement of levels of free fatty acids. 835 49


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