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 prevalence of fatty liver disease at autopsy ranges from 40% to 80% in Europe and North America, and liver injury tests are abnormal in up to 8% of healthy populations. Liver injury tests were therefore examined in a group of 325 workers without exposure to hepatotoxins to identify the influence of obesity and gender. Obesity was a strong predictor of the degree of abnormality for serum levels of arginine and alanine aminotransferase and of alkaline phosphatase, even in the normal range. Women generally demonstrated lower levels of these enzymes. Workers with morbid obesity were substantially more likely to have abnormal liver injury tests. Obesity and gender must be considered in the interpretation of abnormal liver injury tests in hazardous waste workers.
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PMID:Liver injury tests in hazardous waste workers: the role of obesity. 291 8

Health examinations of 108 workers exposed to vinyl chloride monomer (VCM) at a Japanese chemical plant were carried out in 1979. The polymerization of vinyl chloride was started at the plant in 1949. In this study, the highest concentration of VCM in autoclaves was determined to be 250 ppm in 1961. However, the workers at the plant had been exposed to higher concentrations of VCM several times before 1960. More recent VCM exposure was considered negligible. Examinations assessed data on age, height, weight, obesity index, sake consumption, VCM exposure concentration, latent period, cumulative exposure, ICG (indocyano green test), serum bilirubin, GOT (glutamic oxaloacetic transaminase), GPT (glutamic pyruvic transaminase), A1-P (alkaline phosphatase), GGT(gamma-glutamyl transpeptidase), ZTT (zinc turbidity test), LDH (lactate dehydrogenase), cholesterol, TTT (thymol turbidity test), A/G (albumin globulin ratio), and thrombocytes. Variation in VCM exposure did not affect tests of pigment excretion from the liver, such as ICG; thrombocytes; and enzyme activity (such as GPT); nor bilirubin or flocculation reaction in serum.
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PMID:Early detection and signs of hepatoangiosarcoma among vinyl chloride workers. 302 84

Seven patients developed acute hepatitis after receiving Plethoryl for obesity for 4 to 16 weeks. Jaundice was generally associated with or preceded by asthenia, nausea and pruritus. Serum aminotransferase activities were markedly increased whereas alkaline phosphatase and gamma-glutamyltransferase activities were moderately elevated. There was no hepatic failure. In all cases, Plethoryl administration was promptly discontinued. In 6 cases, jaundice disappeared within 2 to 4 weeks, and recovery occurred within 2 to 5 months. In one case, however, jaundice disappeared within 12 weeks and recovery took 10 months.
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PMID:[Hepatitis probably caused by Plethoryl. Apropos of 7 cases]. 337 97

The overfed rat served as the animal model for examining the influence of obesity on the hepatotoxic and nephrotoxic potential of metabolically activated drugs, and acetaminophen served as the prototype drug. Weanling Sprague-Dawley rats were given a standard pellet diet or semisynthetic, energy-dense diet designed to produce obesity. After 24 weeks, when overfed rats outweighed controls by more than 50%, animals received 710 mg/kg of acetaminophen i.p., based on total body weight. Toxicity evaluation included biochemical signs of organ injury over the first 24 hr and histopathologic changes in tissue morphology at 48 hr. Both enzyme release (alanine aminotransferase into plasma, alkaline phosphatase into urine) and frank cellular necrosis in liver and kidney of obese rats greatly exceeded that in pellet-fed controls. Contributing to the potentiation of injury were higher peak plasma concentrations of acetaminophen in obese animals resulting from total body weight dosing. However, liver and kidney injury and mortality remained elevated when peak plasma concentrations were matched by fat-free mass dosing, indicating that increased toxicity also was related to obesity. Incomplete recovery of acetaminophen and metabolites from obese animals (45 vs. 71% in control rats) caused by a functional renal impairment made it impossible to determine the metabolic fate of acetaminophen in overfed animals from the analysis of urine collections. Drug products measured in urine were summed with amounts remaining in carcass at sacrifice, computed as terminal plasma concentrations times respective distribution volumes. These results showed obese rats to form more glucuronide and less sulfate conjugate than did pellet-fed controls, coinciding with clinical evidence for enhanced glucuronidation in obese humans.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Obesity as a risk factor in drug-induced organ injury: increased liver and kidney damage by acetaminophen in the obese overfed rat. 359 8

We performed iliac bone histomorphometry after in vivo double tetracycline labeling 3-14 years after intestinal bypass surgery for obesity in 21 patients, selected because of clinical suspicion of metabolic bone disease, and compared the results with those of 40 age-matched normal control subjects. Osteomalacia defined by rigorous kinetic criteria was found in six cases, histologic features of secondary hyperparathyroidism without significantly impaired mineralization in one case, and possible osteomalacia masked by impaired matrix synthesis in one case. In the patients with definite osteomalacia, nonfracture bone pain was more frequent, corrected plasma calcium lower, plasma alkaline phosphatase and magnesium higher, and secondary hyperparathyroidism more severe than in the other patients. In the patients without osteomalacia there was a 24.5% reduction in trabecular bone volume compared to the controls; in contrast to age-related bone loss and post-menopausal osteoporosis, this was due mainly to reduction in the thickness rather than the density of trabecular plates. About two-thirds of the reduction in trabecular thickness was due to reduction in interstitial bone thickness, representing the cumulative effect of increased depth of osteoclastic resorption cavities, probably due in part to secondary hyperparathyroidism. About one-third of the reduction in trabecular thickness was the result of reduced mean wall thickness, representing insufficient osteoblastic matrix synthesis, probably due in part to malabsorption of an unidentified nutrient necessary for normal bone health. Resorption indices were not increased at the time of the biopsy, but there were persistent defects in the recruitment and activity of osteoblasts. Clinically significant bone loss after intestinal shunt surgery, as in several other clinical situations, results from the combined effects of an unsustained increase in bone resorption and a sustained decrease in bone formation.
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PMID:Metabolic bone disease with and without osteomalacia after intestinal bypass surgery: a bone histomorphometric study. 384 Mar 79

Temporal and spatial patterns of lipid deposition, vascularization and collagen deposition were described for subcutaneous adipose tissue in the fetal pig. Enzyme cytochemical changes were reported as they relate to the morphological differentiation of the subcutaneous depot. There are distinct temporal lags between the appearance of specific enzymes in adipocytes. For example, NADH-tetrazolium reductase activity appeared earliest whereas esterase activity appeared before lipoprotein lipase (LPL) activity. Adipose tissue primordia has been localized around specific tissue components in rat and pig tissues. These tissue components include hair follicles, sweat glands, large nerves, large blood vessels and mammary gland ducts. Lipid and enzyme cytochemistry demonstrates physical continuity between primordial cells and differentiated fat cell clusters. Alterations in maternal and/or fetal endocrine or metabolic profiles result in specific changes in fetal subcutaneous adipocytes. For example, maternal diabetes significantly increases cell size whereas genetic obesity has little effect on cell size but increases cellular LPL activity significantly. A comparison of subcutaneous and perirenal depots in the pig fetus indicated several depot specific anatomical and enzyme histochemical traits. Blood vessel architecture and vascular alkaline phosphatase activity clearly demarcated perirenal and subcutaneous depots in the fetus. These data indicate that site to site variations of adipose tissue characteristics may be reflecting intrinsic stromal-vascular aspects of specific locations.
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PMID:Anatomical and enzyme histochemical differentiation of adipose tissue. 393 90

According to current concepts, soluble phosphatidic-acid phosphatase, converting phosphatidic acid into a diglyceride, is a rate-limiting enzyme in the hepatic biosynthesis of triglycerides. The present paper is the first report on this enzyme in human liver. The enzyme activity was assayed in ammonium sulphate precipitates of cytosol obtained from human liver biopsies. The activity was stimulated by preincubation with alkaline phosphatase and inhibited by Mg-ATP, suggesting that phosphorylation-dephosphorylation may be of some importance for the expression of the activity of the enzyme. When assayed under optimal conditions, the activity obtained in liver biopsies from normal-weight gallstone patients averaged 12.8 +/- 2.0 nmol min-1 (mg protein)-1 (mean +/- SEM) (n = 17). The enzyme activity was slightly higher in liver biopsies from morbidly obese subjects 16.4 +/- 2.8 nmol min-1 (mg protein)-1 (n = 14). The difference between the two groups of subjects was probably in part sex-dependent and was not statistically significant. A similar small and insignificant difference between the two groups of subjects was found when the enzyme activity was assayed in the maximally stimulated state--i.e. after incubation with alkaline phosphate. These findings suggest that an increased capacity of the soluble phosphatidic-acid phosphatase is not of major importance for the increased triglyceride synthesis known to occur in obesity. Other factors (i.e. availability of substrate and cofactors) may be of greater importance.
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PMID:Triglyceride metabolism in human liver: studies on hepatic phosphatidic-acid phosphatase in obese and non-obese subjects. 608 51

Glucagon has been shown to lower blood lipids and to decrease food intake and body weight in short-term studies in man and animals. There is evidence of decreased secretion of glucagon in human obesity. The Zucker obese rat suffers from a genetic type of obesity and has an absolute reduction in circulating glucagon concentration. The effect of long-term administration of glucagon on the body weight in obese Zucker rats was studied. Glucagon caused a marked (-20%) reduction of body weight in obese Zucker rats with no change in feed intake. Urine glucose, urea nitrogen, creatinine, and ketone content, as well as serum triglyceride, cholesterol, alkaline phosphatase, creatinine, and insulin levels remained unchanged. Weights of perirenal fat, kidneys, and heart also remained unchanged. However, glucagon injection in obese Zucker rats caused significant decrease in serum glucose, and increases in SGOT, liver weight, and liver lipid and glycogen content. Further investigations are needed concerning the safety of chronic glucagon administration for weight control.
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PMID:Suppression of weight gain by glucagon in obese Zucker rats. 672 36

With the aim of investigating bone mineral loss after intestinal bypass operation, bone mineral content (BMC) was measured by two-dimensional scanning photon absorptiometry on the distal part of the forearm in 23 consecutive patients who had undergone intestinal bypass operation for obesity. Eleven patients (group 1) were investigated before and 12 months after operation, and 12 (group 2), who had been operated on 2-7 years earlier, were investigated two times at an interval of 12 months. No patient received therapeutic calcium or vitamin D supply. The predominant biochemical findings postoperatively were decreased serum values of calcium, magnesium, albumin, and total protein; there was no change in inorganic phosphate or alkaline phosphatase. Mean BMC was normal in both groups postoperatively as well as in group 1 before operation; there was no significant change in mean BMC during 12 months of observation. However, in BMC measurements on extremely obese subjects, a correction for the excessive fat layer on the forearm was necessary because of different attenuation properties of fat and soft tissues. Neglect of this problem will give a systematic underestimation of BMC, and may lead to false conclusions in cross-sectional as well as longitudinal studies.
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PMID:Bone mineral content before and after intestinal bypass operation in obese patients. 722 14

By means of immunonephelometry, determinations of a number of high molecular weight (HMW) and low molecular weight (LMW) proteins in urine and serum were undertaken in 42 consecutive patients, who had been subjected to jejuno-ileal bypass surgery for treatment of massive obesity two to six years before the study. Five patients demonstrated a distinct LWM proteinuira, ie excessive excretion of free-light lamdba and kappa chains of immunoglobulin and beta-2-microglobulin. The creatinine clearance was normal in four of these five patients. This LMW-proteinuria group differed from the remaining 37 patients in several respects. First, they had lost weight more effectively (P less than 0.01); secondly, they exhibited secondary hyperparathyroidism (P less than 0.05), increased levels of alkaline phosphatase and low serum concentrations of bicarbonate (P less than 0.001). It is suggested that LMW proteinuria may be a manifestation of secondary hyperparathyroidism.
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PMID:Tubular proteinuria following jejuno-ileal bypass surgery. 722 72


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