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

Liver biopsies from 60 patients with acute alcoholic hepatitis (AAH) developing against the background of steatosis, chronic hepatitis and cirrhosis were studied histologically, histochemically and electron microscopically. AAH is characterized by necrosis of hepatocytes with deposition of alcoholic hyalin, obesity of the organ, and polymorphonuclear leukocyte infiltration. Hyperplasia of the smooth endoplasmic reticulum, the appearance of megamitochondria, and an increased amount of peroxisomes reflect the participation of MEOS and the catalase system in alcohol metabolism with a progressive decrease in the activity of alcoholdehydrogenase. Acute alcoholic hepatitis is a connecting link between steatosis and cirrhosis of the liver in which the accompanying autoimmune mechanism and microcirculation disorder followed by activation of lipofibroblasts are conducive to the progression of the pathologic process.
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PMID:[Morphological characteristics of acute alcoholic hepatitis]. 7 56

The effect of obesity on peroxisomal beta oxidation has been studied previously only in the liver of genetically obese animals. We measured activity of peroxisomal acyl CoA oxidase (ACO) in livers, hearts and rectus femoris muscles of gold-thioglucose treated obese mice (n = 17) and control mice (n = 8). Since production of H2O2 by ACO could contribute to oxidative stress, activities of H2O2-metabolizing enzymes, catalase and glutathione peroxidase, were also measured. ACO activity was assayed using dichlorofluorescein and peroxidase as detectors of H2O2. ACO activity was higher in the obese liver and skeletal muscles than in their respective controls, while the heart ACO activity was unaltered. The activities of H2O2-metabolizing enzymes were unchanged or tended to be decreased in the obese tissues. There was a close correlation between the body weight and ACO activity in both liver and rectus femoris muscles. The ACO activity in the liver also correlated with the liver triacylglycerol content. These results suggest that the activation of peroxisomal beta oxidation occurring in both hepatic and extrahepatic obese tissues is closely linked to weight gain (i.e. non-genetic in nature), but that this does not enhance oxidative stress detected as reactive change of the defense system against H2O2.
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PMID:Peroxisomal beta-oxidation in liver and muscles of gold-thioglucose-induced obese mice: correlation with body weight. 201 Feb 57

A study was made of the erythrocytic membranes in patients with stage II-III metabolic and alimentary obesity. The red blood cells may serve as model of the membranes of other cells of the internal organs, that is why their changes are likely to mirror the total impairment of the function of the cell membranes in the illness under consideration. The patients' red blood cells were characterized by high permeability, increased ATPase activity, catalase activation, reduction of the content of the thiol groups, and by the displacement of the thiol-disulfide balance towards oxidized forms. A correlation was discovered between the elevation of red blood cell permeability and red blood cell K+, Na+-ATPase activation. The changes in the thiol-disulfide balance brought about inconclusive shifts in the magnitude of permeability, in the activity of ATPase isoenzymes, and in the content of cholesterol fractions in red blood cells of patients with metabolic and alimentary obesity. The changes thus discovered are of paramount importance for understanding the pathogenesis of metabolic abnormalities associated with obesity and for rational treatment of this patients' group.
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PMID:[New data on characteristics of the chemism of erythrocytes in patients with metabolic-alimentary obesity]. 280 Apr 51

Obese Zucker rats were dosed orally for one week with fenofibrate (100 mg/kg). Liver weights of treated rats as expressed as percent of body weight were slightly increased, while protein, DNA and lipid contents were unaffected per g of liver or increased when expressed in whole liver. Compared with the control animals, activities of fatty acid oxidase, of the peroxisomal fatty acid-oxidizing system and of catalase were markedly increased by fenofibrate both per g of liver and per total liver, while urate oxidase activity was unchanged when expressed per g of liver. The activity of monoamine oxidase and that of cytochrome c oxidase used as marker enzymes for mitochondria were increased only when expressed per total liver. However, fenofibrate treatment induced a pronounced increase in the activities of mitochondrial palmitoyl-CoA dehydrogenase and carnitine acyltransferases, particularly carnitine acetyltransferase. Fenofibrate also caused a significant increase of carnitine content in liver and hepatic mitochondria. The greatest observed increases were in free carnitine and in the rate of carnitine-dependent oleate oxidation, which might be favoured in vivo by a lesser sensitivity of CPT-I to a malonyl-CoA inhibitory effect. The present results suggest that fenofibrate treatment induces increased hepatic mitochondrial beta-oxidation in obese Zucker rats.
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PMID:Effects of fenofibrate treatment on fatty acid oxidation in liver mitochondria of obese Zucker rats. 366 37

We investigated the hepatocellular peroxisomes in 27 patients with steatosis of the liver by means of catalase cytochemistry, light and electron microscopic study, and morphometry. Seven normal human livers were used as controls. In our patients, fatty liver was mainly associated with alcohol abuse or obesity. Indications for a slight decrease in catalase activity and for a proliferation were found in visual evaluation of the peroxisomes. Morphometric analysis showed a significant decrease in mean peroxisomal diameter (to 87%) and a simultaneous significant elevation to numerical density of the peroxisomes (to 188%); this resulted in a normal volume density and a significant increase to (133%) in surface density. However, individual differences were found. No differences in peroxisomal characteristics were found between fatty livers of different causes. A significant inverse linear correlation between mean peroxisomal diameter and numerical density was found in patients with fatty livers. Because a similar correlation was also found when control data were added to the fatty liver data, we hypothesize that the peroxisomal compartment in human fatty livers is adapted in such a way to permit the same metabolic efficiency as in control livers.
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PMID:Alterations of peroxisomes in steatosis of the human liver: a quantitative study. 765 78

Selected parameters of lipid metabolism (cholesterol, HDL cholesterol, LDL cholesterol, atherogenic index, triacylglycerols, vitamin C, vitamin E, vitamin E/cholesterol, plasma fatty acid profile) and pro-oxidative/anti-oxidative parameters (conjugated dienes of fatty acids, activity of catalase and glutathione peroxidase) were estimated in blood of 59 healthy vegetarians aged 19-30 years. When compared to non-vegetarians, no incidence of obesity, low levels of cholesterol, LDL cholesterol, atherogenic index or triacylglycerols, HDL cholesterol levels on the margin of 1.4 mmol/l (boundary level between standard and reduced risk) as well as a higher plasma content of polyunsaturated fatty acids and a higher 18:2/18:1 ratio were all favourable consequences of vegetarianism with respect to atherosclerosis prevention. These factors are completed by higher levels of protective compounds with antisclerotic activity (vitamin C, vitamin E/cholesterol--protecting LDL from lipoperoxidation) as well as by beneficial pro-oxidative/anti-oxidative parameters (low values of conjugated dienes, significantly higher activity of catalase, higher level of vitamin C).
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PMID:Selected parameters of lipid metabolism in young vegetarians. 770 61

The authors subdued 183 vegetarians to examination, the aim of which was to judge the state of health and nutrition of the vegetarian population. The examined group was composed of people with their age ranging from 19-60 years, out of which 102 were of younger (19-39 years) and 81 were of older age. Their average period of vegetarian food consumption was 4.2 years. One third of men and a half of women were lacto-vegetarians, the rest were lacto-ovo-vegetarians. The results were compared with 160 nonvegetarians (64 of younger and 96 of older age). The detected values of lipid parameters were evaluated as favourable for vegetarians (low values of cholesterol, triacylglycerols, atherogenic index, LDL-cholesterol, the share of HDL-cholesterol was 28-33% (vs 24-26% in nonvegetarians) with values converging to 1.4 mmol.l-1--i.e. reduced risk). Additional favourable factors in prevention of atherosclerosis include the absence of obesity in vegetarians and values of antisclerotic active substances in blood (high values of vitamin C, in comparison with nonvegetarians a significantly higher molar ratio of vitamin E/cholesterol and vitamin E/triacylglycerols--more effective protection against peroxidation of lipids). Vegetarian mode of food consumption may be favourably evaluated regarding prooxidative-antioxidative parameters which play an important role in the process of atherogenesis, and carcinogenesis. Significantly lower values of conjugated dienes in plasma of vegetarians and vice versa high values of antioxidant substances (vitamin C, vitamin E/lipid components, catalase activity) were detected. A more pronounced system of detoxication in vegetarians is important due to a possible risk of an increased intake of xenogenous substances. (Tab. 3, Ref. 27.)
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PMID:[Lipid and pro-oxidative and antioxidative parameters in the blood of vegetarians]. 855 57

Lipid parameters (cholesterol CH, HDL-, LDL-cholesterol, triacylglycerols TG, atherogenic index AI) were estimated in four age groups of vegetarians, 82 males and 80 females, aged 15 to 60 years. The period of consumption of vegetarian food was 1.4 to 1.9 years for adolescents (15-18 years old) or 2.4 to 5.4 years for adults (age groups 19-29 years, 30-39 years and 40-60 years). Lacto-vegetarians constituted one half of females and one third of males. Vitamin C content, lipid peroxidation levels (conjugated dienes, CD) and the activities of catalase (CAT) and glutathione peroxidase (GSH-Px) were estimated in the oldest age group of males and females. Low levels of TG and glutathione peroxidase (GSH-Px) were estimated in the oldest age group of males and females. Low levels of TG and CH (in the lower half of the reference range), low calculated values of LDL-CH and AI, as well as values of HDL-CH in the upper region of the standard risk zone or over 1.4 mmol/l (reduced risk level) in males and females of all age groups are the positive factors of vegetarian nutrition in prevention of atherosclerosis. High levels of vitamin C in blood, absence of obesity and low blood pressure should be mentioned here as additional positive factors as well. When considered as a single isolated factor, the nearly significantly elevated values of CD (linked to increased intake of unsaturated fatty acids) could be a negative factor of vegetarian nutrition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipid parameters in blood of vegetarians. 814 53

Dehydroepiandrosterone (DHEA) is an adrenal steroid with chemoprotective effects against a wide variety of conditions including cancer, obesity, diabetes, and cardiovascular disease. However, DHEA is also a carcinogen in laboratory animals, possibly through its function as a precursor of sex steroids or peroxisome proliferation. The structural analog 16 alpha-fluoro-5-androsten-17-one (8354) has been reported to have enhanced chemopreventive activity without the steroid precursor and peroxisome proliferating effects of DHEA. This study compares DHEA and 8354 in rainbow trout, a species that is resistant to peroxisome proliferation but is highly susceptible to the carcinogenic and tumor enhancing effects of DHEA. Trout were exposed as fry to aflatoxin B1 (AFB1) or given a sham exposure, then were fed diets containing 444 ppm DHEA or 8354 for 6 months. Postinitiation treatment with DHEA significantly increased liver tumor incidence, multiplicity, and size compared to initiated controls. The analog 8354 slightly increased tumor incidence (p = 0.06) but had no effect on multiplicity or size. Six percent of trout treated with DHEA alone developed tumors, whereas no tumors occurred in noninitiated trout fed control or 8354-containing diets. Serum levels of androstenedione were elevated by DHEA (48-fold) or 8354 (6-fold) treatment. Serum beta-estradiol titers were increased in DHEA- but not 8354-treated trout. Vitellogenin was induced significantly by either DHEA (434-fold) or 8354 (21-fold). Peroxisomal beta-oxidation was not increased by either compound and catalase activity was decreased in DHEA-treated animals. Both steroids were potent inhibitors in vitro of trout liver glucose-6-phosphate dehydrogenase with IC50s of 24 and 0.5 microM for DHEA and 8354, respectively. This research suggests that in trout the tumor enhancing effects of DHEA may be due to its function as a sex steroid precursor and are unrelated to peroxisome proliferation. These carcinogenic properties are reduced in the analog 8354 which has been advocated as an alternative to DHEA for chemoprevention.
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PMID:Comparison of the enhancing effects of dehydroepiandrosterone with the structural analog 16 alpha-fluoro-5-androsten-17-one on aflatoxin B1 hepatocarcinogenesis in rainbow trout. 893

Obese hypertensive patients with cardiovascular risk factor clustering have increased plasma nonesterified fatty acid levels and are at high risk for atherosclerotic events. Our previous studies demonstrated that oleic acid induces a mitogenic response in rat aortic smooth muscle cells (RASMCs) through protein kinase C (PKC)- and extracellular signal-regulated kinase (ERK)-dependent pathways. In the present study we investigated the possibility that the generation of reactive oxygen species (ROS) constitutes a critical component of the oleic acid-induced mitogenic signaling pathway in RASMCs. We studied the effect(s) of oleic acid on the generation of ROS using the oxidant-sensitive fluoroprobe 2',7'-dichlorofluorescin diacetate. Relative fluorescence intensity and fluorescent images were obtained with laser confocal scanning microscopy from 1 to 5 minutes, since preliminary studies demonstrated that the peak fluorescence intensity occurred within 5 minutes. Oleic acid (100 micromol/L) induced a time-dependent increase of cell fluorescence that was >8-fold of that seen in control cells at 5 minutes. This was blocked by catalase, which suggests that H2O2 was the principal ROS. The oleic acid-induced increases in H2O2 were blocked when PKC was inhibited with the use of bisindolylmaleimide and when PKC activity was downregulated by exposing RASMCs to phorbol 12-myristate 13-acetate for 24 hours. Stearic and elaidic acids, which are weak PKC activators, did not significantly increase H2O2 production. The increase of H2O2 in response to oleic acid was inhibited by the antioxidant N-acetylcysteine. N-Acetylcysteine also completely blocked ERK activation and the increase of thymidine incorporation in response to oleic acid. The data suggest that generation of H2O2 in RASMCs exposed to oleic acid is PKC dependent. Moreover, H2O2 production emerges as a critical intermediary event in the oleic acid-mediated mitogenic signaling pathway between the activation of PKC and ERK. These observations raise the possibility that the elevated plasma nonesterified fatty acids, including oleic acid, in obese hypertensive patients contribute to vascular growth and remodeling by a PKC-dependent mechanism to generate ROS that subsequently activate ERK.
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PMID:Reactive oxygen species are critical in the oleic acid-mediated mitogenic signaling pathway in vascular smooth muscle cells. 985 64


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