Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to determine whether the adrenal glands play a primary or secondary role in the pathogenesis of the spontaneous arteriosclerosis which occurs in repeatedly bred rats, sexually mature female, Sprague-Dawley rats were adrenalectomized and maintained during four successive pregnancies. Some of the breeders were treated with deoxycorticosterone (DOCA) and 0.5% saline. The adrenalectomized breeders did not develop arteriosclerosis, beta cell degranulations, or those which has accesory or regenerated adrenal glandular tissue. Surprisingly, intact DOCA-treated breeders also showed inhibition of arterial disease but they did have fatty livers and beta cell degranulation. Body and organ weights, serum enzymes, lipids, glucose, BUN, and corticosterone were elevated in breeder rats but not to such high levels as is usual in repeatedly bred rats. These findings demonstrate that the presence of the adrenal glands is essential for the pathogenesis of the spontaneous arteriosclerosis, fatty liver, and beta cell degranulation which occurs in repeatedly bred, female rats.
Atherosclerosis 1977 Jul
PMID:Inhibition of spontaneously developing arteriosclerosis in female breeder rats by adrenalectomy. 90 28

Rats were fed for 24 days a liquid diet with ethanol as 36% of calories to produce hyperlipemia and hepatic steatosis. The catabolism of chylomicrons doubly-labeled in the triacylglycerol and cholesteryl ester moieties was studied in conscious rats after ingestion of their usual liquid diets with or without ethanol. A constant intravenous infusion of chylomicrons revealed a defect in chylomicron catabolism after chronic treatment with ethanol. The plasma clearance of chylomicron cholesteryl ester was impaired to a greater extent than clearance of chylomicron triacylglycerol. These findings are consistent with defective catabolism of chylomicron remnants, and suggest that the accumulation of chylomicron remnants in the plasma contributes to the development of increased post-prandial hyperlipemia and chronic hyperlipemia in association with excessive ethanol consumption.
Atherosclerosis 1977 Sep
PMID:Effects of chronic ethanol consumption on the catabolism of chylomicron triacylglycerol and cholesteryl ester in the rat. 91 70

To develop the prophylactics and the curatives for atherosclerosis, thyroxine derivative, CG-635, was assayed for its physiological activities in experimental atherosclerosis in rabbits fed with cholesterol. It was found that CG-635 possessed serum TC/TP value lowering activity (total cholesterol/total phospholipid) in normal and cholesterol fed rabbits for 3 weeks, and prevented the elevation of the value of cholesterol fed rabbits by daily injection for 7 weeks. CG-635 also depressed the hyperlipemia induced by cholesterol feeding, and its inhibitory effect was shown to be more marked on the increase of cholesterol than triglyceride, phospholipid and free fatty acid in serum. CG-635 did not, however, influence GOT, GPT and G-6-Pase activities in serum with increased cholesterol intake. From the histological findings it was proved that this compound prevented to a high degree the occurrence of atherosclerosis and fatty liver of cholesterol fed rabbits. Furthermore, it was recognized that thyroid hormone and the thyroid simulating hormone-like activities of CG-635 were much weaker than thyroxine, except for the action in the lipid metabolism.
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PMID:[Effect of d,l-alpha-methyl-3, 5, 3, 5-tetraiodothyronine ethylester hydrochloride (CG-635) on experimental hypercholesterolemia and atherosclerosis in rabbits (author's transl)]. 117 Oct 31

Non-arteriosclerotic, virgin and arteriosclerotic, breeder rats were treated with aniline to suppress adrenal steroidogenic capacity and responsiveness to the stress of acute myocardial infarction. After two weeks of aniline treatment, some of the non-arteriosclerotic and arteriosclerotic animals were given two injections of isoproterenol, spaced 24 h apart, to induce massive myocardial infraction. On the 3 rd day, when myocardial necrosis reaches its zenith, the animals were sacrificed. Aniline-induced adrenal insufficiency caused increased mortality, absence of congestive heart failure, cardiac and adrenal enlargement but no evidence of the characteristic intense catabolism and increased corticoid production which attends acute myocardial infarction. Serum enzymes, e.g., SGOT, SGPT and LDH, triglycerides, but not glucose, free fatty acids and cholesterol, became acutely elevated in animals treated with aniline and isoproterenol. Animals developed a fatty liver, beta cell degranulation, post hypophy-sectomy-like changes in their adrenal cortices, unusually severe infarction, marked distention of intermuscular spaces, frequent foci of dystrophic calcification and cartilaginous metaplasia of the papillary muscles. It is believed that aniline-induced adrenal suppression altered the usual pathophysiologic response to acute myocardial infarction.
Atherosclerosis
PMID:Adrenocortical suppression and myocardial infarction in non-arteriosclerotic (virgin) and arteriosclerotic (breeder) rats. 126 59

This study was designed to determine whether male Mongolian gerbils (Meriones unguiculatus) develop atherosclerosis (AS) during long-term feeding of diets similar to those consumed by humans. Gerbils were fed diets containing 16% casein (C) or soy (S) protein +/- 0.1% cholesterol (CH) for 15 months. The energy contribution from protein, fat and carbohydrate was similar to the energy distribution reported for the average North American (NA) diet and the level of added dietary CH resembled the average NA intake. At mo 0, 3, 6, 9, 12 and 15, animals were killed and tissue sections were prepared for histologic examination. Microscopic observations of cardiovascular tissues did not reveal any evidence of AS in any of the diet groups. Liver fatty infiltration (FI) was evident in the C+CH and C groups at mo 3 and 9, respectively, and continued to occur at all subsequent sampling times. Livers from gerbils fed S+CH also began to exhibit FI at mo 9, while livers from S-fed gerbils did not show any significant morphologic changes. Biochemical liver total lipid results supported the histological liver findings. Other tissues examined did not reveal any morphological changes related to diet. The gerbil may be a useful animal model to study mechanisms which inhibit AS development.
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PMID:Long-term feeding of casein or soy protein with or without cholesterol in Mongolian gerbils. I. Morphologic effects. 223 27

Extracts of snake venom have been widely used for the treatment of vascular thrombotic diseases, yet the therapeutic mechanism is not clear. The effect of snake venom fractions on atherosclerosis in Japanese quail was studied. The venom of Agkistrodon halys was fractionated by DEAE-cellulose chromatography and the pooled protein fractions that resulted were injected intravenously into the quail with aortic atherosclerosis induced by dietary cholesterol. After 7 weeks of injections on every other day, the quail were killed, blood clotting times and serum cholesterol levels were determined, and aortic atherosclerosis and fatty liver were scored. The results showed that while no regression of atherosclerosis was observed, the lowering of serum cholesterol, prolonged blood clotting time and reduced fatty liver were significantly affected by the injection of one of the pooled protein fractions. This venom fraction contained two major protein components, one of which had arginine esterase activity. From this study we conclude that snake venom has little effect on the regression of atherosclerosis, but it prolongs blood clotting and lowers serum cholesterol.
Atherosclerosis 1990 Oct
PMID:Effect of snake venom of Agkistrodon halys on atherosclerosis and blood characteristics in Japanese quail. 228 93

Whereas up to the end of the last century overweight reflected the privilege of the high society and her relative good health, the recent epidemiological studies have assessed the relations between body weight and general or cause specific morbidity and mortality. The major diseases associated with obesity are hypertension, atherosclerosis and diabetes, as well as certain types of cancer. Less well known complications include hepatic steatosis, gallbladder diseases, pulmonary function impairment, endocrine abnormalities, obstetric complications, trauma to the weight bearing joints, gout, cutaneous diseases, proteinuria, increased hemoglobin concentration and possibly immunologic impairments. From these wide epidemiological studies arise the definition of obesity: with an excess of 20% beyond the desirable weight, the complications bound to the overweight become statistically more frequent. Over there a U or J shaped curve illustrates the relation between the overweight and the degree of these various complications. An excess of 45 kg or more represents the critical level which defined "morbid obesity" with its own complications, the most important are sudden unexplained death, ventilatory disorders, circulatory congestion and functional limitations in activities of daily living and of course psychological consequences. When for certain complications, such as diabetes, the relationship with the overweight is evident, discrepancies between certain studies, especially for the cardiovascular diseases, had focused the attention on the regional patterns of fat distribution. Cross-sectional studies have shown abdominal obesity to be strongly associated with risk factors for cardiovascular disease, stroke and death independent of the total degree of obesity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The contribution of epidemiology to the definition of obesity and its risk factors]. 266 68

The major diseases associated with obesity are hypertension, atherosclerosis, and diabetes, as well as certain types of cancer. Less well-known complications include hepatic steatosis, gallbladder disease, pulmonary function impairment, endocrine abnormalities, obstetric complications, trauma to the weight-bearing joints, gout, cutaneous disease, proteinuria, increased hemoglobin concentration, and possibly immunologic impairment. A U- or J-shaped curve illustrates the relation between body mass index and the degree of these various complications. This relationship can be used to provide guidelines for assessing treatment of obesity.
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PMID:Complications of obesity. 406 25

Ten laying hens with low plasma cholesterol levels and no signs of fatty liver syndrome were examined at necropsy. Liver coloration and deposition of body fat were not abnormal in such hens. Eleven nonlaying hens had signs of fatty liver syndrome. They were out of production for 1 to 3 months and had elevate plasma cholesterol levels. At necropsy, such hens had yellow livers, heavy deposits of body fat, and several involuted egg yolks, which were dark yellow. Intimal plaques were observed by light microscopy in the abdominal aortas of hens with low plasma cholesterol levels; the plaques contained little or no lipid and were composed of three or four rows of modified smooth-muscle cells. Aortic intimal plaques of hens with high plasma cholesterol levels were composed of 16 to 18 rows of modified smooth-muscle cells when examined by light microscopy. The plaques contained intracellular and extracellular lipid, indicating aortic atherosclerosis. Electron-microscopic observations of the abdominal aortas of both groups of hens were similar to light-microscopic observations, except that lipid, including cholesterol clefts, was seen both intracellularly and extracellularly in the thickened tunica intima of hens with high plasma cholesterol values. Thus, the presence of aortic atherosclerosis was confirmed by electron microscopy. It is suggested that the endogenous hypercholesterolemia and cessation of egg production, characteristic of severe fatty liver syndrome, originated from the reabsorption of involuted egg yolks and that such reabsorption caused the development of aortic atherosclerosis and deposition of excess body fat.
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PMID:Aortic atherosclerosis in nonlaying hens with fatty liver syndrome. 663 49

A sub-strain of male and female spontaneously hypertensive rats (SHR) capable of having massively obese or non-obese offspring were bred repeatedly or were maintained as virgin controls. When the male and female breeders had sired or given birth to 5 litters of young, they were autopsied along with their 10-month-old celibate brothers and sisters. Virgin and breeder SHR developed high blood pressure (250 +/- 10 mm Hg). Breeder rats were significantly heavier than their virgin cohorts; pituitary and adrenal glands, hearts, and kidneys were significantly enlarged while thymi were severely involuted in breeder vs virgin SHR. The hyperlipidemia, fatty liver, hyperglycemia, and islet hyperplasia, characteristic of virgin SHR, were greatly exacerbated in breeder SHR. Blood levels of corticosterone, deoxycorticosterone, and aldosterone were greatly elevated in breeder vs virgin SHR. Although breeder rats of genetically normotensive strains develop aortic sclerosis, none of the breeder SHR developed aortic sclerosis. Instead, intimal fibrinohyalin lesions appeared confined to the testes and ovaries. It is suggested that the anatomical appearance or resistance of the arterial wall to the development of lesions is genetically mediated but this genetic programming may be modified by metabolic and hormonal factors with particular emphasis on the participation of adrenocorticoids.
Atherosclerosis
PMID:Hyperlipidemia, hyperglycemia and hypertension in repeatedly bred parents of the obese spontaneously hypertensive rat (obese/SHR) unaccompanied by arteriosclerosis. 674 80


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