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Query: UMLS:C0020473 (hyperlipidemia)
15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes of cholesterol, phospholipid, triglyceride or bile acid levels in serum liver, bile and feces after the treatment with alloxan were examined in Wistar strain male rats. Serum cholesterol, phospholipid and triglyceride levels and liver cholesterol level markedly increased but liver phospholipid and triglyceride levels remained unchanged. The lipid levels in serum very low density and low density lipoproteins were elevated but those in high density lipoprotein were not. Bile flow was not changed but biliary secretion of cholesterol, phospholipid and bile acids markedly increased. Among the biliary bile acid components, cholic acid markedly increased but the amount of chenodeoxycholic acid was similar to that of normal rats. Fecal excretion of deoxycholic acid increased but that of lithocholic and hyodeoxycholic acids decreased, and alpha, beta- and omega-muricholic acids did not change, thus, the total amount of fecal bile acids remained unchanged. Hepatic cholesterol synthesis was markedly depressed, while cholesterol 7 alpha-hydroxylase activity did not change and cytochrome P-450 content was elevated by about 40%. From such evidence, it was apparent that synthesis of cholic acid increased while that of chenodeoxycholic acid decreased and the total amount of bile acids synthesized did not change in the diabetic rats. Furthermore, marked increase of the pool size of cholic acid and hepatic secretion of cholic acid stimulated the absorption of lipids and produced a hyperlipidemia in the diabetic rats.
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PMID:Altered bile acid metabolism in alloxan diabetic rats. 53 73

Dogs were made alloxan-diabetic and randomly distributed into either of two prospective treatment groups. In one group it was intended that the metabolic signs of diabetes be controlled poorly, and commercial insulin was administered in doses inadequate to prevent chronic, severe hyperglycemia and glucosuria. In the other group it was intended that the metabolic disorder be well controlled, and the animals received food and commercial insulin twice daily such that the hyperglycemia and glucosuria became mild or infrequent. Experimental improvement of the carbohydrate disorder was accompanied by amelioration of hyperlipemia and other clinical signs of deficient insulin activity. By 60 months of diabetes, retinal capillary aneurysms, pericyte ghosts, obliterated vessels, and other microvascular abnormalities typical of diabetes were apparent in each animal of the poor-control group. Better control was found to reduce significantly the incidence and severity of microvascular lesions. The data suggest that the mechanism responsible for diabetic retinopathy is initiated as a result of deficient insulin activity and that the development of the microvascular complications of diabetes are preventable and may be inhibited by careful control of the metabolic disorder.
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PMID:Relationship of microvascular disease in diabetes to metabolic control. 88 98

A single s.c. injection (10 mg/100 g bw of alloxan) was given to nonarteriosclerotic, virgin, Sprague--Dawley rats and to breeder rats with preexisting arteriosclerosis, hyperlipidemia and hyperglycemia. All of the animals promptly developed severe diabetes with ketosis, hyperglycemia, and hyperlipidemia. Insulin therapy was deliberately withheld. Mortality was high. Seven days later one group was subjected to hypophysectomy and 30 days later, all of the animals were autopsied. The diabetes + hypophysectomy animals maintained their body weight better, did not have hypertrophied adrenal glands, showed the least elevation of serum enzymes, e.g., CPK, SGOT, SGPT and LDH, less hyperlipidemia and hyperglycemia and reduced corticosterone production than the animals with untreated severe diabetes. Despite the relative amelioration of metabolic derangements prognostic of cardiovascular degenerative changes, the diabetes + hypophysectomy animals manifested extensive renovascular damage and the breeder rats with pre-existing arteriosclerosis showed definite exacerbation of their arterial disease in response to the severe alloxan diabetes regardless of hypophysectomy. It is suggested that although hypophysectomy may alleviate certain metabolic derangements attributed to growth hormone, ACTH and adrenal steroids, the angiopathic damage proceeds inexorably.
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PMID:Effects of hypophysectomy on alloxan-diabetic, arteriosclerotic, breeder vs. non-arteriosclerotic, virgin rats. 98 94

Male and female, arteriosclerotic and nonarteriosclerotic rats were subjected to acute myocardial infarction by two, subcutaneous injections (spaced 24 hr apart) of isoproterenol. During the immediate postinfarct repair phase all of the experimental animals were made severely diabetic with alloxan. Two weeks later the animals were sacrificed and their blood and pertinent organs analyzed for biochemical and pathologic changes. Females survived the myocardial infarct with superimposed diabetes in significantly greater than males. In addition to marked loss in body weight all of the experimental animals developed marked adrenal hypertrophy and thymus gland involution, cardiac hypertrophy, and unusual increase in ovarian or testicular size and weight. The combined conditions of myocardial infarction + diabetes led to substantial increases in serum creatine phosphokinase (CPK) and glutamic oxaloacetic transaminase (SGOT) whereas the enzymes glutamic pyruvic transaminase (SGPT) and lactic dehydrogenase (LDH) were reduced. Although serum triglyceride levels were greatly elevated, total cholesterol and free fatty acids were reduced. All of the animals were severely hyperglycemic and had greatly increased B.U.N. levels. Diabetes caused hypercalcemia but diabetes + myocardial infarction was associated with a definite reduction of this hypercalcemia. Despite marked adrenal hypertrophy, circulating Cmpd. B levels were subnormal. The diabetic condition and its attendant hyperlipidemia did not alter the morphologic nature of the arterial lesions in the breeder rats but the diabetes did cause definite impairment of the usual myocardial repair process observed in these rats with a particularly high incidence of left ventricular aneurysms in males.
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PMID:Metabolic and histopathologic changes in arteriosclerotic versus nonarteriosclerotic rats following isoproterenol-induced myocardial infarction with superimposed diabetes. 119 29

Groups of metabolically normal (controls) and alloxan-diabetic adult female rabbits were fed semi-synthetic diets containing 40 cal % palm-kernel oil (PKO) or sunflower-seed oil (SSO) for 54 weeks. In contrast to control rabbits fed PKO-diet, the alloxan-diabetic rabbits on this diet, developed no or only a negligible degree of atherosclerosis, although the serum levels of all lipid classes had increased in the diabetic rabbits above that of the controls during almost the whole experimental period. The diabetic rabbits and the controls fed SSO-diet were both free from any significant atherosclerotic involvement in spite of the fact that the SSO-diet appeared unable to suppress the very high levels of the various serum lipid classes induced by the diabetic state. On both diets, the diabetic rabbits showed a significantly higher cholesteryl linoleate/oleate ratio than the controls, which was caused by an increase in the cholesteryl linoleate level in the diabetics. No serious aorta atherosclerosis was found in rabbits with a cholesteryl linoleate/oleate ratio higher than 0.6, although no correlation was found between the atherosclerosis indices and these ratios at values lower than 0.6. Rabbits with cholesteryl linoleate/oleate ratios below 0.6 seemed to run a greater risk of developing atherosclerosis. It is suggested that insulin might be required for atherogenesis in addition to hyperlipemia and hypercholesterolemia.
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PMID:Effects of palm-kernel oil and sunflower-seed oil on serum lipids and atherogenesis in alloxan-diabetic rabbits. 120 Nov 41

Diabetes mellitus is associated with hyperlipidemia and increased risk of atherosclerosis. A diabetic animal model has been developed to study the effect of treatment with pravastatin, a potent HMG CoA reductase inhibitor, on plasma lipoprotein levels. Hypercholesterolemia was induced in alloxan diabetic and control rabbits by feeding a diet containing 25% casein and 10% hydrogenated coconut oil for 8 weeks. Feeding the casein-coconut oil diet to the diabetic group resulted in a 5-fold increase in serum cholesterol levels, which was not statistically different from the nondiabetic group fed this diet. However, in the diabetic group, there was more cholesterol in the VLDL fraction and less in LDL as compared to the nondiabetic group. Serum triacylglycerol levels in the diabetic rabbits were variable and ranged from 58-943 mg/dl. The diabetic and nondiabetic animals were then treated with pravastatin at a dose of 10 mg/kg per day for 21 days. In the nondiabetic group, pravastatin treatment significantly lowered serum and LDL cholesterol concentrations by 28.5% (52.3 mg/dl, P less than 0.05) and 36.2% (40.7 mg/dl, P less than 0.05) respectively, relative to the placebo group. Serum and VLDL triacylglycerol levels in the nondiabetic group were also significantly decreased following pravastatin treatment. In the diabetic group, serum and LDL cholesterol levels were decreased by 37.0% (69.1 mg/dl, P less than 0.05) and 52.7% (32.1 mg/dl, P less than 0.01), respectively, relative to the diabetics given the placebo. Pravastatin treatment did not adversely affect serum glucose levels. Thus, pravastatin treatment was effective in controlling the hypercholesterolemia present in these diabetic animals.
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PMID:The effect of pravastatin on serum cholesterol levels in hypercholesterolemic diabetic rabbits. 190 19

1. The effects of isoproterenol (ISO) on the ultrastructure of hearts from 10-week alloxan diabetic rabbits were examined. 2. Following alloxan injection, all rabbits developed severe hyperglycemia, hyperlipidemia and hypoinsulinemia. 3. Injection of ISO induced marked alterations in both control and diabetic rabbit hearts including accumulation of lipid and swelling of sarcoplasmic reticulum. 4. Myofibrils in both groups of animals were dispersed and appeared as a homogeneous mass with poorly defined Z-bands. 5. The most marked effect of ISO treatment in both groups of animals was damage to mitochondria. Mitochondria were extensively damaged and showed partial or complete disruption of their cristae network. 6. Glycogen granules were few in number or not detectable in both groups of animals. 7. The diabetic animals treated with ISO showed greater clumping and margination of nuclear chromatin, fewer intact mitochondria and a greater number of amorphous dense bodies in and around the mitochondria. 8. The presence of greater sarcolemmal damage in diabetic animals was inferred from the significantly greater accumulation of calcium and decreased magnesium in the myocardium.
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PMID:Isoproterenol-induced ultrastructural alterations in hearts of alloxan-diabetic rabbits. 275 45

1. Hyperlipidaemia is associated with diabetes mellitus. 2. A comparison of cholesterol synthesis and utilization in alloxan-induced diabetic rats and rabbits revealed that interspecies differences existed only in the response of the key enzymes regulating cholesterol utilization, namely cholesterol 7 alpha-hydroxylase and ACAT in the liver and intestine respectively. 3. The activity of cholesterol 7 alpha-hydroxylase was enhanced in diabetic rats but was markedly reduced in diabetic rabbits. 4. Intestinal ACAT activity, though unchanged in diabetic rats was reduced in diabetic rabbits. 5. Such species differences in cholesterol utilization may underlie the different degree of susceptibility to hypercholesterolaemia that exists between these two species.
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PMID:A comparative study of the rate-limiting enzymes of cholesterol synthesis, esterification and catabolism in the alloxan-induced diabetic rat and rabbit. 342 2

Male, 5 months old, massively obese, spontaneously hypertensive rats (Obese/SHR) were given 10 mg alloxan/100 g b.w., s.c., to induce diabetes. Control Obese and non-obese/SHR were given saline. Insulin therapy was withheld. All of the animals were killed at 6 months of age. Alloxan caused a slight but statistically significant increase in blood pressure, pituitary and adrenal glandular hyperplasia, hyperlipidemia, hyperglycemia, and increased BUN levels. The giant sized islets of Langerhans in Obese/SHR showed only partial degranulation of the insulin-producing beta cells concomitant with residual but apparently adequate blood insulin levels, whereas the islets of non-obese/SHR exhibited virtually total beta cell degranulation and only trace amounts of blood insulin. The alloxanized, non-obese rats were severely emaciated; the alloxanized Obese/SHR maintained their obesity. Alloxan-treated, Obese and non-obese/SHR manifested gross and microscopic degenerative changes suggesting acceleration of the normal aging process. The genetically-programmed pathogenesis of diabetes, obesity, hypertension, and Cushingoid pathophysiology of Obese/SHR may be due to hyperadrenocorticism.
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PMID:Resistance of obese and non-obese, spontaneously hypertensive rats to alloxan-induced diabetes. 635 Jul 80

In experiments on albino rats it was found that the partial alloxan elimination of the pancreatic incretory elements followed by the normal diet and long-term adaptation of a healthy organism to excessive readily assimilating food carbohydrates are accompanied by a series of morphofunctional shifts, indicating the development of early diabetes mellitus stages, which are characterized by a recurrent increase in the glycemia level over 100 mg/100 ml, in the presence of sugar curves, changed according to a questionable type, hyperinsulinism and hyperlipemia arising. Some pancreatic islets are hypertrophied, whereas their beta-cell number decreases.
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PMID:[Morphofunctional characteristics of the initial phase of the development of experimental diabetes mellitus]. 637 95


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