Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The fasting concentration of cholesterol and triglycerides in serum and in very low (VLDL), low (LDL) and high (HDL) density lipoproteins (LP) was determined 3 months after a myocardial infarction (MI) in 54 men, and the values obtained were compared to those in 61 healthy male control subjects. The mean triglyceride concentration in MI patients was significantly increased in serum, VLDL, LDL and HDL by 74%, 110%, 30% and 12% respectively, compared to controls. The mean cholesterol concentration was significantly raised by 16%, 120% and 14% in serum, VLDL and LDL but decreased by 22% in HDL. Hypertriglyceridaemia occurred in 58% of MI patients. Of these patients, two-fifths had hypertriglyceridaemia only and three-fifths had combined hyperlipidaemia. The hypertriglyceridaemia was caused by elevation of only VLDL triglycerides in 26%, only LDL triglycerides in 19%, VLDL and LDL triglycerides in 23% and by various other combinations of raised LP triglyceride levels in 25% of cases. Hypercholesterolaemia was found in 41% of MI subjects. Of these, one-sixth had elevation of cholesterol levels, while five-sixths had combined hyperlipidaemia. The LP abnormalities underlying hypercholesterolaemia were increased of only VLDL cholesterol levels in 36%, only LDL cholesterol in 14% and both VLDL and LDL cholesterol in 50% of cases. The low HDL cholesterol values in comparison to controls were related to higher VLDL triglyceride values in MI patients, since HDL cholesterol fell significantly with increasing VLDL triglyceride levels. When HDL cholesterol was related to similar VLDL triglyceride levels, there were no major differences between controls and MI.
Atherosclerosis
PMID:Quantitative and qualitative serum lipoprotein analysis. Part 2. Studies in male survivors of myocardial infarction. 114 36

Diet and atherosclerosis are closely linked, both aetiologically and therapeutically. The aetiological association can be demonstrated most satisfactorily in animal experiments. In human beings the evidence must necessarily be more indirect and is largely based on dietary trials and epidemiological surveys linking the intake of cholesterol and saturated fat with morbidity and mortality from coronary disease. A modifying influence which has gained increasing recognition over recent years is the individual response to a given diet. This variability appears to be largely genetically determined, certainly in the defined primary hyperlipidaemic states, and possibly within the normal ranges of serum cholesterol levels. A change in food habits should be fully utilized therapeutically in any form of hyperlipidaemia, whether as a primary preventive measure before clinical diseases of atherosclerotic origin become manifest or in secondary prevention to delay further morbidity and mortality. With good dietary adherence, lipid levels may return to normal and there may be additional favourable effects on intravascular thrombosis. Many problems remain to be solved on the public health issue of advising changes in the national diet. A number of countries in which an atherogenic diet is habitually eaten have decided in favour of such a recommendation. Public education, identification of persons at risk and provision of readily available skilled medical and dietary counselling should constitute a national health project with rewarding long-term results.
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PMID:Diet and atherosclerosis. 115 3

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

A new strain of rat characterized by genetic obesity, endogenous hyperlipidemia, and hypertension was obtained in this laboratory. The abnormal phenotype is inherited as a homozygous recessive trait. The animals exhibit marked hypertriglyceridemia, moderate hypercholesterolemia, and an electrophoretic pattern resembling that of human Type IV hyperlipoproteinemia. The average life-span is less than 1 year, due largely to the development of premature renal and vascular disease. The kidney lesion has both glomerulonephritic and nephrosclerotic components and is accompanied by marked proteinuria. About 12% of animals develop urinary tract calculi. The vascular disease consists of fibrous and fatty-fibrous intimal plaques, and polyarteritis. The obese animal offers a useful model for investigating abnormal lipid metabolism and the etiology and pathogenesis of atherosclerosis.
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PMID:Pathologic findings and laboratory data in a new strain of obese hypertensive rats. 117 27

One hundred and ten patients with radiologically established peripheral atherosclerotic arterial disease were studied. None of them suffered from diabetes, endocrine disorders or renal disease. Their serum cholesterol and triglyceride values were compared with those of a reference group consisting of 548 individuals. When the 95th percentile of the reference values was used for cut-off, the frequency of hyperlipidemias in the patients with peripheral arterial atherosclerosis was about 52%. Combined hyperlipidemia was slightly more common (21%) than isolated increase of either cholesterol (17.9%) or triglycerides (12.6%). Using other cut-off limits for the definition of hyperlipidemia, a striking change in the distribution between these three types of hyperlipidemia occurred. In our patients, the frequencies of different blood groups were not significantly different from those of a comparable population. The serum lipids were at the same level in the different blood groups.
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PMID:Hyperlipidemia in peripheral atherosclerotic arterial disease. 117 25

The morbidity and mortality in 172 males and 164 females with xanthomatosis have been investigated. Symptoms of coronary heart disease (CHD) were the most frequent initial manifestation of atherosclerotic vascular disease. Angina pectoris was the first symptom in about 3/4 of males as well as females; myocardial infarction was the first event in 26% of the males and 9% of the females. Other manifestations of atherosclerosis were comparatively rare and occurred late in life. Half of the subjects were affected with symptoms of atherosclerotic vascular disease by the age of 52 in men and 62 in women, the mean age for first symptoms being 49 and 56 years, respectively. No significant influence of other CHD risk factors than xanthomatosis and hyperlipidaemia was found in these patients. An increase in the number of cardiovascular deaths was seen in xanthomatosis patients, compared with the general population, in particular in the number of "sudden deaths". Half of the males died before the age of 66 and half of the females before the age of 74.5, which is about 10 and 7 years earlier than predicted at 30 years of age for the normal population. The cumulative relative mortality in both men and women was about twice that expected for the general Norwegian population until 70 years of age.
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PMID:The risk of atherosclerotic vascular disease in subjects with xanthomatosis. 118 82

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.
Atherosclerosis
PMID:Effects of palm-kernel oil and sunflower-seed oil on serum lipids and atherogenesis in alloxan-diabetic rabbits. 120 Nov 41

Human growth hormone (HGH) response to i.v. insulin (0.1 U/kg body weight) and arginine infusion (25 g of L-arginine for 30 min) was studied in 9 patients (5 males and 4 females) with primary familial hypercholesterolaemia and belonging to 4 families. Mean age was 28 +/- 2 years (range 18-36) and body weight was less than 105% of ideal body weight. Glucose tolerance and insulin response to oral glucose were normal in all patients. HGH release after insulin and after arginine was slightly increased as compared to 21 normal controls, but the differences were not significant. Insulin and glucagon response to arginine in these patients was within the normal range. Plasma glucose and free fatty acids were normal after both insulin and arginine. Moreover, no significant correlation was found between fasting cholesterol and HGH peaks after insulin and after arginine, nor between cholesterol and insulin and glucagon responses. Despite marked hyperlipidaemia, HGH-deficient patients examined by other authors never present signs of atherosclerotic disease. Our data suggest that HGH, in the presence of elevated cholesterol levels, might play an important role in the development of atherosclerotic lesions.
Atherosclerosis
PMID:Growth hormone response to insulin and to arginine in patients with familial hypercholesterolaemia. 120 Nov 52

This work is the 1st of a research program on the behavior of lipid metabolism during pregnancy and in the 1st years of life. Theories on the subject of the biochemistry of cholesterol and triglycerides are summarized and lipid physiology, particularly from the viewpoint of hormone regulation and the behavior of some important enzyme systems, is examined. Lipid transport systems, in the form of lipoproteins, is discussed, followed by a description and classification of hyper- and hypolipemia and of the relation between some forms of hyperlipemia and atherosclerosis. It is concluded that it would be very useful to obtain an early identification of subjects with a high risk of atherosclerosis in order to begin prophylactic treatment, if possible, during early infancy or even during pregnancy.
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PMID:[Obstetrico-pediatric aspects of physiopathology of lipid metabolism. I. Synthesis of the physiological bases with special regard to hormonal regulation and classification of dyslipidemias]. 122 7

The recent increase in coronary heart disease is real and the causes must mainly be environmental. Consequently the condition should largely be preventable. The application of what is already known is likely to be a far more effective way of reducing the mortality rate than all attempts at palliative treatment, but vigorous action will be necessary. Much greater sums are being expended on coronary-care units and cardiac surgery than in preventing the need for them, although there is little evidence that they have significantly lowered the over-all mortality rate. Conventional treatment is immensely expensive. Prevention could in the long run be much cheaper. Cardiologists on their own are unlikely to succeed in a program of prevention. They need the help of many others, including community nurses, nutritionists, public health workers, sociologists, and of course general practitioners, but they have responsibility for leadership and for providing background knowledge. For the detection of certain risk factors, health examinations are necessary and should be part of general practice. Also, advice is best given on an individual basis. The chief-known risk factors (hyperlipidemia, hypertension, smoking, physical inactivity) could be controlled. CHD occurs in adults but atherosclerosis starts many years before. Prevention should begin with appropriate infant feeding, whenever possible with breast milk, and continue into childhood, when habits are formed and attitudes to life can best be influenced. It should be possible to bring up children virtually free from risk factors. It may never be possible to prove the effectiveness of such a multifactorial program by prospective controlled intervention studies, but the evidence indicates strong probability. The stakes are too high to delay action any longer. Physicians daily give advice in areas where the evidence is much less certain. Such a program for the control of coronary artery disease is urgently needed and could become one of the most rewarding activities for the medical profession.
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PMID:The cardiologist's responsibility for preventing coronary heart disease. 124 24


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