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

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

The effects of acute and chronic differences in the carbohydrate content of the diet on plasma insulin, glucagon, insulin-glucagon molar ratio (I/G), and triglycerides were studied. Acute effects were studied by varying the carbohydrate content of a single test meal, while chronic effects were determined by varying the carbohydrate content of the diet for a week. A test meal containing 0.6 gm of gelatin per kilogram plus 0.6 gm. per kilogram of glucose resulted in much higher levels of insulin and I/G (p smaller than 0.005), lower glucagon levels (p smaller than 0.05), and slightly higher triglycerides (N.S.) than did a meal of 1.2 gm, per kilogram of gelatin alone. One week of a 12 gm. carbohydrate, 2870-calorie diet lowered insulin (p smaller than 0.001), I/G (p smaller than 0.05), and triglycerides (p smaller than 0.001) and increased glucagon (N.S.), whereas a 390-gm. carbohydrate, 2784-calorie intake significantly increased insulin, I/G, and triglycerides (p smaller than 0.005) and lowered glucagon (p smaller than 0.02) within two days; even greater changes in hormones were observed on a 510-gm. carbohydrate intake. Of those patients in whom a high carbohydrate intake induced a triglyceride rise of at least 40 mg. per deciliter, a significant correlation between the change in I/G and the change in triglycerides was noted (r equals 0.85; p smaller than 0.01). The results are compatible with but do not prove the proposal that pancreatic alpha and beta cells play a mediating role in carbohydrate induction of hyperlipidemia.
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PMID:Basal and postprotein insulin and glucagon levels during a high and low carbohydrate intake and their relationships to plasma triglycerides. 109 39

Fasting serum triglyceride and cholesterol measurements, and lipoprotein characterization by ultracentrifugation, were performed in four groups of patients with chronic renal disease (uraemic, short- and long-term haemodialysis and renal transplant recipients) and the results compared with those obtained from age- and sex-matched control subjects. Basal insulin and growth hormone levels, and serum creatinine and albumin concentrations were measured in, and detailed dietary histories taken from patients in each group. The predominant lipid abnormalities were hypertriglyceridaemia and increased very low density lipoproteins (type IV hyperlipoproteinaemia) in both uraemic and haemodialysis patients. Following renal transplantation, a different pattern of hyperlipidaemia was found. Hypercholesterolaemia was more common and hypertriglyceridaemia less common than in the uraemic and haemodialysis group. The lipoprotein abnormalities were increased low density and/or very low density lipoproteins, with types IIa IIb and IV hyperlipoproteinaemia occurring equally frequently. In uraemic and haemodialysis patients, the proportion of carbohydrate in the diet was high, and may have played a role in the genesis of hypertriglyceridaemia. There was a positive correlation between relative body weight and serum triglyceride in the long-term dialysis group. In renal allograft recipients hypertriglyceridaemia could be attributed, at least in part, to obesity, prednisone dosage and the degree of impairment of graft function. The aetiology of hypercholesterolaemia in the transplant recipients was unclear. Neither basal insulin nor growth hormone levels were elevated in any patient group. Uraemic hypertriglyceridaemia is a clearly defined and well documented metabolic abnormality which is not corrected by dialysis. Post-transplantation hyperlipidaemia however, is a condition of variable presentation and multifactorial aetiology.
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PMID:Studies on the nature and causes of hyperlipidaemia in uraemia, maintenance dialysis and renal transplantation. 110 47

Human growth hormone (HGH) response to arginine (25 gm IV in 30 min) and to insulin (0.1 U/kg B.W.) was studied in 12 male patients (mean age 36 +/- 2 years), with normal glucose tolerance and normal body weight, affected with Fredrickson's Type IV primary hyperlipemia. The patients were examined both when plasma triglycerides (TG) were elevated and following clofibrate (2 gm/die for 30-60 days) induced TG reduction. No variations in glucose or FFA behaviour or in body weight were observed after clofibrate. HGH response to arginine was absent, while that to insulin was only inhibited, when plasma TG were elevated. A significant increase in HGH peaks after arginine (from 1.99 +/- 0.59 to 9.34 +/- 1.58 ng/ml) and a slight increment in HGH peaks after insulin (from 23.09 +/- 7.19 to 31.46 +/- 7.95 ng/ml) were observed following reduction in plasma TG. Arginine test was carried out in 7 normal subjects during saline infusion and at the 3rd hour of lipid infusion (Intralipid 20%). HGH response to arginine was absent in all of the subjects during lipid infusion. The HGH response to insulin test, carried out in 9 other normal subjects during saline infusion and at the 3rd hour of lipid infusion (Lipiphysan 15%) was significantly inhibited during lipid infusion. Since lipid infusion provoked an increment, not only in plasma TG but also in FFA, the inhibition of HGH release could be correlated with the elevated plasma levels of both TG and FFA. The results obtained in both spontaneous and experimental hyperlipemia not only confirm the role played by FFA in the regulation of HGH secretion, but also support the hypothesis that elevated TG levels could inhibit HGH response to some stimuli.
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PMID:The influence of plasma triglycerides on human growth hormone response to arginine and insulin: a study in hyperlipemics and normal subjects. 118 14

Blood glucose, free fatty acid and insulin responses to oral glucose and the fasting serum lipids were measured in 3 groups: 32 non-obese (mean age: 47.5 years) and 9 obese (mean age: 84.5 years), male patients with coronary heart disease and 12 non-obese male controls (mean age: 46.5 years). The oral glucose tolerance tests were repeated after 3 years in 16 of the non-obese patients with coronary heart disease. The results were as follows: 1) Glucose tolerance was impaired in 19 of 32 non-obese patients (59.4%). There was a significant correlation between impaired glucose tolerance and hyperlipidemia (hypercholesterolemia and/or hypertriglyceridemia). 2) In obese patients FFA levels at 30, 60, and 120 min after oral glucose administration were significantly elevated and FFA decrease was delayed with a drop to minimum levels at 180 min. 3) The insulin response after oral glucose administration in the group of non-obese patients with normal glucose tolerance was similar to that of non-obese controls. In the group of non-obese patients with impaired glucose tolerance, serum insulin levels went up to normal levels, but the peak was delayed. The serum insulin levels in obese patients were significantly higher than those of controls of 0, 60, 120, and 180 min. After 3 years the change in insulin response to oral glucose was not related to anginal symptoms or ECG findings, but was related to body weight change in patients with minor changes in glucose tolerance. 4) The metabolic pattern in the non-obese group with impaired glucose tolerance resembled that of "mild diabetes" in delayed response of insulin and FFA, and mild hyperlipidemia. These findings suggest that obesity may contribute to hyperinsulinemia in patients with coronary heart disease and that impaired glucose tolerance observed in patients with coronary heart disease is in part due to "latent diabetes".
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PMID:Glucose tolerance, serum insulin and lipid abnormalities in patients with coronary heart disease. 118 89

Transient lowering of blood levels of free fatty acids (FFA) in man and experimental animals after ingestion of fat has been noted by many investigators and has been attributed to inhibition of mobilization of fatty acids from adipose tissue. Studies on lipid mobilizing activity in in vitro systems containing glucagon, insulin and anti-insulin anti-bodies as factors modifying lipolysis indicate that insulin is the basic inhibitor of lipolysis in the blood in the period immediately following feeding of animals. This observation has been confirmed by direct determinations of insulin levels by the radioimmunologic method. Experiments in which substances influencing activity of the autonomic nervous system were used show that ingestion of fats stimulates insulin secretion as a result of cholinergic stimulation. Studies on lipolytic activity of blood serum confirmed an essential role of lipoprotein lipase in the mechanism of deposition of triglycerides in adipose tissue during alimentary lipemia. The role of prostaglandins and intestinal hormones (enteroinsular axis) in the mechanism of regulation of FFA levels during alimentary lipemia is also discussed.
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PMID:Factors regulating blood levels of free fatty acids during alimentary lipemia. 118 13

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

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.
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PMID:Growth hormone response to insulin and to arginine in patients with familial hypercholesterolaemia. 120 Nov 52

The various contraceptive methods available and their suitability and contraindications in the case of diabetic patients are reviewed. After briefly discussing tubal sterilization, condoms, diaphragms and spermicides, and IUDs, and their respective safety and effectiveness, the risks and advantages of contraceptive steroids are analyzed in detail. It is concluded that the metabolic effects of estrogen-progestin combinations are more serious in many diabetics, and their use often increases the need for exogenous insulin, as well as the tendency to hyperlipemia, excessive weight gain, and hypertension, which are all factors that aggravate diabetes. The contraindications apply to cases of subclinical diabetes, because the administration of these drugs to genetically predisposed subjects may precipitate the appearance of clinical diabetes. Oral contraceptives should then be used only if IUDs are contraindicated in a specific case and the desire for future pregnancies precludes sterilization. Patients should then be carefully monitored, and the oral contraceptive used contain the smallest possible effective dose of estrogen (preferably ethinyl estradiol) and progestin (preferably other than the nortestosterone type of a 19-nortestosterone derivative in a very low dose).
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PMID:[Choice of a contraceptive method in the diabetic patient]. 121 58

This summary of management of pill patients covers contraindications, individualizing pill formulations for normal women, and for diabetics, hypertensives, hyperlipidemics and those with personal or familial history of thrombophebitic or vascular disorders. The estrogen or progestagen balance of a pill can be selected to suit the individual. All patients beginning oral contraception should have pelvic exam, breast exam, cervical smear, fasting blood glucose, hematology and SMA-12, repeated in 3 months and yearly thereafter. Normally the pill causes transitory deterioration in glucose tolerance, increased growth hormone, a permanent change in insulin response, effects that are irreversible in 20% of users. Prediabetics should be given sequentials; diabetics should be followed weekly or monthly during oral contraception. Severe hypertension occurs in about 1% of pill users, but the risk is 4 times higher in women who had hypertension in pregnancy. Patients with increased personal or familial risk should be checked every 3 months and pills stopped immediately if blood pressure exceeds 150/100. In pill users cholesterol and free fatty acids remain normal, but lipoproteins, lecithins and triglycerides increase after 6 weeks to a plateau by 6-18 months, in proportion to estrogen dose. Since patients normally only discover hyperlipidemia after a clinical event such as xanthoma or vascular accident, those with related familial or personal history should have blood lipid studies every 3 months, and be given a progestagen only pill. Adolescents who are at high risk of pregnancy should receive progestagen or sequential pills, if their growth, bone age, hypothalamic function and reproductive organs are mature. The risk of idiopathic or posttraumatic thromboembolism is 3-9 times higher in pill users than in the normal population, but the only way of testing for risk in an individual is to do a detailed series of coagulation tests. Those predisposed should be given progestagen only or low dose pills.
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PMID:[Program of surveillance of patients under oral contraceptives]. 122 Jan 2


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