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

The coexistence of partial lipodystrophy of unusual distribution (limbs, back and head) with insulin-resistant diabetes and severe retinal, renal, neurological and arterial complications is reported. The lipodystrophy followed juvenile arthritis (Still's disease) and the diabetes, initially asymptomatic, became insulin dependent and technically insulin resistant (200 - 300 units insulin/day). Severe hyperlipidaemia has been a feature of this syndrome, probably contributing to the conspicuous peripheral arterial disease. The mother was diabetic but three sisters had normal glucose tolerance and there is no lipodystrophic member of the family. Underlying mechanisms of this syndrome remain obscure.
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PMID:Partial lipodystrophy and insulin-resistant diabetes. 68 Mar 14

We have estimated rates of fatty acid synthesis from glucose carbon and from all 2-carbon units in liver and carcass of mice using [U-14C] glucose and 3H2O under four different nutritional states. The liver synthesized only a small fraction (2--9%) of the fatty acids that were formed from glucose carbon in mice that were fasted 24 hr, fasted--refed, or fed ad libitum. However, in fed-refed mice, the liver's role increased and now accounted for 40% of the fatty acids that were formed from glucose carbon. Under the latter conditions (fed-refed), the liver synthesized 50% of the fatty acids that were formed from all 2-carbon units. At least five-sixths of all the fatty acids synthesized de novo in the fed-refed mouse were derived from carbon fed in the glucose test meal. These studies, in contrast to most earlier studies, provide direct evidence in mice of the major contribution that dietary carbohydrate makes, especially in the liver, to the synthesis of fatty acids. In addition, we have shown that lipogenic inhibition (fasting) and activation (feeding) are most marked in liver and greater for glucose than for non-glucose-carbon. Possible implications for dietary control of carbohydrate-induced hyperlipemia and obesity are discussed.
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PMID:Re-evaluation of lipogenesis from dietary glucose carbon in liver and carcass of mice. 71 47

Growth of Ehrlich ascites carcinoma induces hyperlipemia in mice. In the present study using male Swiss-Webster mice, we examined whether the usual elevations of plasma triglyceride levels in cancerous mice would occur in the absence of dietary fat. Hypertiglyceridemia developed at a similar rate and to a comparable degree in tumerous mice eating a fat-free (58% glucose) diet and in those fed Purina chow. Maximal hyperlipidemia was observed on day 6 or day 8 in tumorous mice fed either diet. To determine whether the endogenous cancer-induced hyperlipidemia was due to hypersecretion of triglycerides by the liver, triglyceride secretion rates were studied 0, 2, 4, 6, 8, 10, and 12 days after tumor inoculation using Triton WR-1339. The secretory rates did not increase prior to or during the development of hypertriglyceridemia in tumorous mice and were not significantly different from those of control mice. On days 10 and 12, triglyceride secretion actually decreased in tumorous mice. Other possible causes for hypertriglyceridemia are discussed in light of the present findings of undetectable differences in triglyceride secretion rates accompanying growth of Ehrlich ascites carcinoma in mice.
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PMID:The role of dietary fat and hepatic triglyceride secretion in cancer-induced hypertriglyceridemia. 75 Aug 29

In fed rats the effects of catechloamines and adrenergic antagonists on blood glucose, free fatty acids (FFA), and liver glycogen levels were investigated in order to determine the role of alpha- and beta-adrenergic receptors in metabolic responses to catechloamines. Hyperglycemic responses to dopamine (DA), noradrenaline (NA), adrenaline (A) and isoprenaline (ISP) were dose-related and accompained by a depletion of liver glycogen. The relative potencies in producing hyperglycemia and in causing liver glycogenolysis were in descending order of potency, A, NA, DA and ISP. Hyperlipemic response was most potent to NA and DA, weaker to ISP, and least potent to A. Phentolamine antagonized completely both hyperglycemia and hepatic glycogen depletion induced by all catecholamines. Propranolol impaired only hyperglycemic responses to A and ISP. Phentolamine antagonized hyperlipemia induced by DA and NA but only partially impaired hyperlipemia after A. Propranolol only partially antagonized hyperlipemic responses to NA and ISP without influencing DA--and A-induced hyperlipemia. The results indicate that in fed rats hyperglycemic responses to catecholamines are mediated mainly by an alpha-adrenergic receptor, and hyperlipemic responses do not fit inton the alpha-receptor or beta-receptor classification.
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PMID:Effect of catecholamines and adrenergic antagonists on blood glucose, free fatty acids and liver glycogen levels in fed rats. 75 44

Diabetes mellitus occurs in many animals species. However, only a few have been utilized in systematic studies designed to answer unsolved problems associated with the disorder in man such as molecular basis, pathogenesis of the vascular and neural lesions, and the roles of diet, exercise and obesity. Among the animal models available, rodents have been studied most thoroughly for a number of reasons: a) short generation time (sexually mature at about 3 mo of age, gestation time 21 days) and life-span is approximately 3 yr; b) hyperglycemia and/or obesity is known to be inherited in several species; c) environmental factors can be controlled easily in the laboratory because of small size; and d) economic considerations. The better-known rodent diabetes/obesity syndromes may be categorized as follows: 1) hyperglycemic with ketoacidosis, nonobese (Chinese hamster, South African hamster); 2) hyperglycemic with insulin hypersecretion, moderate obesity and may develop ketoacidosis (diabetic mouse (db/db), spiny mouse, sand rat); and 3) less pronounced hyperglycemia with hyperinsulinemia, insulin "resistance" and marked obesity (obese (ob/ob), yellow (Ay) and New Zealand obese (NZO) mice, and the Zucker "fatty" rat). The PBB/Ld mouse, described here in detail for the first time, is a new strain of mouse that also fits into the latter category. Members of this strain following maturity develop an obesity that is characterized by increasing cellularity of adipose tissue, increased serum immunoreactive insulin, reduced glucose tolerance, fatty liver, and hyperlipidemia. Therefore, this strain of mouse represents another model for study of adult onset obesity.
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PMID:Animal models of diabetes and obesity, including the PBB/Ld mouse. 77 Jan 97

A brief survey of the literature on the side effects of oral contraceptives is given. Of the many influences on laboratory results those related to (reversible) cholestasis or to a change in protein synthesis are the most important ones. A decrease of the tolerance for glucose is sometimes observed. Few of the clinical side effects attributed to oral contraceptives can be directly correlated with the pharmaceutical action of these drugs. Many so-called side effects of the pill are due to other factors such as altered psychosociological or sexual behavior, etc. However, among users of oral contraceptives there is a significant decrease in the number of benign tumors, particularly of the breast, the uterus and the ovaries. It is still an open question if this also signifies protection against cancer. Anemias due to iron deficiency are less frequent among users of the pill. According to recent studies arterial hypertension and cholecystopathies are probably directly related to oral contraceptives, but a causal relation has not been proven for migraine, headaches, depression etc. An elevated risk for vascular complications seems to be well established: there is a 4-6-fold increase of the estimated risk for venous thrombo-embolism and a 4-9-fold increase for cerebrovascular accidents among users of oral contraceptives when compared with nonpregnant women of the same age not using the pill. Oral contraceptives act as a supplementary factor of risk which may cumulate with other similar factors, such as arterial hypertension, hyperlipidemia, overweight, smoking etc. Mortality due to oral contraceptives is very much 10-50 x) inferior to the one caused by delivery and the post partum state. Since the number of failures in prevention of pregnancies is less for oral contraceptives than for any other method of contraception, the overall risk of death under oral contraceptives in this age group of women is least.
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PMID:[Real and seeming side-effects of oral contraceptives with an emphasis on medical and haematological problems. Review of literature (author's transl)]. 79 Mar 74

43 male and 30 female patients with various types of hyperlipemia were treated with Lipostabil, Lipostabil forte and 2 placebo preparations, each treatment lasting one month. The effect on the serum lipid level, lipoprotein electrophoresis, coagulation, coronary and peripheral vascular diseases, blood pressure and glucose tolerance was examined. Lipostabil caused a significant decrease of the serum triglyceride level in Type IV. To us, the use of "Essential" phospholipids alone does not appear to be sufficient for the drug therapy of hyperlipemia, but it might play a supporting role in the treatment.
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PMID:[The therapeutic value of "Essential" phospholipids]. 80 90

The long term use of a glucose free dialysate in a group of 15 maintenance hemodialysis patients is associated with a significant decrease in serum cholesterol in 50% of the patients and a significant decrease in serum triglycerides in 25%. The lipid changes appear to be independent of changes in body weight. Hyperlipidemia is believed to be an associated risk factor in the genesis of atherosclerosis in the general population and perhaps in maintenance hemodialysis patients. The long term correction or palliation of the hyperlipidemia of some maintenance hemodialysis patients by the use of glucose free dialysate may be beneficial.
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PMID:Long-term effect of dialysate glucose on the lipid levels of maintenance hemodialysis patients. 82 Dec 4

The disappearance rate of plasma. free glycerol, free fatty acids and triglycerides following the termination of short-term (6-hr) infusion of fat emulsion (Intralipid) was studied in 12 low-birth-weight infants. The mean K values for each lipid component were found to be higher in infants receiving 10% glucose. Owing to the wide individual variation of responses and the small number of infants studied, only the disappearance rate of free fatty acids reached the level of significance. It is concluded that increased amounts of glucose given simultaneously with fat emulsion could diminish hyperlipidaemia by increasing the clearance of lipids from the plasma.
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PMID:The elimination of free fatty acids, free glycerol and triglycerides from the plasma of low-birth-weight infants receiving intravenous fat emulsion and glucose. 82 38

Statistical analyses were performed in order to determine the effects of the control of the diabetes as well as the food intake on serum lipid levels of 73 diabetic outpatients. They had had elevated fasting blood glucose levels, mostly complicated by various grades of hyperlipidemia, before the initiation of treatment. Hyperlipidemia was found to be ameliorated in nearly half of those patients after the start of diabetic treatment. However, the elevation of serum triglyceride persisted in 30 per cent of controlled diabetics, and no differences were found in occurrence of hypertriglyceridemia between diet-treatment group, sulfonylurea group, biguanide group, combined group and insulin group. Estimation of diet intake revealed that the controlled hypertriglyceridemic patients consumed slightly (but significantly) greater amounts of sucrose, alcohol, and total calories than the controlled normotriglyceridemic patients. In addition to such inadequate diet consumptions, the tendency to be overweight and the subtle increment of fasting blood glucose levels were also shown to have contributed to hypertriglyceridemia. It is thus concluded that the lipid disorder in controlled diabetic outpatients is the result of multifactorial influences and that well-conducted diet therapy and stricter regulation of blood glucose are essential in the management of posttreatment hyperlipidemia.
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PMID:Dietary intake and hyperlipidemia in controlled diabetic outpatients. 83 68


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