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

The effect of two synthetic heparinoids, SP-54 and Depot-Thrombocid, on serum lipids was studied in 17 patients with primary hyperlipidaemia (types IIb, IV and V of Fredrickson) and 15 healthy persons. SP-54 had no lipid-lowering effect, neither on oral nor rectal suppository application. Intramuscular injection of Depot-Thrombocid, however, resulted in a decrease of serum triglyceride concentrations of maximally 50% after six hours. There was a marked increase in the activity of the two lipolytic enzymes, lipoprotein lipase and hepatic triglyceride lipase in plasma, as well as an increase in free fatty acids and an extension of thrombin time and PTT. Twenty-four hours after injection all values returned to pretreatment levels. Intramuscular administration of Depot-Thrombocid two or three times a week for seven weeks had no lasting effect on serum lipids. However, there were considerable side effects such as haemorrhagic diatheses, hair loss and thrombocytopenia.
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PMID:[Mechanism of action of synthetic heparinoids: results in patients with hypertriglyceridaemia (author's transl)]. 7 86

Labeled chylomicrons in thoracic duct lymph were collected after test meals containing 14C cholesterol and 2-3H glyceryl trioleate and were given by intravenous injection to groups of control rats, rats made diabetic by treatment with streptozotocin, and rats made hypothyroid and hypercholesterolemic by a diet containing cholesterol, peanut oil, cholic acid, and thiouracil. In the diabetic rats clearances from the plasma of chylomicron triacylglycerol and cholesteryl ester were impaired. A large variability in triacylglycerol clearance in diabetic rats was ascribed to variability in plasma triacylglycerol concentrations. Adipose tissue lipoprotein lipase activity was not impaired in the female diabetic rats used in this study. In the hypothyroid hypercholesterolemic rats chylomicron cholesteryl ester clearance from the plasma was impaired but chylomicron triacylglycerol was cleared efficiently, and adipose tissue lipoprotein lipase activity was similar to or greater than activity in controls. Ten minutes after intravenous injection most plasma radioactivity was recovered in lipoproteins of density less than 1.006 g/ml in all groups of rats, but relatively more was recovered at this density in both treatment groups. We suggest that chylomicron remnants accumulate in the plasma and contribute to the development of hyperlipemia in both treatment groups, but that the remnants formed in the diabetic rat are less depleted of triacylglycerol than the remnants formed in the hypothyroid hypercholesterolemic rat. It is suggested that factors other than measured lipoprotein lipase activities of adipose tissues may be important in determining the initial extent of hydrolysis of chylomicron triacyglycerol. We propose that the hypercholesterolemic hypothyroid rat is a useful model for the experimental production of the remnants of triacylglycerol-rich primary lipoproteins.
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PMID:Clearance of chylomicron triacylglycerol and cholesteryl ester from the plasma of streptozotocin-induced diabetic and hypercholesterolemic hypothyroid rats. 13 29

In order to elucidate the mechanism(s) of hyperlipidemia following glucocorticoid administration, dexamethasone (0.125 mg/Kg) was administered daily intramuscularly for 2 wk to male Sprague-Dawley rats and the effects on plasma triglyceride (TG) and cholesterol (Chol), lipoprotein neutral lipids, hepatic triglyceride secretion rates (TGSR; Triton), and epididymal fat lipoprotein lipase (LPL) were determined. Special measures were taken to maintain positive caloric balance and keep the weights of control and dexamethasone-treated animals comparable. Significant increases (p less than 0.001) in TG and very-low density lipoprotein (VLDL) triglyceride associated with no change in Chol and actual reduction in both triglyceride and cholesterol in low density lipoprotein (ldl) were observed in the steroid-treated animals. Dexamethasone treatment was associated with increased basal insulin and glucose levels, an insignificant increment in TGSR, and a highly significant reduction (p less than 0.001) in LPL. These findings suggest that glucocorticoid treatment increases splanchnic triglyceride production rates, but the resulting hypertriglyceridemia is primarily a consequence of impaired VLDL removal due to low adipose tissue LPL activity.
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PMID:Glucocorticoids and triglyceride transport: effects on triglyceride secretion rates, lipoprotein lipase, and plasma lipoproteins in the rat. 17 40

A subnormal activity of postheparin plasma hepatic lipase was demonstrated in nine of 16 patients with familial type II hypercholesterolemia. On the other hand, in patients with combined hyperlipidemia (type II b) the hepatic lipase activity was mostly in upper normal range. The postheparin plasma lipoprotein lipase activity was normal in both patient groups. It is suggested that the low hepatic lipase activity may have a role in the patholgenesis of one form of familial hypercholesterolemia.
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PMID:Low postheparin plasma hepatic lipase activity in familial type IIa hyperlipoproteinemia. 18 Aug 67

There are several causes for hyperlipemia in the diabetic: (a) an increase in hepatic synthesis of prebetalipoproteins, and (b) reduced elimination of prebetalipoproteins and chylomicrons from the bloodstream, due to diminished activity of lipoprotein lipase in insulin deficiency. The role of heredity has been put in doubt by the observation that diabetes and hypertriglyceridemia are not transmitted by the same genetic factor. The shortterm and longterm implications of diabetic hyperlipemia are discussed, together with the treatment.
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PMID:[Hyperlipemia and diabetes]. 18 65

The activity of two triglyceride lipases was determined by an immunochemical method in the postheparin plasma of 60 diabetic patients and of 47 age- and sex-matched nondiabetic control subjects. The results were related to the type of diabetes, to plasma triglyceride and insulin concentrations, to removal of exogenous fat from the blood, and to turnover of VLDL-triglycerides . The mean postheparin plasma lipoprotein lipase (LPL) activity was decreased by 44 per cent (p less than 0.001) in patients with untreated ketotic diabetes and by 20 per cent (p less than 0.01) in patients with untreated mild to moderate nonketotic early-onset diabetes. Insulin treatment of ketotic diabetes resulted in a rapid increase in the activity of LPL and decrease in serum triglycerdie level, whereas sulfonylurea treatment of non-insulin-requiring diabetics did not significantly influence the enzyme activity. In insulin-treated chronic diabetics the average postheparin plasma LPL activity was not different from that of nondiabetic controls, but some of these patients had high LPL values. In normolipidemic maturity-onset-type diabetics the LPL activity was within normal range, but in those having hypertriglyceridemia the average LPL value was decreased by an average of 26 per cent (p less than 0.01). The LPL activity showed a significant negative correlation with the logarithm of serum triglyceride concentration (r = -0.62) and a positive correlation with fractional removal of Intralipid (r = +0.64) and fractional turnover of V triglyceride (r = +0.40). The activity of LPL was correlated to basal plasma insulin concen tration in the insulin-deficient diabetes r = +0.34) but not in patients with maturity-onset-type diabetes. The hepatic lipase (HL) activity of postheparin plasma was similar in diabetes and controls, with the exception of hypertriglyceridemic maturity-onset diabetics, who had higher mean HL activity than the corresponding control group (p greater than 0.01). The activity of HL was not related to triglyceride removal but showed a significant correlation to VLDL-triglyceride production rate. On the basis of these results it seems that a deficiency of LPL accounts for a great deal of the elevation of serum triglyceride in insulin-deficient human diabetes but has a smaller role in the pathogenesis of the hypertriglyceridemia that is associated with maturity-onset diabetes. The latter abnormality is caused mainly by an increased secretion of triglycerides into the blood even though a decreased LPL may contribute to development of hyperlipemia in cases with gross elevation of serum triglycerides.
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PMID:Postheparin plasma lipoprotein lipase and hepatic lipase in diabetes mellitus. Relationship to plasma triglyceride metabolism. 18 16

Primary type V hyperlipoproteinemia was identified in two preadolescent children. The propositus (kindred N) was a 10-year-old girl with severely creamy plasma, lipemia retinalis, hypertriglyceridemia (triglyceridelevel, 6,800 mg/100 ml), and ypercholesterolemia (cholesterol level, 490 mg/100 ml). Her parents and an 8-year-old sister all had endogenous hypertriglyceridemia (type IV hyperlipoproteinemia). In kindred A, an 11-year-old boy had triglyceride levels as high as 1,100 mg/100 ml and recurrent abdominal pain. His father had type V hyperlipoproteinemia; his mother was normal. All three of his older teenage siblings had type IV hyperlipoproteinemia. The enzymatic activities of lipoprotein lipase (LPL), hepatic triglyceride lipase (HTL), and histaminase (H) were studied in postheparin plasma. The LPL level was low in the children and both parents in kindred N. LPL level in kindred A was normal, except for one child with type IV hyperlipoproteinemia. HTL level was normal to above normal in both kindreds. Most patients had a normal H level, but one parent (kindred N) had no preheparin H and very low levels of postheparin H. There was a strong correlation (r = 0.58, significant at less than 1% level) between release of LPL and H but not between HTL and H (r= 0.22). The mean (+/- 1 S.D.) levels of the enzymes were as follows: LPL, 2.8 +/- 0.7 micronmol/ml/hr in kindred N and 5.4 +/- 2.2 micronmol/ml/hr in kindred A; H, 13.4 +/- 6.8 units/ml in kindred N and 22.0 +/- 11.9 units/ml in kindred A; and HTL, 18.0 +/- 7.1 micronmol/ml/hr in kindred N and 14.9 +/- 6.3 micronmol/ml/hr in kindred A. The enzymatic activities of kindreds N and A were significantly different for LPL (P less than .001) and H (.025 less than P less than .05) but not for HTL. All but one child had at least one high insulin level, which was accompanied by hyperglycemia in two children. The hypertriglyceridemia in all but one child was ameliorated on therapeutic diets. These data suggest that the genetic basis of the hypertriglyceridemia in these two families is different and that hyperchylomicronemia in childhood is not confined to the rara type I hyperliporproteinemia.
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PMID:The clinical, biochemical, and familial presentation of type V hyperlipoproteinemia in childhood. 19 90

A system for classification of genetic and acquired forms of hyperlipidemia in humans based on lipoprotein physiology is described. Most hyperlipidemia can be accounted for by defects in one of four sites of physiologic regulation: (1) triglyceride-rich lipoprotein production, (2) lipoprotein lipase-mediated triglyceride catabolism, (3) remnant lipoprotein catabolism, and (4) extrahepatic cholesterol-rich lipoprotein catabolism.
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PMID:Pathophysiology of lipoprotein transport. 21 Mar 52

The mechanism of hyperlipidaemia in the nephrotic syndrome has not been fully established. We propose that it results from hypoalbuminaemia due to inhibition of the reaction catalysed by lecithin cholesterol acyltransferase converting cholesterol of high density lipoproteins to cholesterol esters and to an inhibition of high density lipoprotein particle formation from very low density lipoproteins due to reduced activity of lipoprotein lipase.
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PMID:The mechanism of hyperlipidaemia in the nephrotic syndrome. 23 35

The aim of this study was to discover which of three major abnormalities of the genetically obese Zucker rat (fa/fa), namely hyperphagia, excess adiposity, and hyperlipidemia, is the first to appear prior to manifest obesity, i.e., before weaning. Suckling fa/fa rats, bred from heterozygous parents, were detected by sizing fat cells obtained from an inguinal fat pad biopsy. Cell hypertrophy was observed in fa/fa rats, compared to Fa/-littermates of the same sex, as soon as 5-7 days after birth. Prediction of fa/fa genotype at this age by this method was assessed using a series of 80 pups and proved to be totally successful. The identity of the "predicted" obese pups was confirmed morphologically at 6 weeks of age. Food (milk) intake was estimated from water turnover rates determined on 86 pups aged 2-8 days using tritiated water. The results show that 7-day-old fa/fa rats had heavier inguinal fat pads with larger adipocytes and higher lipoprotein lipase activity than their lean controls. There was no genotype effect on water intake adjusted to body weight during the first week of life. Moreover weight of stomach contents and triglyceridemia were similar in all animals at 7 days. These results show that excess adiposity develops in the fa/fa rat during the first week of life, before hypertriglyceridemia and hyperphagia, and raises the question of whether this adiposity results from a defect in energy expenditure or an abnormality of fat cell storage capacity, or both.
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PMID:Onset of genetic obesity in the absence of hyperphagia during the first week of life in the Zucker rat (fa/fa). 29 Jul 21


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