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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma lipolytic activity (lipoprotein lipase and hepatic lipase), free fatty acids (FFA), triglycerides, cholesterol, and glucose levels were measured in 21 premature infants [gestational age 26-37 weeks (mean +/- SEM 30.4 +/- 0.63 weeks), aged 1-8 days (mean +/- SEM 3.00 +/- 0.35 days)]. All infants were maintained on total parenteral nutrition with heparin (1 U/ml) and were given Intralipid, 1, 2, and 3 g/kg/day, over 15 h on days 1, 2, and 3, respectively. Blood samples were drawn before and at the end of Intralipid administration. Baseline plasma lipolytic activity, before the start of lipid infusion, was 1.54 +/- 0.24 U/ml (1 U = 1 mumol [3H]oleic acid released from tri[3H]olein/h). Lipolytic activity increased after lipid infusion to 4.04 +/- 0.96, 4.32 +/- 0.63, and 6.09 +/- 1.00 U/ml on days 1, 2, and 3 of the study. Hepatic lipase amounted to 38-47% of total lipolytic activity. During the 3 days of lipid infusion, there were dose-dependent increases in plasma FFA, triglyceride, and cholesterol. Whereas FFA and triglyceride concentrations returned to prelipid infusion levels 9 h after stopping the infusion of Intralipid, 1, 2, or 3 g/kg, there was a cumulative increase in plasma cholesterol and glucose concentrations. The close correlation between FFA concentrations and plasma lipolytic activity (r = 0.655, p less than 0.001) suggests considerable intravascular lipolysis. The positive correlation between plasma FFA and triglycerides (r = 0.632, p less than 0.001) and FFA and cholesterol (r = 0.582, p less than 0.001) indicate, however, that intravascular lipolysis does not prevent the lipemia associated with Intralipid infusion to low birth weight infants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Total parenteral nutrition with intralipid in premature infants receiving TPN with heparin: effect on plasma lipolytic enzymes, lipids, and glucose. 312 35

Serum lipoproteins and postheparin plasma lipoprotein lipase and hepatic lipase (HL) activities were determined in 23 hypothyroid women treated with graded doses of thyroxine (T4) (50, 100, and 150 micrograms/day), each given for 3 weeks. Since the sex hormone-binding globulin (SHBG) and thereby serum sex steroid concentrations are sensitive to thyroid status, we also measured serum testosterone, estradiol, and SHBG at each time. Stepwise T4 treatment resulted in gradual improvement in thyroid status. Concomitantly, serum low density lipoprotein (LDL) cholesterol decreased in a linear fashion from a mean of 4.72 +/- 0.31 (+/- SEM) to 3.21 +/- 0.18 mmol/L (P less than 0.001) after the largest dose. In contrast, serum high density lipoprotein (HDL) cholesterol decreased, although not in a dose-dependent fashion, from 1.61 +/- 0.07 to 1.44 +/- 0.05 mmol/L (P less than 0.001) after the largest dose. Serum SHBG increased along with improvement of thyroid function, but this increase did not have major impact on the changes in LDL during T4 treatment, as judged by multiple regression analysis. Thus, serum LDL correlated independently only with T4 (r = -0.38; P less than 0.001). The serum HDL changes were almost exclusively due to those in the HDL2 subfraction, and these were related to HL activity, which increased from 13.4 +/- 1.76 to 18.9 +/- 2.08 U/L after the largest dose. We conclude that thyroid hormones regulated serum HDL (HDL2) cholesterol mainly through their effect on HL.
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PMID:Lipoproteins, lipolytic enzymes, and hormonal status in hypothyroid women at different levels of substitution. 333 9

Twenty six preterm infants were studied at the age of 2, 7, and 26 days. The activities of lipoprotein and hepatic lipase in plasma taken 15 minutes after a heparin bolus of 100 IU/kg had been given and the concentrations of carnitine in serum and urine were measured. The mean gestational age was 31 weeks (range 26-35 weeks) and birth weight 1580 g (range 840-2280 g). Thirteen infants weighed under 1500 g at birth (very low birth weight), 20 were of appropriate weight for gestational age and six were small for gestational age. Lipoprotein lipase activity was higher in the preterm infants of appropriate weight than in the infants of very low birth weight and those who were small for gestational age. At the age of 2 or 7 days the activity of lipoprotein lipase in the preterm infants (mean (SEM) 46.2 (4.3) mumol free fatty acid/ml/hour) was, however, higher than in term infants and adults. Multivariate regression analyses showed that weight and relative birth weight together explained 58% of the variance of lipoprotein lipase activity but only 3% of the variance of hepatic lipase activity. Serum carnitine concentration was lower in the preterm infants than in term infants. Urinary excretion of carnitine increased progressively with age but was independent of serum concentration and carnitine intake. Urinary excretion of total carnitine was significantly greater in the infants who were small for gestational age (mean (SEM) 754 (203) nmol/mg of creatinine, n = 6) than in the infants of appropriate weight (161 (22.0) nmol/mg of creatinine, n = 12) but acyl/free carnitine ratio was smaller in the infants who were small for gestational age than in infants of appropriate weight (0.56 v 5.5). The results indicate that the slow elimination of fat from the circulation in preterm infants less mature than 32 weeks of gestation can hardly be explained by low lipoprotein lipase activity.
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PMID:Lipoprotein lipase, hepatic lipase, and carnitine in premature infants. 334 61

To study postheparin plasma lipase activities in nonfed newborn infants immediately after birth and to investigate the possible influence of fetal hyperinsulinemia on lipoprotein lipase activity, we measured lipoprotein and hepatic lipase activities in 55 macrosomic newborn infants: group I consisted of 21 infants born to mothers with insulin-dependent diabetes. The infants were hyperinsulinemic at birth and had hypoglycemia and poor lipolysis at the age of 2 h. Group II consisted of 18 infants born to mothers with gestational diabetes. Group III consisted of 16 large-for-date infants born to nondiabetic mothers. The mean postheparin plasma lipoprotein lipase activities at 2 h of age were similar (mean 36 mumol free fatty acids/ml/h; SEM 15) in groups I-III. Lipoprotein lipase activity correlated negatively with cord-serum triglycerides (range 0.13-1.2 mmol/liter) but did not correlate with serum insulin (range 5.4-524 microU/ml) or C-peptide (range 0.6-21.0 micrograms/liter). Hepatic lipase activity was somewhat higher in group I (mean 68 mumol free fatty acids/ml/h; SEM 23) than in groups II and III (mean 55 mumol free fatty acids/ml/h; SEM 14). Hemoglobin Alc was the only important factor explaining the difference in hepatic lipase activities between groups. Lipoproteins and apolipoproteins A-I, A-II, and B were similar in all three groups. We conclude that in large-for-date infants lipoprotein lipase is active at birth without exogenous fat induction, and that these infants are capable of hydrolyzing fat, their main source of energy, immediately after birth. In addition, we conclude that postheparin plasma lipoprotein lipase activity is not affected by fetal hyperinsulinemia.
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PMID:Postheparin plasma lipoprotein and hepatic lipase activities in hyperinsulinemic infants of diabetic mothers and in large-for-date infants at birth. 352 12

Ten men with hypogonadism of pituitary origin were studied before and during testosterone substitution therapy with regard to effects on the activities of hepatic lipase (HL) and lipoprotein lipase (LPL) in postheparin plasma, and on plasma lipoprotein concentrations. The mean (+/- SEM) testosterone level increased from 1.8 +/- 0.5 to 16.3 +/- 2.4 nmol/l. The mean activity of HL rose from 327.1 +/- 35.2 to 432.8 +/- 57.2 mU/ml (p less than 0.02), while the activity of LPL did not change significantly, 71.0 +/- 9.1 mU/ml before and 62.2 +/- 3.8 mU/ml after treatment. No significant alterations in lipoprotein concentrations were recorded. These results indicate that a normal testosterone level is of importance for maintaining the activity of HL in men, thereby contributing to the sex difference previously recorded for HL activity.
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PMID:Increase in hepatic lipase activity after testosterone substitution in men with hypogonadism of pituitary origin. 360 52

Post-heparin plasma lipoprotein lipase activity was measured in 28 cancer patients with varying degrees of weight loss, and in 16 normal volunteers. Total lipoprotein lipase activity was decreased by 35.4% (P less than 0.001) in the cancer group. The component lipase activities, hepatic (HLPL), and peripheral (PLPL), were decreased by 40% (P less than 0.001) and 38% (P less than 0.005) respectively. In addition, the level of total peripheral lipoprotein lipase correlated well with the percent body weight lost by these patients (r = 0.6, P less than 0.01). Regardless of extent of disease, patients with lung cancer showed the lowest enzyme activity (mean 191 mU/ml +/- 30 SEM, P less than 0.001) and the greatest percent of weight loss (mean 16%), while patients with breast cancer had nearly normal lipase activity (mean 315 mU/ml +/- 50 SEM, normal 340 mU/ml +/- 22 SEM, P less than 0.10) and minimal weight loss (mean 8.4%). Fasting serum triglycerides were significantly elevated in the patient group (mean 120 mg/dl +/- 9.7 SEM) as compared to normal (mean 71 mg/dl +/- 7 SEM, P less than 0.001). The mean fasting insulin level was elevated in the patient group (13 mU/ml +/- 3.0 SEM), although in the majority of the patients it was found within the normal range (4-24 mU/ml). We conclude that the significant decrease in the total LPL activity may be responsible in part for the characteristic hypertriglyceridemia present in cancer patients.
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PMID:Reduced plasma lipoprotein lipase activity in patients with malignancy-associated weight loss. 378 75

Normal rats fed an isocaloric sucrose-rich diet (SRD) for 3 weeks developed high levels of triacylglycerol in plasma (P) (mmol triacylglycerol I-1) heart (H) and liver (L) tissues (mumol triacylglycerol mg DNA-1) as compared to control rats fed the standard chow (STD) (X +/- SEM; P: SRD 1.32 +/- 0.06 vs STD 0.49 +/- 0.05, P less than 0.001; H: SRD 2.1 +/- 0.17 vs STD 0.94 +/- 0.01, P less than 0.001; L: SRD 8.48 +/- 1.47 vs STD 1.71 +/- 0.12, P less than 0.001). A simultaneous drop in the activities (mumol glycerol ml-1 hr-1) of several plasma post heparin lipolytic enzymes was observed; total triglyceride lipase (T-TGL): SRD 5.32 +/- 0.34 vs STD 7.48 +/- 0.64, P less than 0.01; lipoprotein lipase (LPL): SRD 1.61 +/- 0.26 vs STD 2.42 +/- 0.41, P less than 0.05; hepatictriglyceride lipase (H-TGL): SRD 3.71 +/- 0.28 vs STD 5.05 +/- 0.69, P less than 0.05 and monoglyceride hydrolase (MGH) (mumol glycerol I-1 min-1): SRD 558 +/- 108 vs STD 1165 +/- 45, P less than 0.001. Rats fed the SRD presented glucose intolerance after i.v. glucose (Kg X 10(-2); 1.06 +/- 0.09 vs 2.61 +/- 0.14 of STD, P less than 0.001) in spite of the presence of hyperinsulinism (sigma plasma IRI microU/ml from 0 to 30 min: 184.6 +/- 23.6 vs 100.5 +/- 9.7 of STD, P less than 0.01) suggesting that a state of insulin resistance had developed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of tiadenol and clofibrate on plasma post heparin lipolytic hepatic, extrahepatic and monoglyceride hydrolase activities in rats with hypertriglyceridemia induced by a sucrose rich diet. 400 66

We have previously reported that normal Wistar rats fed an isocaloric, sucrose-rich (63%) diet (SRD) developed glucose intolerance and elevated triglyceride levels in plasma as well as in heart and liver tissue. This metabolic state was accompanied by hyperinsulinism both in vivo and in vitro, suggesting that a state of insulin resistance has developed. The aim of this study was to gather information on the various plasma post-heparin lipolytic activities in rats fed a SRD. Hepatic triglyceride lipase (H-TGL) was evaluated by both, protamine sulfate inhibition (PSI) of extrahepatic lipoprotein lipase (LPL) and heparin-Sepharose affinity chromatography (H-SAC). Both methods rendered comparable results. Total triglyceride lipase (T-TGL) was measured after Krauss et al. and monoglyceride hydrolase (MGH) after Vogel et al. Our results have shown a significant decline of plasma T-TGL (5.32 +/- 0.34 means +/- SEM vs. 7.48 +/- 0.64 mumol glycerol ml-1 h-1; p less than 0.01), H-TGL (3.71 +/- 0.28 vs. 5.05 +/- 0.69; p less than 0.05), LPL (1.61 +/- 0.26 vs. 2.42 +/- 0.41; p less than 0.05) and MGH (558 +/- 108 mumol glycerol l-1 min-1 vs. 1,165 +/- 45; p less than 0.001) activities. Thus, feeding a sucrose-rich diet induced a state of hyperlipemia and insulin resistance in which not only plasma T-TGL but also H-TGL and MGH activities were significantly decreased. This suggests that the latter two enzymes are also under nutritional and/or hormonal control.
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PMID:Post-heparin plasma hepatic triglyceride lipase and monoglyceride hydrolase activities in hyperlipemia induced by a sucrose rich diet. 661 28

Seven men took part in a study in which the diet was changed from an ordinary mixed one to a fat-rich diet [greater than 70% energy (E)] for 3 days followed by a carbohydrate-rich diet (greater than 70% E) for 3 days. Blood was drawn and muscle biopsies [for analysis of lipoprotein-lipase (LPL) activity] were taken before the study and at the end of each diet period. Insulin, apolipoprotein (apo) B, A-I and A-II, cholesterol and triglyceride concentrations were determined in serum and the lipids also in the high density lipoproteins (HDL). Serum insulin was higher (p less than 0.01) during the carbohydrate-rich diet than during the fat-rich diet (12.0 +/- 0.9 vs. 7.5 +/- 0.5 microunits/l, mean +/- SEM), as were serum-triglycerides (2.42 +/- 0.27 vs. 0.98 +/- 0.07 mmole/1, p less than 0.001). Muscle LPL activity, on the other hand, was lower (p less than 0.01), 27.3 +/- 6.1 vs. 75.1 +/- 13.2 microunits/g. HDL-cholesterol was 1.22 +/- 0.08 during the carbohydrate-rich diet which was lower (p less than 0.01) than during the fat-rich diet, 1.45 +/- 0.11. The concentration of apo A-I and A-II did not vary significantly. It is suggested that the increased insulin concentrations during a short-term, carbohydrate-rich diet may have a down-regulating effect on muscle LPL activity. Low muscle LPL activity may account for part of the elevation of serum triglycerides. An ineffective hydrolysis of VLDL-triglycerides may contribute to the variation in HDL-cholesterol concentration seen under these circumstances.
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PMID:Decrease of lipoprotein lipase activity in skeletal muscle in man during a short-term carbohydrate-rich dietary regime. With special reference to HDL-cholesterol, apolipoprotein and insulin concentrations. 675 38

Human and guinea-pig placental activity was measured in tissue extracts and in medium in which tissue fragments have been incubated. Lipase activity was estimated from measured rates of release of 3H-labelled fatty acids from a 3H-labelled triacylglycerol substrate. Whole tissue lipase activity was 1.6 +/- 0.3 units/g (mean +/- SEM, mumol of unesterified fatty acid release/min) in the human, and 87.1 +/- 7.3 units/g in guinea-pig placental tissue. 70% of the human and 56% of the guinea-pig placental activity was lost on treating the tissues with cold acetone. Sodium chloride (0.75 M) decreased activity by 50% in extracts from both species. Lipase activity was released into media when placental fragments were incubated. The addition of heparin increased the release of lipase from human placenta but not significantly from that of the guniea-pig. Insulin had no effect on placental lipase activity from either species. It is concluded that the placentas of both species contain at least two lipases. One of these, which constituted a large of the total, had the characteristics of lipoprotein lipase.
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PMID:Lipoprotein lipase activity in human and guinea-pig placenta. 714 75


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