Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.34 (lipoprotein lipase)
7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of hormone administration on the activity of lipoprotein lipase in the lung was studied in the rat. The following hormones were administered: dexamethasone, L-thyroxine, estradiol-17beta and progesterone. In addition, lung lipoprotein lipase activity was studied in diabetic and lactating rats. Lipoprotein lipase activity was measured in dried, defatted preparations of rat lung using double labeled ([14C]palmitate, [3H]glycerol) chylomicron triacylglycerol as substrate. Dexamethasone administration caused a rise of 70% in the level of activity of lipoprotein lipase in acetone powders of lung and a 100% increase in the amount of enzyme released during heparin infusion into isolated, perfused lungs. Enzyme activity was higher in lungs of females than of male rats; however; the level of activity was unaffected by estrogen or progesterone administration to either male or ovariectomized rats. Diabetes, hyperthyroidism or lactation did not change lipoprotein lipase activity in the lung. The constant presence of lipoprotein lipase activity in the lung suggests that this organ is able to maintain a steady supply of triacylglycerol-fatty acids under a variety of physiological and pathological conditions. Stimulation of enzyme activity by dexamethasone could lead to increased uptake of triacylglycerol-fatty acids by the lung and may thus be a contributing factor to corticosteroid-induced enhanced surfactant synthesis.
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PMID:Lipoprotein lipase in rat lung. Effect of dexamethasone. 13 65

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

The mechanisms by which insulin and glucocorticoids modulate lipoprotein lipase (LPL) synthesis and degradation were examined in human adipose tissue fragments maintained in organ culture. Tissue fragments were cultured for 7 days in serum-free medium supplemented with or without insulin (7 nM) and with or without dexamethasone (30 nM), a synthetic glucocorticoid. Responses of LPL activity to both insulin and dexamethasone were obtained at doses within the physiological range. At a maximal dose, insulin increased heparin-releasable and total LPL activity (approximately 7-fold) by specifically increasing the rate of LPL synthesis (approximately 5-fold) determined by pulse labeling with [35S]methionine and [35S]cysteine and immunoprecipitation. Dexamethasone added in the presence of insulin increased heparin-releasable and total LPL activity approximately 8-fold but did not alter rates of LPL synthesis compared with insulin alone. Pulse-chase studies showed that the rate of LPL degradation was markedly slowed in the presence of dexamethasone plus insulin compared with insulin alone. These data suggest that, in human adipose tissue, insulin is essential for maintaining rates of LPL synthesis and that cortisol may play a key role in regulating human adipose tissue LPL at the posttranslational level by inhibiting the degradation of newly synthesized LPL.
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PMID:Effects of insulin and dexamethasone on lipoprotein lipase in human adipose tissue. 159 Mar 79

The effect of macrophage differentiation agents on lipoprotein lipase (LPL) secretion by macrophages at different stages of differentiation/maturation was investigated. Phorbol myristate acetate (TPA) had an augmenting effect on LPL secretion by in vitro-derived bone marrow macrophages (BMMs), thioglycollate-elicited peritoneal macrophages (TgM phi), and resistant macrophages. Augmentation was time dependent and reached approximately two-fold and approximately threefold increase over control cells within 16 and 96 hr, respectively. TPA did not affect LPL secretion from J774.1 cells treated with the agent for 16-72 hr. L-cell conditioned medium (L-CM), a source of macrophage colony-stimulating activity, augmented LPL secretion by BMMs and Tg-M phi, and when added together with TPA had an additive augmenting effect on LPL secretion in these cells. Retinoic acid (RA) exerted a time-dependent suppressive effect on LPL secretion by BMMs (46% within 16 hr and 83% within 6 d), had a relatively small effect on secretion from J774.1 cells (approximately 20% in 72 hr) and had no effect on LPL secretion by Tg-M phi. Dexamethasone suppressed LPL secretion by BMMs, Tg-M phi, and J774.1 cells. Optimal suppression of LPL secretion by BMMs required more than 24 hr. Thus, TPA and L-CM, agents that exert a mitogenic effect on BMMs and Tg-M phi, augmented the secretion of LPL in these cell types, and RA and dexamethasone, agents which induce differentiation patterns in myeloid cells, suppressed LPL secretion.
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PMID:Control of lipoprotein lipase secretion by macrophages: effect of macrophage differentiation agents. 229 53

The effects of insulin and dexamethasone on the secretion of lipoprotein lipase (LPL) by mouse peritoneal macrophages were examined in vitro. Macrophages from either normal or thioglycollate-primed mice continuously secreted LPL into the culture medium. The time courses and the amounts of enzyme secretion and the responses to the hormones were essentially the same in resident or thioglycollate-primed macrophages. Insulin did not enhance the secretion of this enzyme by macrophages, even though a marked effect of this hormone on the enzyme in adipose tissue has been well established. Dexamethasone, which has been reported to stimulate the secretion of LPL in the heart, suppressed the secretion of LPL by macrophages. The present study is the first report to deal with the effect of hormones on the secretion of LPL by macrophages, and clearly demonstrates that insulin does not play an important role in the regulation of LPL activity in macrophages. Dexamethasone also showed a different effect on macrophage LPL compared to that on the enzyme in other tissues. This difference in the regulation of LPL may be relevant to the possibly different role of this enzyme in macrophages as compared to other tissues such as adipose tissue, muscle, or heart.
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PMID:Lipoprotein lipase in mouse peritoneal macrophages: the effects of insulin and dexamethasone. 354 81

Dexamethasone was administered by continuous subcutaneous infusions (16 microgram/kg/h) to pregnant rats from day 16 of gestation. Administration of the hormone markedly affected maternal and fetal weight gain, fetal lung:body weight ratio and lipoprotein lipase activity of the lung. Cumulative maternal weight gain from days 15-21 of gestation was 80 +/- 4.0 g in control and 30 +/- 10 g in dexamethasone-treated rats. Fetal weight at 22 days of gestation and 1 day after birth was 5.5 +/- 0.39 and 8.6 +/- 0.30 in control and 4.65 +/- 0.26 and 5.9 +/- 0.34 in dexamethasone-treated rats. The ratio of lung weight to body weight was lower throughout the last 5 days of gestation in dexamethasone-treated than in control rats. Dexamethasone administration led to a 2- to 3-fold increase in lipoprotein lipase activity levels in fetal rat lung at 19 and 20 days' gestation and prevented the decline in enzyme activity shortly before birth. Stimulation of fetal lung lipoprotein lipase activity suggests that increased uptake of triglyceride-fatty acids by the lung could be a contributory factor to corticosteroid-enhanced surfactant synthesis.
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PMID:Effect of dexamethasone on lipoprotein lipase activity of fetal rat lung. 728 97

An in vitro system was used to study the regulation of lipoprotein lipase (LPL) activity in bovine adipose tissue. The utilization of two energetic and lipogenic substrates, acetate and glucose, and the activity of glucose-6-phosphate dehydrogenase (G6PDH), an enzyme involved in de novo lipogenesis, were also studied. Nine nonlactating, nonpregnant Holstein cows were given limited amounts of feed for 10 d, then they were overfed for 3 to 5 wk. Samples of perirenal adipose tissue were incubated for 24 or 48 h. Insulin (2 mU/mL) increased (P < .001) daily glucose and acetate utilization and attenuated (P < .001) the loss of G6PDH activity detected after 1 or 2 d of incubation. Dexamethasone (DEX, 10 nM) added to the insulin-supplemented medium decreased (P < .02) glucose utilization, but it did not change acetate utilization or G6PDH activity. A higher concentration of DEX (100 nM) potentiated (P < .004) the ability of insulin to attenuate the decrease in G6PDH activity without changing substrate utilization. Under basal conditions, LPL activity was decreased by approximately 66% after 2 d of incubation. The decline in LPL activity was attenuated by insulin addition (P < .02) and was further attenuated (P < .004) by 100 nM of DEX. The addition of 10% fetal bovine serum alone to the medium had no effect on LPL activity, and fetal bovine serum decreased this activity when it was added to the insulin-supplemented medium.
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PMID:Lipoprotein lipase and metabolic activities in incubated bovine adipose tissue explants: effects of insulin, dexamethasone, and fetal bovine serum. 813 88

There are marked variations in the activity of lipoprotein lipase (LPL) among adipose depots, particularly in women. Consistent with data on LPL activity, the level of expression of LPL mRNA was lower in omental (OM) than subcutaneous (SQ) adipose tissue of women. To investigate the cellular basis of these differences, OM and SQ adipose tissues obtained at surgery from obese men and women were placed in organ culture for 7 d with varying concentrations of insulin and dexamethasone. Insulin increased levels of LPL mRNA and LPL activity in abdominal SQ but not OM adipose tissue. Dexamethasone also increased LPL mRNA and LPL activity, and these effects were more marked in the OM adipose tissue, particularly in men. When insulin and dexamethasone were added together, synergistic increases in LPL activity were seen in both depots, and this was in part explained at the level of LPL mRNA. The SQ depot was more sensitive to the effects of submaximal doses of dexamethasone in the presence of insulin. The maximum activity of LPL induced by insulin or insulin plus dexamethasone was higher in the SQ than in the OM depot of women, and this was associated with higher levels of LPL mRNA. Rates of LPL synthesis paralleled LPL mRNA levels. These data show that insulin and glucocorticoids influence human adipose tissue LPL activity at the level of LPL gene expression, as well as posttranslationally, and that responsiveness to these hormonal effects is dependent on adipose depot and gender.
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PMID:Lipoprotein lipase regulation by insulin and glucocorticoid in subcutaneous and omental adipose tissues of obese women and men. 822 34

The in vitro regulation of lipoprotein lipase (LPL) and glucose-6-phosphate dehydrogenase (G6PDH) activity in bovine and ovine adipose tissue was investigated. Adult non-lactating non-pregnant cows (n = 5) or ewes (n = 5) were given limited amounts of feed for 8 or 10 days and then overfed for 10 (ewes) or 21 (cows) days. Perirenal adipose tissue explants were incubated for 2, 4 or 7 days. Regardless of the experimental conditions, the activity of LPL and G6PDH after 2 days of incubation was lower than in fresh tissue. Insulin significantly increased LPL activity in bovine but not in ovine adipose tissue, and it had no effect on G6PDH activity in the two species. Dexamethasone addition to the insulin-supplemented medium significantly increased LPL activity in ovine adipose tissue, whereas it was decreased in bovine adipose tissue on days 4 and 7. Moreover, dexamethasone addition to the insulin-supplemented medium did not change G6PDH activity in the two species on day 2, whereas it was increased in bovine and ovine adipose tissue on days 4 and 7. Therefore, the effects of insulin and/or dexamethasone on LDL and G6PDH differed with ruminant species and incubation time.
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PMID:Lipoprotein lipase and glucose-6-phosphate dehydrogenase activities in bovine and ovine adipose tissue incubated for 7 days: effects of insulin and/or dexamethasone. 865 94

Expression of the ob gene and production of leptin have been examined on differentiation of rat fibroblastic preadipocytes to adipocytes in primary culture. Preadipocytes were obtained from the inguinal fat pad of suckling rats, and following differentiation the cells contained lipid droplets and the mRNAs for both lipoprotein lipase and adipsin were detected by Northern blotting. ob mRNA was not, however, detected on Northern blots, but analysis by RT-PCR indicated that the ob gene was expressed, particularly after differentiation. Measurement of leptin in the culture medium by ELISA showed that the ob gene product was secreted by adipocytes from approximately 4 days after the induction of differentiation. Leptin production was sustained over a 2-week period with a peak at 8-10 days post-induction. Dexamethasone stimulated leptin production, while an inhibition was observed with the beta-adrenoceptor agonist isoprenaline. These results demonstrate that following the differentiation of fibroblastic preadipocytes to adipocytes in primary culture, leptin is secreted with the cells responding to stimuli which regulate production of the hormone.
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PMID:ob gene expression and secretion of leptin following differentiation of rat preadipocytes to adipocytes in primary culture. 901 84


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