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 effects of several prostaglandins on lipoprotein lipase activity of mammary gland and adipose tissue and serum triacylglycerol were studied during late pregnancy in rats. Prostaglandins were injected twice daily for 2 days before and once on the day of analysis. In rats pregnant 20 days, prostaglandin F(2alpha) (PGF(2alpha)) increased the activity of lipoprotein lipase in mammary gland fourfold, reduced the activity in adipose tissue about 60%, and decreased serum concentration of triacylglycerol 50%. PGF(2alpha) also reduced serum concentration of progesterone 90% and increased that of prolactin fivefold, but had no effect on serum concentrations of either immuno-reactive insulin or 17beta-estradiol. Injections of 13,14-dihydro-15-keto PGF(2alpha), a metabolite of PGF(2alpha), had similar effects in rats pregnant 20 days, whereas prostaglandins E(1) and E(2) did not. In rats pregnant 16 days, PGF(2alpha) did not affect lipoprotein lipase activity in the tissues or the concentration of triacylglycerol and prolactin in serum, although it decreased serum progesterone 80%.2-Br-alpha-ergocryptine prevented the increase in serum prolactin in response to PGF(2alpha), but did not alter the effect of PGF(2alpha) on lipoprotein lipase activity or serum triacylglycerol. Progesterone completely blocked the effects of PGF(2alpha) on lipoprotein lipase activity and serum triacylglycerol and prolactin concentrations. These findings indicate that the changes in lipoprotein lipase activity and serum triacylglycerol in PGF(2alpha)-treated rats are probably related to the inhibitory action of PGF(2alpha) on progesterone secretion. They also suggest that endogenous F prostaglandins may play a role in the regulation of lipoprotein lipase activity in mammary gland and adipose tissue near parturition.
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PMID:Regulation of mammary and adipose tissue lipoprotein lipase and blood triacylglycerol in rats during late pregnancy. Effect of prostaglandins. 89 73

The effect of 17beta-estradiol or progesterone administration on adipose tissue lipoprotein lipase activity was studied in male and ovariectomized female rats. Lipoprotein lipase activity was measured in acetone-ether-extracted preparations of adipose tissue with doubly labeled (14C-fatty acid, 3H-glyceryl) chylomicron triglyceride as substrate. Administration of 17beta-estradiol to male rats lowered adipose tissue lipoprotein lipase activity from 8.22 plus or minus 1.8 U/g (1 U = 1 mumol triglyceride hydrolyzed per h) to 4.96 plus or minus 0.5 U/g in the treated group. Ovariectomy increased adipose tissue lipoprotein lipase activity from 10.4 plus or minus 1.8 U/g in controls to 22.7 plus or minus 4.3 U/g. 17beta-Estradiol administration to ovariectomized rats cuased a marked fall in adipose tissue lipoprotein lipase activity: 17beta-estradiol (2.5 mug/day) lowered the enzyme activity to 9.00 plus or minus 1.2 U/g, whereas 25 mug/day further decreased lipoprotein lipase activity to 3.2 plus or minus 0.6 U/g. Blood triglyceride levels increased from 0.8 plus or minus 0.05 mumol/ml in ovariectomized rats to 1.4 plus or minus 0.09 mumol/ml in 25 mug/day 17beta-estradiol-treated rats. Progesterone administration did not affect adipose tissue lipoprotein lipase activity in either male or ovariectomized rats. Heart and lung lipoprotein lipase activity was unaffected by hormone treatment. We suggest that the rise in blood triglyceride concentrations, which accompanies high palsma estrogen levels, could be due to the marked inhibition of adipose tissue lipoprotein lipase activity.
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PMID:The effect of estrogen on the lipoprotein lipase activity of rat adipose tissue. 112 25

Lipolytic activity measured at pH 8.6 in bovine corpora lutea exhibited classical properties of lipoprotein lipase (LPL) in terms of serum and heparin stimulation and NaCl inhibition. LPL activity was measured in 23 corpora lutea collected at different stages of the estrous cycle and early pregnancy. The LPL activity in cyclic corpora lutea (mumole FA released/hr/100 mg acetone powder) was low at Days 4-8 of the estrous cycle (3.1 +/- 1.5: mean +/- SE) and at Days 19-20 (1.6 +/- 0.6). However, high activity of the enzyme was found at Days 12-15 of the cycle (11.8 +/- 1.8); these concentrations were significantly (P less than 0.01) elevated over those found at Days 4-8 and 19-20. The enzyme activity began to decline at Days 16-18 of the estrous cycle (5.1 +/- 1.7). Low enzyme activity was found in the corpora lutea removed from two cows at Day 22 of pregnancy. Progesterone concentrations were measured in 16 of the 23 corpora lutea and a good correlation (r = 0.75, P less than 0.01) was found between lipoprotein lipase and progesterone concentrations of the tissue. The data suggest that LPL may be involved in controlling the transfer of fatty acids, including arachidonic, from plasma lipoproteins to luteal tissue.
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PMID:Lipoprotein lipase activity in the bovine corpus luteum during the estrous cycle and early pregnancy. 126 48

Recently, it was shown that lipoprotein lipase (LPL) was produced in neonatal but not in adult rat liver. In an attempt to further define the mechanism involved in liver LPL expression, we identified a neonatal mouse hepatoma cell line, BWTG3, capable of producing LPL. The regulation of LPL expression by various extracellular stimuli was investigated in this cell line. Progesterone caused a rise in LPL production by BWTG3 cells. Other hormones tested, such as insulin, glucagon, adrenalin, testosterone, and thyroid hormone, had no effect on LPL production. The effects of progesterone on LPL production showed slow kinetics reaching a maximum 24 h after addition. Cotransfection of a progesterone receptor expression vector with a 5'-LPL-CAT reporter construct resulted in an induction of CAT activity, suggesting that the increase in LPL accumulation after progesterone was linked to transcriptional induction of the LPL gene. Stimuli causing an elevation of protein kinase A activity in the cells also increased LPL production. Three agents capable of elevating intracellular cAMP levels, i.e., forskolin, dBcAMP, and choleratoxin, caused an elevation of LPL production. The increase in LPL activity caused by forskolin and choleratoxin was paralleled by an elevation of LPL mRNA levels, while dBcAMP only induced a small elevation of LPL mRNA levels. The increase in LPL production was shown to be linked to the stimulation of the PKA signal transduction pathway and was apparently transmitted via the transcription factor CREB. No effect of the stimulation of protein kinase C or calcium/calmodulin-dependent kinase on LPL production was detected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein lipase expression in undifferentiated hepatoma cells is regulated by progesterone and protein kinase A. 132 33

Recent studies have shown the predictive power of abdominal distribution of adipose tissue for the development of cardiovascular disease, stroke, diabetes as well as strong associations to the previously known risk factors for these endpoints. The reason for the accumulation of abdominal fat might be due to an imbalance between cortisol and sex steroid hormones. Cortisol receptor density seems to be particularly high in abdominal adipose tissue, leading to expression of lipoprotein lipase activity primarily here. Progesterone and testosterone seems to counteract this, the former perhaps through competition with the cortisol receptor. Accumulation of intraabdominal fat, particularly in the tissues drained by the portal circulation, probably leads to high free fatty acid concentrations in the portal vein, because of the high lipolytic sensitivity of these tissues. This in turn seems to inhibit hepatic clearance of portal insulin, leading to peripheral hyperinsulinemia, insulin resistance, perhaps hypertension as well as hyperlipidemia via drive by free fatty acids of lipoprotein synthesis in the liver. These are risk factors for diabetes, cardiovascular disease and stroke. It is of interest that subjects with abdominal adipose tissue have several factors leading to increased cortisol and low sex steroid hormone secretion, including stress, high alcohol consumption and smoking. This might provide some of the background to this syndrome.
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PMID:Obesity and adipose tissue distribution as risk factors for the development of disease. A review. 214 Jan 8

The effects of oestrogen and progesterone, alone or in combination, on regional adipose tissue metabolism and oestrogen binding were examined in rats which were not only ovariectomized but also adrenalectomized to allow a study under conditions such that no endogenous sex steroid production occurred. Under these conditions no effects on food intake of the sex steroid hormones were found. 17-beta-oestradiol plus progesterone tended to increase lipoprotein lipase in the parametrial but not retroperitoneal fat depot, but no effects were found of oestrogen or progesterone alone. Oestradiol alone or in combination with progesterone clearly increased basal and norepinephrine-stimulated lipolysis, most pronounced in the retroperitoneal depot. Progesterone alone had no effect. Cytoplasmic 17-beta-oestradiol binding was highest in the parametrial fat depot in non-substituted rats and decreased dramatically after oestrogen administration. It was concluded that in ovariectomized-adrenalectomized rats, oestrogen alone or in the presence of progesterone facilitates lipolysis, a clear effect which is thus possible to elicit without adrenal hormones. Both sex steroid hormones alone or in combination, have no or weak effects on food intake and lipoprotein lipase activity, respectively. These metabolic events as well as cytoplasmic oestrogen binding show regional variations.
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PMID:Sex steroid hormones and adipose tissue metabolism in ovariectomized and adrenalectomized rats. 329 58

Phospholipase C and 1,2-diacylglycerol lipase activities were demonstrated in human endometrium using 1-stearoyl-2-[1-14C]arachidonyl phosphatidylinositol as substrate. Phosphatidylinositol is hydrolysed by phospholipase C to inositol phosphates and to 1,2-diacylglycerol which is then further metabolized by 1,2-diacylglycerol lipase to release free arachidonic acid. In the present study the radiolabelled products formed (1,2-diacylglycerol and arachidonic acid) were measured following chloroform/methanol extraction and thin-layer chromatography. Phospholipase C activity was calcium dependent and optimal at pH 5.0-5.5 and 7.5; 1,2-diacylglycerol lipase activity was also calcium dependent, with an optimum pH of 5.5. A significant increase in 1,2-diacylglycerol production was stimulated by steroid sulphates. Pregnenolone sulphate, oestrone sulphate, testosterone sulphate and dehydroepiandrosterone sulphate stimulated 4, 3.2-, 1.8- and 2.6-fold increases in release respectively. Oestradiol sulphate stimulated a 25% increase in diacylglycerol release which was not significantly different from the control value. Progesterone stimulated a fourfold increase but other free steroids had no effect. Arachidonic acid release was increased in the presence of oestradiol sulphate, oestrone and oestradiol but reduced by oestrone sulphate, dehydroepiandrosterone sulphate, progesterone, dehydroepiandrosterone and, to a lesser extent, by pregnenolone sulphate and testosterone sulphate. 5-Androstene-3 beta,17 beta-diol had no effect on the liberation of either product. This study demonstrates a potential route for the liberation of arachidonic acid from phosphatidylinositol in human endometrium. The opposing effects of steroids on phospholipase C and 1,2-diacylglycerol lipase activity could be important in regulating the release of arachidonic acid by this pathway.
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PMID:Hydrolysis of phosphatidylinositol by human endometrium: modulating effects of steroids on arachidonic acid and 1,2-diacylglycerol release. 337 59

The effects of estradiol-17 beta and progesterone on multiplication, differentiation and lipid filling of adipose precursor cells were examined in primary cell cultures of cells prepared from adipose tissue of both male and ovariectomized female rats. Progesterone down to a concentration of 10(-7) mol/liter, alone or in the presence of estradiol-17 beta stimulated the development of glycerophosphate dehydrogenase and lipoprotein lipase activity. Estradiol-17 beta alone had no effects. These effects were essentially parallel to increases in the rate of lipid filling of the cells. Furthermore, the formation of cells with a lipid vacuole greater than 20 micron was markedly stimulated, suggesting that new fat cells were formed by the stimulation of differentiation of the adipose precursor cells. No effects of the sex steroid hormones were seen on the rate of multiplication. These results suggest a role of sex steroid hormones in the regulation of triglyceride storage capacity in adipose tissue by facilitating the differentiation of precursor cells to form new adipocytes.
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PMID:Effects of sex steroid hormones on differentiation of adipose precursor cells in primary culture. 369 65

Prolactin implants prevented the decline in milk yield and the resumption of oestrous cycles which occurred between days 22 and 28 in untreated lactating rats. Ovariectomy and progesterone implants only partially prevented the decline in milk yield despite preventing the occurrence of oestrous cycles. All three treatments increased total RNA content of the mammary gland compared with controls. In untreated rats there were no changes in mammary DNA content or the number of insulin receptors whereas lipoprotein lipase (LPL) activity decreased significantly during the declining phase of lactation. In contrast, the number of insulin receptors, LPL activity and glucose incorporation into lipid increased in adipose tissue. Prolactin prevented the increase in insulin receptors and lipid synthesis and significantly decreased LPL activity in adipose tissue. Progesterone stimulated LPL activity in the mammary gland and also prevented the increase in lipid synthesis and insulin receptors in adipose tissue but was without effect on LPL activity whereas ovariectomy stimulated LPL activity in the mammary gland but prevented only the increase in the number of insulin receptors in adipose tissue. The results show that raising the serum prolactin concentration can prevent the decline in milk yield during extended lactation and whilst part of this effect may be due to a direct effect on the mammary gland and an indirect effect due to inhibition of oestrous cycles, prolactin may also produce part of its effect on milk synthesis by inhibiting competitive metabolic processes in tissues such as adipose tissue.
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PMID:Effects of prolactin, progesterone and ovariectomy on metabolic activities and insulin receptors in the mammary gland and adipose tissue during extended lactation in the rat. 674 1

Although estrogen has effects on the heart, little is known regarding which genes in the heart are directly responsive to estrogen. We have shown previously that lipoprotein lipase (LPL) expression was increased in female hearts compared with male hearts. To test whether LPL gene expression in heart is regulated by estrogen, we perfused mouse hearts from ovariectomized females with 100 nM 17beta-estradiol or vehicle for 2 h, after which hearts were frozen, and RNA was isolated. The SYBR green real-time PCR method was used to detect LPL gene expression. We found that addition of 17beta-estradiol to hearts from ovariectomized females resulted in a significant increase in LPL mRNA. This estrogen effect on LPL gene expression in mouse heart can be blocked by the estrogen receptor (ER) antagonist ICI 182,780 or by progesterone. We also identified a potential estrogen receptor element (ERE) enhancer sequence located in the first intron of the mouse LPL gene. The potential ERE sequence was linked to a TATA-luciferase (LUC) reporter plasmid in HeLa cells. Both ERalpha and ERbeta stimulated strong activity on the heterologous promoter reporter in Hela cells upon estrogen addition. Both ERalpha and ERbeta activities on the LPL ERE reporter were abrogated by the ER antagonist ICI 182,780. Progesterone also dose dependently inhibited the estrogen-mediated increase in LPL ERE reporter activity. These results show that heart LPL is an estrogen-responsive gene exhibiting an intronic regulatory sequence.
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PMID:Estrogen-enhanced gene expression of lipoprotein lipase in heart is antagonized by progesterone. 1797 24


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