Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.34 (lipoprotein lipase)
 7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in the volume, the rates of fatty acid synthesis and synthesis of the glycerol moiety of acylglycerols, the activity of lipoprotein lipase, and the number and affinity of insulin receptors of adipocytes, and concentrations of serum insulin, prolactin and progesterone were determined in virgin rats and in rats at various stages of pregnancy and lactation. Changes in the metabolic activities of adipose tissue appeared to be synchronized and primarily comprised a marked decrease in anabolic activity around parturition. In contrast, the number of insulin receptors (Kd 1.5 nM) per adipocyte doubled during pregnancy before returning to normal values around parturition. It is postulated that the increase in the number of insulin receptors is an adaptation to counteract the effects of insulin-antagonistic hormones during pregnancy and that the decrease in the number of receptors is primarily responsible for the loss of anabolic activity around parturition.
 ...
PMID:Role of insulin receptors in the changing metabolism of adipose tissue during pregnancy and lactation in the rat. 50 93

DELTA1-tetrahydrocannabinol (delta1-THC), a highly lipid soluble and active principle of cannabis, was injected each day (25 mg/kg) s.c. in mice from the estimated 13th day of pregnancy. Delta1-THC-treated mice showed no increase in the wet weight or DNA content of their mammary glands during the period of investigation from before parturition until the 12th day post-partum. A marked increase in mammary-gland lipoprotein lipase activity w,s found in control mice at parturition and this was suppressed by delta1-THC. Prolactin rose to a peak level in plasma earlier in lactation in the control mice than in the delta1-THC-treated mice. This delayed rise in plasma prolactin due to delta1-THC may account for the depression of mammary gland growth and development by the drug and for the delay in the appearance of high activities of lipoprotein lipase until later in lactation.
 ...
PMID:The effects of delta1-tetrahydrocannabinol on mammary gland growth, enzyme activity and plasma prolactin levels in the mouse. 69 71

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.
 ...
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 prolactin on lipoprotein lipase activity of crop sac, omental adipose tissue, and esophagus was studied in adult female pigeons. Prolactin injected for 4 days, 1 mg/day, increased lipoprotein lipase activity from 17 to 177 U/g in crop sac and from 68 to 118 U/g in adipose tissue, but had no effect on the activity in esophagus, 4 U/g. (10 = 1 mumol of chylomicron triglyceride hydrolyzed to free fatty acid and glycerol per hour.? Prolactin increased the weight of crop sac from 1.4 to 7.2 G. The effect of prolactin on lipoprotein lipase activity and weight of crop sac occurred mostly during the 3rd and 4th days of treatment, whereas the effect on the activity of adipose tissue occurred later, during the 4th day of treatment. Crop "milk" collected from pigeons injected with 2 mg of prolactin daily for 4 days contained a small amount of lipoprotein lipase activity, 12 U/g, is smaller than 10% of that found in crop sac. The finding of markedly increased lipoprotein lipase activity in crop sac of prolactin-treated pigeons suggests that blood triglyceride may be used by crop sac for the formation of crop milk lipid.
 ...
PMID:Effect of prolactin on lipoprotein lipase in crop sac and adipose tissue of pigeons. 113 May 58

Inhibition of prolactin secretion with bromocriptine and neutralization of GH action with a specific antiserum to rat GH (rGH) were used to explore the modes of action of GH and prolactin in maintaining lactation in the rat. Treatment of dams with anti-rGH caused a small reduction in litter weight gain whilst bromocriptine reduced litter weight gain by 50%. When both treatments were combined, however, milk yield ceased completely and this was accompanied by a wide variety of effects on mammary lipid metabolism including decreases in the mRNA concentrations of acetyl CoA carboxylase, fatty acid synthase, malic enzyme and lipoprotein lipase. Activities of acetyl CoA carboxylase and lipoprotein lipase were also significantly reduced. Reciprocal changes were evident in adipose tissue with increases in acetyl CoA carboxylase and lipoprotein lipase activities. In conjunction with a decreased lipolytic response to noradrenaline in adipose tissue of animals given the combined treatment of bromocriptine and anti-rGH, this represented a co-ordinated series of changes to reduce lipid synthesis in the mammary gland and enhance lipogenesis and triglyceride storage in adipose tissue as milk production ceased. All of these effects could be prevented in part by concurrent treatment with GH, but insulin-like growth factor-I (IGF-I) and IGF-II failed to affect any of the parameters measured.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The role of growth hormone, prolactin and insulin-like growth factors in the regulation of rat mammary gland and adipose tissue metabolism during lactation. 147 26

Pyrularia thionin is a 47 amino acid peptide isolated from the nuts of Pyrularia pubera. This peptide does not have intrinsic phospholipase A2 activity, but it increases the liberation of arachidonate from several tissues. Exposure of anterior pituitary cells to this toxin increases the liberation of arachidonate, increases the cellular levels of lysophospholipids, and decreases cellular phospholipids. Thus, phospholipase A2 is involved in the liberation of arachidonate stimulated by this peptide. Because this toxin also increases stearate liberation from the pituitary cells, either diacylglycerol lipase, phospholipase A1 or lysophospholipase may be directly or indirectly activated by this toxin. In addition to increasing fatty acid liberation, Pyrularia thionin increases the release of prolactin and growth hormone from anterior pituitary cells over the identical concentration ranges that this toxin liberates the fatty acids. Pyrularia thionin increased arachidonate liberation and prolactin release from perifused pituitary cells within 2 min, and following withdrawal of the toxin, arachidonate liberation and prolactin release returned to near basal levels within 6 min. Dopamine, a physiological inhibitor of prolactin release that closes calcium channels, decreased prolactin release stimulated by Pyrularia thionin. However, dopamine had no effect on the arachidonate liberation stimulated by this peptide. Similarly, D-600, an organic calcium channel blocker, decreased the prolactin and growth hormone release stimulated by the toxin without affecting the toxin-stimulated arachidonate liberation. Therefore, Pyrularia thionin increases arachidonate liberation through the rapid activation of phospholipase A2 by a mechanism that is not dependent on calcium uptake via D-600-inhibitable calcium channels. In contrast, the prolactin and growth hormone release stimulated by this toxin requires calcium uptake via D-600 inhibitable calcium channels.
 ...
PMID:Pyrularia thionin increases arachidonate liberation and prolactin and growth hormone release from anterior pituitary cells. 148 65

The effect of monomeric (glycosylated and unglycosylated) and dimeric form of porcine prolactin on change of the blood levels of triglycerides (TG) and cholesterol in lipoproteins (LP) of different density and the activity of the main enzymes of plasmatic and liver lipid metabolism were studied under the conditions of experimental hyperprolactinemia in rabbits. It was shown to be accompanied by dyslipoproteinemia, characterized by a stable rise of TG in LP of very low, high and low density as well as by a rise of cholesterol concentration in VLDL and its decrease in HDL. Such changes in LP showed correlation with lowered activity of lipoprotein lipase, triglyceride lipase of the liver and plasmatic postheparin lipolytic activity. Analysis of prolactin-induced dyslipoproteinemia has shown that changes in plasma lipoproteins are of atherogenic nature.
 ...
PMID:[Change in the blood lipoprotein spectrum in experimental hyperprolactinemia]. 202 69

The principal lactogenic hormone, prolactin, secreted by the anterior pituitary is critical to the establishment of lactation, milk macronutrient content and milk production. The concentration of circulating prolactin increases during pregnancy so that by the end of gestation, levels are 10 to 20 times over normal amounts. However, prolactin is prevented from exerting its effect on milk secretion by elevated levels of progesterone. Following clearance of progesterone and estrogen at parturition, copious milk secretion begins. The minimal hormonal requirements for normal lactation to occur are prolactin, insulin and hydrocortisone. Prolactin stabilizes and promotes transcription of casein mRNA; may stimulate synthesis of alpha-lactalbumin, the regulatory protein of the lactose synthetase enzyme system; and increases lipoprotein lipase activity in the mammary gland. Prolactin levels decrease as lactation is established but nursing stimulates prolactin release from the pituitary which promotes continued milk production. Prolactin is secreted into milk at levels representative of the average circulating concentration. The physiological significance of milk prolactin to the infant is uncertain. Prolactin exists in three heterogenic forms which possess varying biological activity. The monomer with a molecular weight of 23 kDa is found in greatest quantity and is the principal biologically active form. The pattern of heterogeneity changes during pregnancy to favor even more monomer in proportion to the dimer. However, during lactation, the proportion of the monomer in circulation decreases in response to selective uptake of the monomer by the mammary gland. Over 90 percent of the prolactin in milk is present as the monomer. Prolactin may exert some of its biological effect by a shift in the ratio of active to less active forms of the molecule.
 ...
PMID:A review of the hormone prolactin during lactation. 209 40

Mammary gland lipase activity of the mouse increased 45-fold compared to that in unmated gland at the 15th day of pregnancy and was 65-fold at the 20th day of pregnancy. After parturition, the activity abruptly decreased during 3 days to 38% of that at the 20th day of pregnancy. On the other hand, only a very small lipoprotein lipase activity was observed in the pregnant gland, the activity increased to 15-fold that of 20 day pregnancy at the 3rd day of lactation. These facts suggest that the mammary epithelial cells (mammary gland lipase activity was detected only in epithelial cells) utilize the fat reserved in the gland during pregnancy, but the lactating mammary epithelial cells utilize the fat supplied from the blood circulation. Mammary gland lipase activity was decreased by treatment with epinephrine which increased the fat mobilization in other adipose tissues. Hydrocortisone and prolactin decreased the mammary gland lipase activity in the glands of pregnancy and lactation. In addition, no hormone-sensitive lipase activity was observed in the mammary gland. Thus, the control of fat mobilization in the mammary gland must be different from that in other adipose tissues.
 ...
PMID:[Changes in lipase activity during pregnancy and lactation in the mouse mammary gland]. 234 21

The cleavage of arachidonate from pituitary phospholipids may contribute to the process that regulates the release of prolactin. To test this hypothesis, primary cultures of anterior pituitary cells from female rats were preincubated with [3H]arachidonate to label their phospholipid-containing components. The cells were then washed and incubated with vehicle or test agents and the release into the medium of prolactin and [3H]arachidonate cleaved from the phospholipids was measured. Thyrotropin-releasing hormone (TRH) and neurotensin significantly increased the release of both [3H]arachidonate and prolactin. Although basal [3H]arachidonate release was not affected by dopamine or somatostatin, both of these agents reduced [3H]arachidonate release induced by TRH. The relationship between calcium mobilization and arachidonate release was investigated by exposing the cells to agents that modify calcium balance. Maitotoxin, a calcium channel activator, stimulated prolactin and arachidonate release. In contrast cobalt, a calcium channel blocker, penfluridol, a calcium-binding protein inhibitor, and low-calcium medium decreased basal and TRH-induced prolactin release and diminished the TRH-induced release of arachidonate. RHC 80267, an inhibitor of diacylglycerol lipase, decreased TRH-induced prolactin and arachidonate release. BW755c, an inhibitor of the conversion of arachidonate to its metabolites, decreased TRH-induced prolactin release but predictably increased arachidonate release. These findings support the hypothesis that arachidonate metabolites may be involved in the process regulating prolactin release.
 ...
PMID:A possible role of arachidonate metabolism in the mechanism of prolactin release. 242 Feb 3


1 2 3 4 5 Next >>