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)

Some alterations in lipid metabolism in mice were observed by the intraperitoneal injection of endotoxin from Salmonella typhimurium. The content of serum triglyceride increased markedly in poisoned mice 16-24 hr postintoxication. The level of free fatty acid (FFA) in the serum of endotoxin-administered mice decreased in inverse proportion to an increase in the injected dose of endotoxin. The electrophoretic analysis of the serum lipoprotein on cellulose acetate membrane showed that pre beta-lipoprotein increased markedly and that FFA fraction in the poisoned mice sera disappeared 18 hr postintoxication. The activity of hormone-sensitive lipase in adipose tissue was elevated appreciably 2 hr after injection, but decreased more significantly after 18 hr than that in fasted control mice. On the other hand, the activity of lipoprotein lipase decreased in the post-heparin serum and adipose tissue 3 hr postintoxication, and decreased significantly after 16 hr. There were no significant differences between changes in the formation of active glycerol (alpha-GP) and in the activity of alpha glycerophosphate dehydrogenase (alpha-GPDH) in the mice liver with or without administration of endotoxin, and after 16 hr levels of both hepatic alpha-GP content and alpha-GPDH activity in poisoned mice showed a tendency to be slightly lower than those in fasted control mice.
 ...
PMID:Alterations of lipid metabolism in mice injected with endotoxin. 37 51

In the murine preadipocyte cell line Ob 17, T3 is known to be necessary at an early step of adipose differentiation for the expression of late phenotypes [lipogenic enzymes such as malic enzyme, glycerol-3-phosphate dehydrogenase (GPDH), etc.] and not necessary for the expression of lipoprotein lipase (LPL), which emerges earlier, at growth arrest. These cells contain nuclear T3 receptors, which mainly belong to products of the c-erbA alpha gene and are down-regulated by T3. In this work, retinoic acid (RA) added to Ob 17 cells at growth arrest impaired morphological differentiation and the development of both late (malic enzyme and GPDH) and early (LPL) phenotypes regardless of whether T3 was added. T3 sensitized the cells to the inhibitory action of RA; the ED50 for GPDH activity was shifted from 0.5 microM to 3 nM in cells cultured with 1.5 nM T3. Later addition of RA (6 days after growth arrest) did not inhibit the differentiation. RA also brought out a marked and fast decrease in nuclear T3 receptors. This was observed whatever the stage of cell development and related to both a rapid decrease in the relative abundance of c-erbA alpha-related mRNA species and an increased disappearance rate, suggesting the involvement of pre- and posttranslational events. RA and T3 acted additively in decreasing the T3 receptor and c-erbA alpha mRNA levels. The effects of RA on T3 receptors were rapidly reversed after RA withdrawal; the reversal was large (75%) when RA was introduced at growth arrest and total when introduced later. The cell sensitivity to RA, considering the T3 receptors, was higher at growth arrest (ED50 for RA, 0.2 and 1.5 microM in assays with RA added at growth arrest and 5 days later, respectively). The results suggest intricated regulatory pathways between RA and T3 at an early step of adipose differentiation and also suggest that among different mechanisms through which RA may impair this differentiation, a decreased level of nuclear T3 receptors at an early period should play a role.
 ...
PMID:Retinoic acid decreases nuclear triiodothyronine receptor expression and impairs an early step of adipose differentiation in the thyroid hormone-sensitive mouse Ob 17 preadipocyte cell line. 131 Dec 41

In order to study the role of collagens in the differentiation of TA1 preadipose cells in vitro, ethyl-3,4-dihydroxybenzoate (EDHB) was used as a specific inhibitor of collagen synthesis. The secretion of collagenous proteins only was severely decreased after exposure to EDHB, and this was accompanied by a decrease of differentiation as indicated by low activity levels of glycerophosphate dehydrogenase. The effect of EDHB was dose-dependent and also dependent upon the stage of cell differentiation. Northern-blot analysis show that EDHB addition to undifferentiated cells did not prevent the induction of A2COL6 gene, a marker of the preadipose state, but prevented the induction of the gene encoding for the adipocyte lipid binding protein and the modulation of the expression of the lipoprotein lipase gene which are both indicators of the adipose state. These results demonstrate that differentiation of preadipose cells into adipose cells requires active synthesis of collagens during the preadipose state.
 ...
PMID:Essential role of collagens for terminal differentiation of preadipocytes. 141 7

The effect of arachidonate metabolites on the differentiation of the adipogenic cell line 1246 was investigated. Among the metabolites examined, only prostaglandin F2 alpha (PGF2 alpha) inhibited differentiation in a dose-dependent fashion with an ED50 of 3 x 10(-9) M. PGF2 alpha inhibited the mRNA expression of lipoprotein lipase, clone 154, and fatty acid-binding protein, which are early markers of differentiation, as well as glycerol-3-phosphate dehydrogenase specific activity and triglyceride accumulation, which are late markers of differentiation. Chronic exposure of 1246 cells to PGF2 alpha before and during differentiation indicated that the cells that have just initiated their differentiation program were the most susceptible to the inhibitory effect of PGF2 alpha. Since 1246 cells produce PGs, we determined whether the PG produced by the cells influenced adipose differentiation. Cyclooxygenase inhibitors added to the culture medium stimulated differentiation of 1246 cells up to 18-fold depending on the type and concentration of inhibitor used. In contrast, lipoxygenase inhibitors had no effect. Treatment of 1246 cells with arachidonic acid resulted in a dose-dependent inhibition of cell differentiation. Oleate or linoleate had no effect. These data indicate that PGF2 alpha inhibits early and late events of adipose differentiation and that the endogenous production of PGs (particularly PGF2 alpha) plays an important role as a negative paracrine or autocrine regulatory pathway of adipose differentiation.
 ...
PMID:Paracrine regulation of adipose differentiation by arachidonate metabolites: prostaglandin F2 alpha inhibits early and late markers of differentiation in the adipogenic cell line 1246. 144 97

Transforming growth factor-beta (TGF-beta) inhibits morphologic differentiation of BALB/c 3T3 T cells as well as other proadipocyte models. Our prior studies suggested that TGF-beta may act only during the early stages of differentiation induction. However, we did not determine whether TGF-beta was differentially effecting expression of any of the various differentiation-specific genes or if it could cause down-regulation of these genes in differentiated cells. Therefore, in the current study we tested the effects of exogenous TGF-beta (0.01-5.0 ng/ml) on morphologic differentiation and on differentiation-dependent gene expression (Northern and slot blot analyses) at various times during differentiation. When induced to differentiate, 3T3 T cells first undergo predifferentiation growth arrest and from this state molecular, biochemical, and morphological differentiation proceeds. Here it was found that when added prior to the onset of differentiation, TGF-beta was a potent inhibitor or morphologic differentiation as well as of the expression of differentiation-specific genes such as lipoprotein lipase (LPL) and glycerol-3-phosphate dehydrogenase (GPD). However, once morphologic differentiation began, TGF-beta was ineffective in blocking differentiation. In addition, exposure of fully differentiated cells to TGF-beta for up to 72 hours caused no decrease of differentiation-specific genes and even a 7-day treatment caused no morphologic dedifferentiation. Tumor necrosis factor also had no detectable effect on fully differentiated cells.
 ...
PMID:TGF-beta blocks early but not late differentiation-specific gene expression and morphologic differentiation of 3T3 T proadipocytes. 153 85

Cytokines like tumor necrosis factor (TNF), interferon-gamma (IFN-gamma), and interleukin-1 (IL-1) are known to interfere with the differentiation of cultured cell lines of adipocyte precursors. In the present study, the effect of mouse and rat IFN-gamma, as well as human IL-1 beta, was investigated on rodent preadipocytes in primary cultures, either in the presence of fetal bovine serum (FBS, 10%) or in serum-free defined medium. IFN-gamma exerted an antiproliferative action that was more pronounced when cells reached confluency than during the growth phase of the culture. Morphological observation and quantifications of undifferentiated and differentiating cells revealed that IFN-gamma caused a decrease in the proportion of cells devoid of lipid droplets which would correspond to fibroblast-like cells, whereas preadipocytes remained unaffected. IFN-gamma induced a marked retardation of adipoconversion, resulting in a partial inhibition of lipoprotein lipase (LPL) activity and a severe decrease in glycerol-3-phosphate dehydrogenase (GPDH) activity. The antiproliferative and anti-LPL effects of IFN-gamma were neutralized by adding anti-IFN-gamma antibodies, while these antibodies prevented only partially the depressing effect of IFN-gamma on GPDH activity. Contrary to IFN-gamma, IL-1 beta slightly enhanced the proliferation in preadipocyte cultures. IL-1 beta also depressed adipoconversion, inhibited markedly LPL activity, and partially reduced GPDH activity. These results show that the influence of cytokines on adipoconversion observed in preadipocyte cell lines can be found in normal preadipocytes in culture.
 ...
PMID:Interferon-gamma and interleukin-1 beta inhibit adipoconversion in cultured rodent preadipocytes. 157 4

The effects of all-trans retinoic acid (RA) on the lipoprotein lipase (LPL) activity, synthesis and mRNA content in 3T3-L1 adipocytes were studied. When fully differentiated 3T3-L1 adipocytes were exposed to RA, dose-dependent suppression of LPL activity was observed. The loss of activity reached a maximum of 60% of the control level and appeared to be due to an effect on synthesis of the enzyme, as judged from the decreased incorporation of [35S] methionine and [35S] cysteine into immunoprecipitable LPL. The LPL mRNA level remained unchanged under the same conditions. In contrast, no significant reduction in glycerol-3-phosphate dehydrogenase activity or change in the morphological signature occurred on 24 hr exposure of 3T3-L1 adipocytes to RA. These results suggest that RA can specifically down-regulate LPL enzyme expression in adipocytes at the posttranscriptional level.
 ...
PMID:Lipoprotein lipase enzyme expression in 3T3-L1 adipocytes is posttranscriptionally down-regulated by retinoic acid. 161 Mar 91

Stromal vascular cells were isolated from adipose tissue obtained from three different anatomical locations: epididymal (EPI), retroperitoneal (RP), and dorsal subcutaneous (SC), and allowed to differentiate in primary tissue culture. Cell number, protein concentration, glycerophosphate dehydrogenase, and lipoprotein lipase activity were similar in cells obtained from the EPI, RP, and SC regions, as were total insulin binding and the affinity of insulin for its receptor. However, both maximal insulin receptor tyrosine kinase activity and insulin-stimulated phosphorylation of the insulin receptor were significantly lower (P less than 0.05) in cells cultured from the SC region. In addition, newly differentiated adipocytes from the SC region were less sensitive to the ability of insulin to stimulate glucose uptake, and maximal insulin-stimulated glucose uptake by these cells was also significantly lower (P less than 0.05) when compared to cells obtained from the two other regions. Since these studies were performed on adipocyte precursor cells, allowed to differentiate to a similar degree in primary culture, the observed differences in insulin receptor phosphorylating activity, as well as the ability of insulin to stimulate glucose uptake appear to be intrinsic to adipose tissue from the three sites.
 ...
PMID:Differences in insulin action as a function of original anatomical site of newly differentiated adipocytes obtained in primary culture. 165 46

We studied the role of cAMP in the regulation of the expression of the adipsin gene and of some other adipose-specific genes including lipoprotein lipase (LPL), glycerophosphate dehydrogenase (G3PDH), and adipocyte P2 (aP2) in 3T3-F442A adipocytes. Northern blot analysis of isoproterenol (10(-6) M)-, forskolin (10(-5) M)- or 8-bromo-cAMP (10(-3) M)-treated adipocytes showed that the steady-state levels of adipsin mRNA were strongly reduced in a time-dependent and reversible manner. The concentration of isoproterenol giving a half-maximal effect in the down-regulation of the adipsin message was approximately 5 x 10(-8) M. Similarly, cell treatment by forskolin elicited a down-regulation of LPL and G3PDH mRNA levels but did not alter aP2 mRNA level. As determined by nuclear run-on assays, the rate of transcription of adipsin, LPL and G3PDH in isoproterenol-treated adipocytes was respectively 3, 3, and 2 times lower than in control adipocytes. These results indicate (1) that cAMP plays a dominant antilipogenic role in the fat cell through the transcriptional down-regulation of the expression of two major genes involved in triglyceride biosynthesis; (2) that cAMP does not reverse the adipocyte character; (3) hence, that cAMP suppresses adipsin expression at the transcriptional level, providing additional support for the role of adipsin protein in adipocyte metabolism.
 ...
PMID:Beta-adrenergic-cyclic AMP signalling pathway modulates cell function at the transcriptional level in 3T3-F442A adipocytes. 166 51

The effects of physiological glucocorticoids such as cortisol and corticosterone, as well as dexamethasone, on proliferation and differentiation of rat fat cell precursors kept in primary culture were analyzed. In serum-containing medium (10%), glucocorticoids markedly decreased cell proliferation, either on subconfluent or on confluent cultures. This effect was independent of the presence of insulin. In contrast, acute amplification of adipose conversion was observed mainly when glucocorticoids and insulin were added simultaneously. Morphological quantification of lipid-containing cells confirmed acceleration of the maturation process, and an early and specific reorganization of the cytoskeleton was detected at the ultrastructural level. In the presence of insulin, glucocorticoids also enhanced the main marker enzymes, lipoprotein lipase, and glycerol phosphate dehydrogenase. Glucocorticoid effects on precursor proliferation and differentiation were clearly dose-dependent, dexamethasone being 10 times more potent than cortisol and corticosterone. Similar results were obtained in serum-free medium, as well as in preadipocyte cultures derived from different fat deposits. This study demonstrates that in addition to an acute inhibition of precursor growth, glucocorticoids exert a clear stimulation of adipose conversion, which depends mainly on the presence of insulin and the glucocorticoid concentration.
 ...
PMID:Glucocorticoids induce a drastic inhibition of proliferation and stimulate differentiation of adult rat fat cell precursors. 189 38


1 2 3 4 5 6 7 8 9 10 Next >>