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)

Ageing results in decreased replicative potential of preadipocytes, as well as reduced capacities for the lipid accumulation and increases in lipogenic enzyme activities during differentiation of preadipocytes into fat cells. To determine whether decreased differentiation is associated with decreased levels of mRNA for differentiation-dependent genes and whether early as well as late components of the differentiation programme are affected by ageing, we measured beta-actin, alpha-tubulin, lipoprotein lipase, and glycerol-3-phosphate dehydrogenase mRNA levels in undifferentiated and differentiated epididymal preadipocytes from 3-, 17-, and 24-month-old Fischer 344 rats. During ageing, diminished differentiation-related changes occurred in mRNAs affected early (actin, tubulin), midway through (lipoprotein lipase), and late (glycerol-3-phosphate dehydrogenase) in the preadipocyte differentiation process. Hence, early as well as late phases of the differentiation programme were affected by ageing. The effects involved changes in gene transcription or mRNA processing. Our results were not consistent with the hypothesis that age-related decreases in replication are caused by an increased tendency for cell differentiation.
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PMID:Ageing, differentiation, and gene expression in rat epididymal preadipocytes. 819 92

Prostaglandin F2 alpha (PGF2 alpha) is a potent adipose differentiation inhibitor for the adipogenic cell line 1246 and for adipocyte precursors in primary culture with an ED50 of 3 x 10(-8) M. In this paper, we examined the effect of several prostaglandins which have structural similarities with PGF2 alpha on the differentiation of 1246 cells and of adipocyte precursors in primary culture. The results show that only 9 alpha,11 beta-PGF2 alpha is as potent as PGF2 alpha to inhibit differentiation of adipocyte precursors in primary culture and of the adipogenic cell line 1246. In the presence of 9 alpha,11 beta-PGF2 alpha, the cells remained fibroblast-like, typical of undifferentiated adipocyte precursors. Triglyceride accumulation and increase of specific activity for glycerol-3-phosphate dehydrogenase were inhibited. In addition, mRNA expression of early markers of differentiation such as lipoprotein lipase (LPL) and fatty acid binding protein (FAB) was decreased. The isomer 9 beta,11 alpha-PGF2 alpha and other PGF2 alpha derivatives were inactive. These results provide new information on the biological activity of 9 alpha,11 beta-PGF2 alpha as an inhibitor of adipose differentiation and about the structural characteristics of prostaglandins required for maintenance of a high adipose differentiation inhibitory effect.
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PMID:Inhibition of adipose differentiation by 9 alpha, 11 beta-prostaglandin F2 alpha. 829 81

Nontransformed 3T3 T mesenchymal/proadipocyte stem cells can be readily induced to differentiate, yet previous work has shown that 3T3 T cells that are spontaneously or virally transformed not only lose their normal growth control mechanisms but also lose the ability to differentiate. Loss of growth control can be due to autocrine mechanisms in some transformed cells, but the mechanisms involved in disrupting differentiation control are poorly understood. Our goal is to further define the growth and differentiation defects that arise in neoplastically transformed cells and the mechanisms underlying those defects. For example, exogenous transforming growth factor beta and tumor necrosis factor, both of which are secreted aberrantly by some tumor cells, are known inhibitors of different steps of the normal 3T3 T adipocyte differentiation process, suggesting a potential role as autocrine factors in disrupting differentiation of transformed 3T3 T cells. In the current study we transformed 3T3 T cells in vitro with chemical or UV irradiation treatment in order to determine if the acquisition of the transformed phenotype after these treatments is also associated with loss of differentiation control as it is with spontaneously or virally transformed cells. Four chemically and two UV-treated 3T3 T cell lines were isolated from type III foci and all have been found to be tumorigenic in syngeneic animals and to have lost the ability to differentiate. Relative to the parental cell line the differentiation abilities of the transformed clones ranged from 0 to less than 5%. In this regard, we also analyzed the normal and aberrant expression of three growth factors and differentiation inhibitors in transformed cells. Both transforming growth factor alpha and beta were found to be expressed in non-transformed 3T3 T cells as determined by Northern blot analyses. In addition, both were found to be down-regulated during differentiation of 3T3 T cells. Transformed/differentiation-defective 3T3 T cells expressed varied levels of transforming growth factor alpha and beta. Three of the new transformed clones expressed particularly high levels of transforming growth factor alpha. Very low levels of tumor necrosis factor expression were found in the normal cells and the transformed cells appeared to express tumor necrosis factor at similar levels. In contrast, none of the transformed cells expressed any of the differentiation-specific genes tested (lipoprotein lipase, glycerol-3-phosphate dehydrogenase, etc.). Even a transformed clone which could undergo growth arrest but not morphological differentiation expressed no differentiation-specific genes. Together, these data suggest that neoplastic transformation in general disrupts differentiation control.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Loss of differentiation control in transformed 3T3 T proadipocytes. 846 95

mRNA levels of the ob gene product, leptin, were investigated by quantitative competitive RT-PCR in a mouse cell line (3T3-L1) which can be induced to differentiate into adipocytes. During conversion to fat cells, the level of leptin mRNA increased several-fold and in parallel to that for typical adipocyte markers like lipoprotein lipase, adipsin and glycerophosphate dehydrogenase. Leptin transcription, however, did not correlate with the size of the adipocytes measured as total triglycerides. On the other hand, mRNA levels for leptin in fully differentiated adipocytes were increased 2-3 fold by insulin. In contrast, free fatty acids exerted a concentration-dependent inhibition of leptin transcription while the corticosteroid dexamethasone and an elevation of intracellular cAMP displayed only marginal inhibitory effects on leptin mRNA levels.
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PMID:Regulation of ob gene mRNA levels in cultured adipocytes. 856 29

Acylation Stimulating Protein (ASP) is a human plasma protein that stimulates both triacylglycerol synthesis and glucose transport. ASP is identical to C3adesArg and is generated by the interaction of factor B, complement C3 and adipsin. We have demonstrated that mature fat cells express messages for factors B, complement C3 and adipsin; that human pre-adipocytes, when cultured under differentiating conditions to produce adipocytes, generate ASP in the culture medium; and that human adipocytes also become more responsive to ASP as they differentiate. The aim of this study, therefore, was to examine the temporal production of ASP during adipocyte differentiation in relation to other adipose specific factors involved in lipogenesis. The results demonstrate that (i) there was little ASP production by differentiating adipocytes over the first 7 days, with a marked increase in ASP thereafter (up to sixfold); (ii) this increase was paralleled by large increases in the message level of factor B and complement C3 and moderate increases in adipsin message; (iii) increases in lipoprotein lipase (LPL) message and glycerol-3-phosphate dehydrogenase (GPDH) activity (both key enzymes for substrate supply for triacylglycerol synthesis) occurred earlier than the increase in ASP; and (iv) in spite of the increase in LPL and GPDH, triacylglycerol synthetic capacity only markedly increases following the increase in ASP production in adipocytes. Although the present study cannot be interpreted as showing causality with respect to triacylglycerol synthesis, it does point to an important role for ASP in human adipose tissue physiology.
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PMID:Differentiation-induced production of ASP in human adipocytes. 858 46

Fat and liver are the major sites for the deposition of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) given in vivo to rats. Although a great deal of information is available on the effects of TCDD in liver, very little is known of the effects in fat. The epididymal fat pads were removed and the stromal-vascular cells, released by collagenase digestion, were put into primary culture, 2, 4, 6 and 8 days after intubating 175 micrograms/kg TCDD into male Sprague-Dawley rats. Following 7 days in culture, the cells were examined morphologically, and assayed for an early (lipoprotein lipase, LPL) and late marker of fat cell differentiation (glycerol-3-phosphate dehydrogenase, GPDH). With rats sacrificed 6 or 8 days after TCCD intubation, the harvested cells from pair-fed rats contained significantly more fat and had a significantly higher level of GPDH enzyme activity, indicating more differentiation. The mRNA for LPL and GPDH genes was also higher for cells from pair-fed rats. In addition, for the rats that were sacrificed 4-8 days after TCDD intubation, despite similar food intake, the pair-fed control rats gained more total body weight than the treated rats. Although there was a body weight difference, there was no significant different between the weights of the epididymal fat pads. This is the first report to demonstrate that TCDD inhibits the differentiation of fat cells.
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PMID:2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) inhibition of fat cell differentiation. 859 78

The aim of this study was to investigate the role of cell replication for the differentiation of human adipocyte precursor cells in primary culture. When cells were seeded in a medium supplemented with 10% fetal bovine serum, they started to proliferate within 48 h after exposure, as assessed by cell counting and [3H]thymidine autoradiography. When cells were inoculated in the absence of serum, a significant degree of cell proliferation was not detectable. Histochemical investigations using bromodeoxyuridine incorporation demonstrated that cells replicating their DNA did not accumulate lipid droplets. Inoculating adipocyte precursor cells under completely serum-free conditions resulted in a 30-50% higher expression of lipogenic enzymes such as glycerol-3-phosphate dehydrogenase and lipoprotein lipase than keeping cells in serum-supplemented medium for the initial 16 h. Addition of cytosine arabinoside at concentrations that effectively block mitosis did not interfere with adipocyte development. In conclusion, adipocyte precursor cells from human adipose tissue do not require cell division to enter the differentiation process in vitro. These cells may have already undergone possibly critical cell divisions in vivo and may be in a late stage of adipocyte development.
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PMID:Relationship between replication and differentiation in cultured human adipocyte precursor cells. 892 27

The objective of this study was to establish optimal conditions for the primary culture of pig preadipocytes. We cultured pig preadipocytes for 10 d and studied the effects of insulin, hydrocortisone, and triiodothyronine (T3) added to serum-free basal medium on differentiation and gene expression of lipoprotein lipase an early marker, and adipsin, a late marker of preadipocyte differentiation. Insulin alone and hydrocortisone alone stimulated a low level of cell differentiation, as indicated by an increase in glycerol-3-phosphate dehydrogenase activity. When added together, insulin and hydrocortisone had a synergistic effect on cell differentiation. When combined with insulin or hydrocortisone, T3 had no effect on cell differentiation, indicating that T3 is not required in porcine preadipocyte culture. Gene expression studies also showed that removal of insulin or hydrocortisone from complete serum-free medium reduced both early and late marker mRNA. As expected, removal of T3 had no effect on the gene expression of early and late marker mRNA. We conclude that insulin and hydrocortisone, but not T3, are required for the differentiation of pig preadipocytes in primary culture.
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PMID:Insulin and hydrocortisone, but not triiodothyronine, are required for the differentiation of pig preadipocytes in primary culture. 902 54

We studied the effect of retinoic acid on the differentiation of cultured porcine preadipocytes. Porcine preadipocytes were cultured in serum-free medium (DME/F12 medium containing 100 nM insulin, 10 micrograms/mL transferrin, and 50 ng/mL hydrocortisone). Addition of increasing amounts of retinoic acid (1 nM to 20 microM) to the medium reduced glycerol-3-phosphate dehydrogenase (GPDH) activity, a late marker of preadipocyte differentiation. At lower concentrations (0.1 to 10 nM), retinoic acid had no effect on the GPDH activity. Addition of retinoic acid (10 microM) for 24 h during the early stage of development (d 1) greatly inhibited the GPDH activity. After the cells were differentiated, however, retinoic acid no longer had any effect. Therefore, retinoic acid was most effective in undifferentiated cells. Following a 24-h exposure of porcine preadipocytes to retinoic acid at d 1, Northern blot analysis showed that there was a decrease in lipoprotein lipase and adipsin mRNA levels. The results suggest that retinoic acid is a potent inhibitor of porcine preadipocyte differentiation in primary culture.
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PMID:Effect of retinoic acid on differentiation of cultured pig preadipocytes. 902 55

Molecular mechanisms of lipid synthesis and their controls in hepatic stellate cells are not known. We have previously proposed that, in contrast to other fat storing cells, hepatic stellate cells are not involved in energy storage, but they represent a particular cell population specialized in storage of lipid-soluble substances, the major one being probably retinol. In agreement with this hypothesis, induction of the lipocyte phenotype in stellate cells is not under the control of insulin, but responds to retinoids and other molecules that modify the gene expression program in these cells. In the present study we have monitored the activity of the two major enzymes involved in lipid synthesis during the induction of the lipocyte phenotype in hepatic stellate cells: glycerol-3-phosphate dehydrogenase (GPDH) that mediates the de novo lipid synthesis, and lipoprotein lipase that mediates incorporation of plasma lipids. In early stages of lipocyte induction, both pathways of lipid synthesis are activated. When lipocytes have already constituted the lipid droplets, lipoprotein lipase pathway is downregulated, while GPDH activity remains high. Adult liver has been reported to lack lipoprotein lipase, but under stress, lipase activity was detected around and at the surface of the intrahepatic vasculature. We have now shown that the lipase activity can be induced in the hepatic stellate cells, located in the Disse's space. The high lipoprotein lipase activity under acute induction of lipocyte phenotype, followed by the low activity under conditions of metabolic equilibrium, are in compass with the increased activity of this enzyme under stress, and its low activity in adult liver parenchyma under normal conditions.
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PMID:Lipid metabolism during in vitro induction of the lipocyte phenotype in hepatic stellate cells. 906 91


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