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 possibility that circulating immune complexes (IC) could modify lipoprotein lipase (LPL) activity or release was explored in in vitro systems. IC were precipitated at antibody-Ag equivalence by using specific rabbit antisera and Ag from inactivated rubella virus and hemagglutinins from purified whole virions from three prototype strains of influenza (A/Brazil, A/Bangkok, and B/Singapore) as well as from a combined diphtheria and tetanus toxoid adsorbed with inactivated pertussis. After resolubilization, these IC were exposed to delipidated homogenates of rat epididymal fat pads before assay for LPL activity. LPL activity was stimulated two- to three-fold by the presence of 20 to 40 micrograms IC protein. This effect is not caused by the individual components of the IC because neither the specific Ag nor the individual antisera had any significant effect on LPL activity. With the rubella IC, a greater stimulatory effect was seen with increase in IC protein. With the influenza and diphtheria, pertussis, tetanus (DPT) IC, however, inhibition occurred when IC protein exceeded the amount of protein used for the LPL assay. C did not appear to be involved because IC prepared with heated antisera had similar effects. When intact rat epididymal fat pads were exposed to the rubella, influenza, or DPT IC, LPL activity recovered in the suspension medium was increased in each instance compared with pads exposed to a comparable amount of albumin. These findings may have implications for specific lipid changes that may occur during the immediate post-infectious period following rubella, influenza, or infections with the several bacteria whose Ag were present in the DPT IC used in these studies.
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PMID:Effects of in vitro prepared immune complexes on rat adipose tissue lipoprotein lipase. 278 30

I mouse strain displays adipocyte hypoplasia responsible for smaller fat pad size compared with C57BL mice. We investigated possible alterations in the proliferation and/or differentiation capacity of preadipocytes from the stroma-vascular fraction of adipose tissue in the I mouse strain. Control C57BL and I mice were studied at 8 weeks of age, and both adipose and stromal cells were isolated from epididymal and inguinal adipose tissue localizations. Results showed that the lower epididymal adipose mass in I mice was accompanied by a decrease in stromal cell number compared with C57BL mice. In inguinal fat pads, total cell number in the stroma-vascular fraction was unmodified; lipoprotein lipase activity significantly increased in stromal cells from I mice compared with control mice. In this depot, further characterization of cells from the stroma-vascular fraction by separation of cells according to density showed an increased number of preadipocytes in the I mouse whole stromal cell population. These preadipocytes seemed unable to undergo terminal maturation, thus leading to a decrease in the number of mature adipocytes. These results indicated that resistance to fat accumulation in I mice is characterized by site-dependent impairment of both the proliferative rate and the differentiation capacity of adipocyte precursors.
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PMID:Impaired fat storage capacity in adipocyte precursors of I versus C57BL mice. 279 37

4 h after intravenous injection of recombinant HuTNF-alpha to fed rats, an increase in heart, diaphragm, and plasma lipoprotein lipase activity was observed. At the same time, a 40-60% decrease in enzymic activity in epididymal fat pad and kidney and 40% decrease in hepatic lipase activity in liver had occurred. Similar results were obtained 20 h after injection of recombinant HuTNF-alpha into fasted rats. Pretreatment with Indomethacin did not affect the changes in tissue lipoprotein lipase activity observed following recombinant HuTNF-alpha administration. Serum triacylglycerol concentration increased by 2- and 6-fold; 4 and 20 h after recombinant HuTNF-alpha administration. Disappearance of 14C-labeled triacylglycerol from the circulation after injection of small chylomicrons, biosynthetically labeled in their triacylglycerol and cholesterol moieties, was lower in TNF-treated than in control rats. However, the clearance rate of triacylglycerol was the same or even higher in recombinant HuTNF-alpha treated rats (assuming that 14C-labeled chylomicron triacylglycerol represents the serum triacylglycerol pool). The livers of recombinant HuTNF-alpha-treated rats and controls contained similar amounts of 14C-labeled lipids, but less [3H]cholesterol, suggesting that in recombinant HuTNF-alpha-treated rats, the liver took up chylomicron remnant particles enriched with triacylglycerol. Separation of the d less than 1.04 g/ml fraction of serum obtained from control and recombinant HuTNF-alpha treated rats by zonal ultracentrifugation revealed that in recombinant HuTNF-alpha-treated rats the lipoprotein particles were less lipolyzed than in controls. The secretion rate of [3H]triacylglycerol into the serum was determined 90 min after injection of [3H]palmitate albumin complex and Triton WR 1339. In recombinant HuTNF-alpha-treated rats, the secretion of [3H]triacylglycerol into plasma was 48% higher than in controls. It is suggested that the increase in lipoprotein lipase activity of heart and diaphragm resulted from an indirect effect of TNF. It is concluded that the increase in serum triacylglycerol in the recombinant HuTNF-alpha-treated rats is due mainly to an increased secretion of triacylglycerol by the liver. Impaired lipolysis, probably due to a fall in hepatic lipase could also contribute to the rise in plasma triacylglycerol.
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PMID:Mechanism of the hypertriglyceridemia induced by tumor necrosis factor administration to rats. 291 56

Conflicting data have been reported on the influence of (excess) glucocorticoids on lipoprotein lipase (LPL) activity in adipose tissue. To solve this problem hypercorticism was induced in rats by treatment for varying periods with Synacthen, a synthetic corticotrophin-1-24 preparation, and LPL was measured in the epididymal fat pads using different methods. In extracts of defatted tissue preparations from overnight fasted rats treated for 3 days with Synacthen we observed an increase in LPL activity (acetone-ether powder LPL) to values similar to those found in normally fed controls. In contrast, the heparin-elutable part of LPL activity in the tissue was not influenced by the Synacthen treatment. This activity remained significantly lower in overnight fasted animals, Synacthen treated or not, than in normally fed rats. Adrenalectomy lowered the acetone-ether powder LPL activity of the epididymal adipose tissue in fasted as well as in fed rats. In fasted rats it prevented the stimulation of the LPL activity by Synacthen.
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PMID:The effect of Synacthen administration on lipoprotein lipase activity in the epididymal fat pad of the rat. 299 75

Cultured rat epididymal preadipocytes exposed for 24-72 h to either bezafibrate or clofibrate added to the culture medium were extensively converted to fat-loaded adipocytes. Adipocyte conversion increased during the first 5-7 days following plating, reaching a level of 100% and 60% conversion with bezafibrate and clofibrate, respectively, as compared to 10% conversion in their absence. Adipocyte conversion in culture was a saturable function of the hypolipidemic effectors and was associated with an increase in the incorporation rate of exogenous palmitate into triacylglycerols, in glycerol-3-phosphate dehydrogenase and hormone-sensitive lipase activities but not in lipoprotein lipase activity. Adipocyte conversion by hypolipidemic drugs was much more prominent than that exerted by dibutyryl cAMP, and the relative conversion efficiency of the two fibrate drugs did not correlate with their respective cAMP content of the culture. Hence, hypolipidemic drugs and dibutyryl cAMP appear to act independently in initiating adipose conversion in primary epididymal preadipocytes.
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PMID:Adipose conversion of cultured rat primary preadipocytes by hypolipidemic drugs. 301 19

The mechanisms by which adrenaline brings about a reduction in the lipoprotein lipase activity of adipose tissue in vitro were investigated. The incorporation of [3H]leucine into lipoprotein lipase was measured during 1-h pulse incubations of rat epididymal fat bodies that had been preincubated for 4 h in the presence of glucose, insulin and dexamethasone. When adrenaline was added to the incubation medium at the start of the pulse, the incorporation of [3H]leucine was markedly reduced, suggesting that the rate of the enzyme's synthesis had decreased. On the other hand, the degradation of lipoprotein lipase, as measured by the loss of 3H-labelled enzyme protein during pulse-chase incubations of the epididymal fat bodies, was found to be significantly increased by the addition of adrenaline to the incubation medium at the start of the chase period. It is concluded that adrenaline is able both to inhibit the synthesis of lipoprotein lipase and to stimulate its degradation.
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PMID:Effects of adrenaline on the turnover of lipoprotein lipase in rat adipose tissue. 301 19

Rats were treated with Synacthen, a synthetic corticotrophin analogue, to induce hypercorticism. The epididymal fat pad was selectively cannulated and perfused. In fasted rats acetone ether powder lipoprotein lipase (LPL) activity rose during treatment to levels found in fed controls. In fed animals no further rise in LPL activity was observed during Synacthen treatment. However, the heparin-elutable LPL activity did not change during this treatment in fasted nor fed animals. Pharmacologic levels of insulin in the perfusion medium caused an increase in heparin-releasable LPL activity as a percentage of total fat pad LPL activity (15% v 48%). Hydrolysis of chylomicrons was higher in fasted three days treated animals then in controls (10 +/- 4% v 2 +/- 2%). In this group a higher uptake of liberated free fatty acids was found (2.6 +/- 1.5% v 1.0 +/- 0.5% in controls). The increase in hydrolysis rate and uptake of fatty acids in the treated fasted animals could not be explained by an increase in releasable LPL activity. Fatty acid release from the fat pad was lower in treated animals than in controls (fasted and fed), basally as well as after adrenalin stimulation. The observation that the epididymal fat pad retains its weight during hypercorticism may therefore be ascribed to an increased influx of fatty acids from increased hydrolysis of TG-rich particles and to an inhibited efflux of fatty acids from the adipocyte. The discrepancy between the LPL activity extractable from an acetone ether powder and the heparin releasable LPL activity suggests impairment of the transport of LPL from the adipocyte to the heparin releasable pool at the endothelium.
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PMID:Effects of synacthen on lipid metabolism in the perfused epididymal fat pad of the rat. 303 21

Female mice treated with 14C-2,4,5,2',4',5'-hexachlorobiphenyl (6-CB) two weeks prior to mating eliminated virtually their entire body burden of the compound through milk during one lactation cycle. 6-CB was shown to distribute among rat and human plasma lipoproteins and protein in vitro. It was readily transferred among plasma constituents and its distribution was related to the triacylglycerol:protein ratio in plasma. At one hour following its intravenous administration to virgin rats, 6-CB was primarily distributed to LDL. With the hypertriglyceridemia of late pregnancy, more than 70% of circulating 6-CB was associated with VLDL. VLDL is a major substrate for mammary gland lipoprotein lipase which is elevated during lactation. When 6-CB was complexed with human VLDL and injected i.v. into late pregnant mice, mammary gland concentrations of 6-CB exceeded those of adipose tissue at all sacrifice times between 5 min and 6 h. No differences between adipose tissue and mammary gland concentrations of 6-CB were observed with Emulphor:ethanol:saline as vehicle until 6 h. Isolated hepatocytes were capable of secreting protein and triacylglycerol in the form of VLDL into serum-free media. Eighty percent of 6-CB released from hepatocytes was in association with VLDL, with the remainder in association with protein. Adipocytes isolated from epididymal fat pads of male rats which were pretreated with 6-CB released progressively less radioactivity to incubation media with time after treatment even though PCB content of these cells increased. 6-CB may not be evenly distributed among adipocyte lipids.
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PMID:Potential mechanisms for redistribution of polychlorinated biphenyls during pregnancy and lactation. 310 24

Male Long-Evans rat pups were either fed by continuous intragastric infusion of a milk formula to match the growth rate of their normally reared siblings, or overfed by continuous infusion of a fat-supplemented formula from d 4 through d 18 postpartum. The early overfeeding accelerated growth and the overfed rats remained significantly heavier than normally reared siblings as adults. Early overfeeding with this procedure led to an adult obesity at 14 mo characterized by significantly larger epididymal and retroperitoneal fat depots resulting from an increase of both fat cell size and number, and by an increase in adipose tissue lipoprotein lipase activity. Gastrostomy rearing per se, without overfeeding, resulted in adult rats that weighed the same as normally reared siblings but had significantly larger retroperitoneal fat depots because of more adipocytes. These findings suggest that the quantity of food consumed during early growth and development, and the quality of early nutrition and/or the early rearing environment affect adipose tissue development and have long-term consequences that persist in the rat.
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PMID:Long-term effects on adiposity after preweaning nutritional manipulations in the gastrostomy-reared rat. 311 35

Testis growth is stimulated when short photoperiod-regressed Siberian hamsters are exposed to a lengthening photoperiod, an effect presumably mediated by the pineal gland through a decrease in the peak nocturnal duration of secretion of its hormone melatonin (MEL)(D. S. Carter and B. D. Goldman, Endocrinology 113: 1268-1273, 1983). We examined this stimulatory or "progonadal" effect of MEL in short photoperiod-regressed, adult male Siberian hamsters that were pinealectomized (PINX) and given timed daily subcutaneous 1) injections of MEL (1 or 10 micrograms/day) or saline or 2) infusions of MEL that were "long day-like" (4 h, 10 or 100 ng/day), "short day-like" (10 h, 10 ng/day), or control saline infusions (4 h/day). Photoregressed sham PINX hamsters were transferred to long days at this time. After 5 wk of treatment, 1-microgram MEL-injected hamsters and both groups of 4-h MEL-infused hamsters had stimulatory responses that mimicked those of the long-day-exposed, sham PINX group [i.e., increased testes, body, and epididymal white adipose tissue (EPIWAT) weights, total body fat, EPIWAT lipoprotein lipase activity, and serum prolactin and follicle-stimulating hormone levels]. These effects were not observed in 10-micrograms MEL- or saline-injected and 10-h MEL- or saline-infused hamsters. Thus the peak nocturnal duration of serum MEL is the critical parameter of the MEL secretion profile for stimulating a variety of photoperiodic responses when photoregressed hamsters are exposed to lengthening daylengths.
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PMID:Effects of melatonin on long-day responses in short-day housed adult Siberian hamsters. 314 82


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