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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

LPL activity, total lipogenesis and rates of growth were determined for stromal-vascular cells derived from epididymal and inguinal depots of 13 1/2-week-old obese and lean Zucker rats. LPL activity, in cells of both depots, was found to increase between days 4 and 6 and decrease by day 8 in the presence of insulin. Inguinal derived fatty cell LPL activity increased between days 4 and 8 in contrast to lean cells which peaked at day 6 under basal growth conditions. LPL activity was elevated in fatty versus lean cells at days 6 and 8 in inguinal derived stromal vascular cells while in epididymal derived stromal vascular cells, LPL activity was elevated in lean versus fatty derived cells at day 4 and 6 but by day 8 the genotypic effect was reversed. Lipogenesis was elevated in lean versus fatty derived epididymal and inguinal cells at all concentrations of insulin and lean cells showed a dose-dependent response to insulin in contrast to fatty cells. There were no effects of genotype on the proliferative capacity of cells from either depot but some regional differences in growth were observed. These data illustrate that fa gene effects can be studied in primary cell culture.
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PMID:Regional and genotypic differences in stromal-vascular cells from obese and lean Zucker rats. 306 68

Functional lipoprotein lipase activity was recently described in rat brain. The present study was performed to further characterize the biologic significance of brain lipoprotein lipase (heparin releasable component) and elucidate regulatory factors. Comparative studies were performed on tissue (brain, adipose, and heart) heparin releasable lipoprotein lipase in the fasted and diabetic (streptozotocin 100 mg/kg BW IP) rat. Both fasting (96 hours) and diabetes (ten days) significantly decreased brain (cortical) (P less than .05) and adipose (epididymal fat pad) (P less than .001) lipoprotein lipase activity. In contrast, heart muscle enzyme activity was significantly increased (P less than .001) in response to fasting and diabetes. Refeeding (Purina chow 96 hours) and insulin replacement (96 hours) reversed these changes in tissue lipoprotein lipase consequent to fasting and diabetes, respectively. There was a positive correlation between the changes in serum insulin concentration and adipose lipoprotein lipase, but there was no correlation between this parameter and brain or heart lipoprotein lipase. In addition, although T3 therapy normalized the low T3 state associated with both fasting and diabetes, it had no effect on the enzyme activity in the studied tissues. However, subsequent studies demonstrated that hypothyroidism (2 weeks post thyroidectomy) significantly decreased brain lipoprotein lipase activity (P less than .001) and increased both the adipose (P less than .025) and heart (P less than .025) enzyme activity. T3 replacement (0.8 micrograms/100 BW/d for 1 week) reversed the effects of hypothyroidism. However, the relationship between brain enzyme activity and serum T3 was nonlinear as hyperthyroidism tended to reduce brain LPL activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Brain lipoprotein lipase is responsive to nutritional and hormonal modulation. 330 44

BAY g 5421 (acarbose) inhibits carbohydrate digestion in the gut, thereby reducing the rate of glucose absorption. This experiment tested whether long term administration of acarbose to developing Zucker "fatty" (fafa) rats would, by reducing several lipogenic factors, attenuate lipid deposition and reduce the hyperphagia and increased food motivated behavior of these animals. From 7 to 20 weeks of life groups of fatty and lean (FaFa) control rats were fed 0, 20 or 40 mg acarbose/100 g maintenance diet (45% carbohydrate, 35% fat, 20% protein calories), while an additional fatty and lean group were pair-fed to respective 40 mg acarbose groups. Lean groups fed acarbose exhibited dose dependent reductions of body weight, insulin, triglycerides, retroperitoneal and epididymal pad weight, adipocyte size, LPL activity/cell (retroperitoneal pad only), and lipid deposition both in total grams of fat and as a percentage of carcass weight. Fatty groups fed acarbose exhibited dose dependent reductions of insulin, blood glucose, retroperitoneal pad weight, and, at one of the two doses used, significantly lowered body weight, (40 mg), triglycerides (20 mg) and cholesterol (20 mg). However, acarbose-fed fatty groups failed to show significant reductions of adipocyte size, number or LPL activity/cell in retroperitoneal and epididymal fat pads, and maintained their obese body composition, on a percentage basis, at levels not significantly different from that of the 0 mg fatty control group. Acarbose administration led to an initial dose dependent reduction of food intake in both genotypes, which persisted for the lean groups. Fatties fed the 20 mg dose showed a gradual tendency (ns) towards increased daily intake, lever pressed at elevated rates for food pellets, and refed at faster rates following fasting. Fatties fed the 40 mg dose maintained their daily intake at fatty control levels, did not lever press at elevated rates, and showed significantly reduced refeeding following fasting. The 40 mg fatty and both lean acarbose treated groups had decreased sucrose solution preference. Possible bases for these differing effects of the drug on feeding behavior by the groups are considered.
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PMID:Effects of a glucosidase inhibitor (acarbose, BAY g 5421) on the development of obesity and food motivated behavior in Zucker (fafa) rats. 662 10

The purpose of the present study was to characterize the time course of adaptation (i.e., circulating metabolites and hormones, fat pad mass, lipoprotein lipase) to a high-fat diet in obesity-prone (OP) and obesity-resistant (OR) male Wistar rats. Delineation of OP and OR was based on body weight gain (upper tertile for OP; lower tertile for OR) after 1 wk on a high-fat diet (60% of kcal from corn oil). Rats were killed after 1, 2, or 5 wk of the dietary period. Increased body weight and percent body fat in OP rats at 1 wk could not be accounted for by increased retroperitoneal or epididymal fat pad weight. Plasma nonesterified fatty acids and triglycerides, as well as blood concentrations of glucose, lactate, and glycerol, were similar throughout the study. Plasma insulin was significantly greater in OP vs. OR rats and low-fat diet (LFD; 20% of kcal from corn oil) controls at 5 wk only, and blood beta-hydroxybutyrate (mM) was significantly higher in OR compared with OP and LFD rats at 1, 2, and 5 wk. Lipoprotein lipase mRNA and activity were significantly greater in epididymal fat pad and significantly lower in gastrocnemius muscle of OP vs. OR rats at 1 wk. Results suggest that early (i.e., 1 wk) differences in body weight and fat weight between OP and OR rats are not due to fat deposition in retroperitoneal or epididymal fat depots, and tissue-specific changes in LPL (increase in epididymal fat pad and decrease in gastrocnemius muscle) that occur in OP compared with OR rats after 1 wk on a high-fat diet provide a metabolic environment favoring fat storage.
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PMID:Time course of adaptation to a high-fat diet in obesity-resistant and obesity-prone rats. 809 9

Although there have been a number of studies of effects of diet and hormones on lipoprotein lipase (EC 3.1.1.34; LPL) activity and levels of LPL mRNA (Raynolds et al. 1990), there have been no studies which have investigated effects of different dietary fatty acids on LPL gene expression. In the present study male Wistar Albino rats were pair-fed diets containing 50 g fat/kg of different fatty acid composition for 2 weeks. The diets fed were (1) a mixed oil (450 g saturated fatty acids, 420 g monounsaturated fatty acids, 130 g polyunsaturated fatty acids/kg; n 8), (2) maize oil (n 8), or (3) fish oil (n 8). Animals were killed, RNA was extracted from liver and perirenal and epididymal fat pads, and analysed by 'Northern methodology'. Samples were hybridized to a human cDNA probe for LPL (Gotoda et al. 1989). Two transcripts were identified in epididymal and perirenal adipose tissue which were approximately 3.7 and 1.7 kb in size. The results suggested that (1) fish oil-fed animals had significantly greater production of LPL mRNA in epididymal adipose tissue compared with maize oil-fed animals (P < 0.05), (2) maize oil-fed animals had significantly greater production of LPL mRNA in perirenal fat compared with the other dietary groups (P < 0.05), (3) expression in the liver was not significant. Rats fed on a fish oil diet had significantly reduced plasma triacylglycerol concentrations compared with the mixed-oil group (P < 0.05), but there were no significant differences in plasma cholesterol. The differences in LPL could not be explained directly by the changes in plasma immunoreactive-insulin and glucose-dependent insulinotrophic polypeptide levels in the three groups.
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PMID:Pretranslational regulation of the expression of the lipoprotein lipase (EC 3.1.1.34) gene by dietary fatty acids in the rat. 829 11

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

Thiazolidinediones are antidiabetic agents, which not only improve glucose metabolism but also reduce blood triglyceride concentrations. These compounds are synthetic ligands for PPAR gamma, a transcription factor belonging to the nuclear receptor subfamily of PPARs, which are important transcriptional regulators of lipid and lipoprotein metabolism. The goal of this study was to evaluate the influence of a potent thiazolidinedione, BRL49653, on serum lipoproteins and to determine whether its lipid-lowering effects are mediated by changes in the expression of key genes implicated in lipoprotein metabolism. Treatment of normal rats for 7 days with BRL49653 decreased serum triglycerides in a dose-dependent fashion without affecting serum total and HDL cholesterol and apolipoprotein (apo) A-I and apo A-II concentrations. The decrease in triglyceride concentrations after BRL49653 was mainly due to a reduction of the amount of VLDL particles of unchanged lipid and apo composition. BRL49653 treatment did not change triglyceride production in vivo as analyzed by injection of Triton WR-1339, indicating a primary action on triglyceride catabolism. Analysis of the influence of BRL49653 on the expression of LPL and apo C-III, two key players in triglyceride catabolism, showed a dose-dependent increase in mRNA levels and activity of LPL in epididymal adipose tissue, whereas liver apo C-III mRNA levels remained constant. Furthermore, addition of BRL49653 to primary cultures of differentiated adipocytes increased LPL mRNA levels, indicating a direct action of the drug on the adipocyte. Simultaneous administration of BRL49653 and fenofibrate, a hypolipidemic drug that acts primarily on liver through activation of PPAR alpha both decreased liver apo C-III and increased adipose tissue LPL mRNA levels, resulting in a more pronounced lowering of serum triglycerides than each drug alone. In conclusion, both fibrates and thiazolidinediones exert a hypotriglyceridemic effect. While fibrates act primarily on the liver by decreasing apo C-III production, BRL49653 acts primarily on adipose tissue by increasing lipolysis through the induction of LPL expression. Drugs combining both PPAR alpha and gamma activation potential should therefore display a more efficient hypotriglyceridemic activity than either compound alone and may provide a rationale for improved therapy for elevated triglycerides.
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PMID:Regulation of lipoprotein metabolism by thiazolidinediones occurs through a distinct but complementary mechanism relative to fibrates. 932 74

We have previously shown in in vivo experiments that adipose tissue glyceroneogenesis is increased in rats adapted to a high-protein, carbohydrate-free (HP) diet. The objectives of the present study were (1) to verify if the increased glyceroneogenic activity is also observed in isolated adipocytes and (2) to investigate the role of preformed fatty acids in the production of the increased adipose tissue glyceroneogenesis. Control rats received a balanced diet, with the same lipid content of the HP diet. Glyceroneogenic activity was found to be higher in adipocytes from HP rats than in controls, as evidenced by increased rates of conversion of pyruvate and lactate to triacylglycerol (TAG)-glycerol. Administration of Triton WR 1339, which blocks the removal of TAG incorporated into circulating lipoproteins, to HP diet-adapted rats caused a significant reduction in the incorporation of 14C-pyruvate into TAG-glycerol by adipose tissue, which was accompanied by a marked inhibition of phosphoenolpyruvate carboxykinase activity, the key enzyme of glyceroneogenesis. The inhibitory effect of Triton on TAG-glycerol synthesis by adipose tissue was also observed in vivo, after administration of 3H2O. Adaptation to the HP diet induced a marked increase in the activity of retroperitoneal and epididymal fat LPL, which was restored to control values 24 hours after replacement of the HP diet by the balanced diet. The data suggest that in rats adapted to a carbohydrate-free diet, adipose tissue glyceroneogenesis is activated by an increased use of diet-derived fatty acids.
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PMID:Increased glyceroneogenesis in adipose tissue from rats adapted to a high-protein, carbohydrate-free diet: role of dietary fatty acids. 1632 24

Using a new serum-free primary culture system, we have previously reported genotypic differences between adipoblasts derived from the epididymal adipose deposit of lean and obese 8-week-old Zucker and Wistar Diabetic Fatty (WDF) rats (15). In these strictly controlled culture conditions, obese-derived adipoblasts expressed low levels of the late markers of differentiation (lipid accumulation, GPDH). In order to further characterize obese-derived adipoblasts and analyze the critical relationship between growth and differentiation, growth arrest was induced in lean- and obese-derived cultures using sodium butyrate treatment. Addition of 2.5 mM sodium butyrate to the serum-free medium from day 1 reduced markedly the growth of lean as well as obese-derived cells. Adipoconversion of lean-derived adipoblasts was not altered, similar levels of LPL and GPDH activities being obtained in control and butyrate-treated groups. By contrast, a marked increase in both activities was observed in obese-derived cultures, restoring the level of both markers of differentiation to the lean level. Similar results were obtained with adipoblasts derived from subcutaneous inguinal (ING) fat pad of obese Zucker as well as adipoblasts derived from ING and EPI fat deposits from obese WDF rats. Taken together, these results suggest that adipose deposits of these genetically obese rats contain a specific adipoblast population which differs from lean-derived adipoblasts in respect to its adipoconversion capacity and/or its stage of commitment to differentiation.
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PMID:Positive modulation of the adipoconversion of adipoblasts derived from genetically obese rats by sodium butyrate. 1635 85

Fenofibrate, a selective (1)PPAR-alpha activator, is prescribed to treat human dyslipidemia. The aim of this study was to delineate the mechanism of fenofibrate-mediated reductions in adiposity, improvements in insulin sensitivity, and lowering of triglycerides (TG) and free fatty acids (FFA) and to investigate if these favorable changes are related to the inhibition of lipid deposition in the aorta. To test this hypothesis we used male LDLr deficient mice that exhibit the clinical features of metabolic syndrome X when fed a high fat high cholesterol (HF) diet. LDLr deficient mice fed HF diet and simultaneously treated with fenofibrate (100 mg/kg body weight) prevented development of obesity, lowered serum triglycerides and cholesterol, improved insulin sensitivity, and prevented accumulation of lipids in the aorta. Lowering of circulating lipids occurred via down-regulation of lipogenic genes, including fatty acid synthase, acetyl CoA carboxylase and diacyl glycerol acyl transferase-2, concomitant with decreased liver TG and cholesterol, and TG output rate. Fenofibrate also suppressed liver apoCIII mRNA levels and markedly increased lipoprotein lipase mRNA levels, known to enhance serum TG catabolism. In addition, fenofibrate profoundly reduced epididymal fat and mesenteric fat mass to the levels seen in lean mice. The reductions in body weight were associated with elevation of hepatic uncoupling protein 2 (UCP2) mRNA, a concomitant increase in the ketone body formation, and improved insulin sensitivity associated with tumor necrosis factor-alpha reductions and phosphoenol pyruvate carboxykinase down-regulation. These results demonstrate that fenofibrate improves lipid abnormalities partly via inhibition of TG production and partly via clearance of TG-rich apoB particles by elevating LPL and reduced apoCIII. The prevention of obesity development occurred via energy expenditure. Fenofibrate-mediated hypolipidemic effects together with improved insulin sensitivity and loss of adiposity led to the reductions in the aortic lipid deposition by inhibiting early stages of atherosclerosis possibly via vascular cell adhesion molecule-1 (VCAM-1) modulation. These results suggest that potent PPAR-alpha activators may be useful in the treatment of syndrome X.
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PMID:Peroxisome proliferator-activated receptor-alpha selective ligand reduces adiposity, improves insulin sensitivity and inhibits atherosclerosis in LDL receptor-deficient mice. 1647 80


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