Chronic mild prenatal stress exacerbates the allergen-induced airway inflammation in rats.
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The effects of chronic mild prenatal stress on leukocyte infiltration into the airways was investigated in rat offspring. The chronic prenatal stress consisted of transitory and variable changes in the rat's living conditions. Offspring at adult age were actively sensitized (day 0) and intratracheally challenged (day 14) with ovalbumin. Bronchoalveolar lavage was performed in the offspring at 48 h after intratracheal challenge with ovalbumin. A significant increase in total leukocyte infiltration was observed in the non-stressed offspring group and this was associated with a marked recruitment of eosinophils without a significant effect on the influx of neutrophils and mononuclear cells. In the prenatal stressed offspring, the counts of both total leukocyte and eosinophils, as well as mononuclear cells, was increased by 50% compared to the non-stressed offspring. We provide here the first experimental evidence that chronic mild unpredictable prenatal stress produces a marked increase in the allergen-induced airway inflammation in the rat offspring. (+info)
Orally administered leucine stimulates protein synthesis in skeletal muscle of postabsorptive rats in association with increased eIF4F formation.
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We investigated the protein synthetic response of skeletal muscle to an orally administered dose of leucine given alone or in combination with carbohydrate. Male rats were freely fed (F) or food deprived for 18 h; food-deprived rats were then administered saline (S), carbohydrate (CHO), leucine (L) or a combination of carbohydrate plus leucine (CL). CHO and CL meals were isocaloric and provided 15% of daily energy requirements. L and CL meals each delivered 270 mg leucine. Muscle protein synthesis in S was 65% of F (P<0.01) 1 h after meal administration. Concomitant with lower rates of protein synthesis, phosphorylation of the translational repressor, eukaryotic initiation factor (eIF)4E-binding protein 1 (4E-BP1), was less in S, leading to greater association of 4E-BP1.eIF4E, and reduced formation of the active eIF4G.eIF4E complex compared with F (P<0.01). Oral administration of leucine (L or CL), but not CHO, restored protein synthesis equal to that in F and resulted in 4E-BP1 phosphorylation that was threefold greater than that of S (P<0.01). Consequently, formation of 4E-BP1.eIF4E was inhibited and eIF4G.eIF4E was not different from F. The amount of eIF4E in the phosphorylated form was greater in S and CHO (P<0.01) than in all other groups. In contrast, no differences in the phosphorylation state of eIF2alpha or the activity of eIF2B were noted among treatment groups. Serum insulin was elevated 2.6- and 3.7-fold in CHO and CL, respectively, but was not different in L, compared with S (P<0.05). These results suggest that leucine stimulates protein synthesis in skeletal muscle by enhancing eIF4F formation independently of increases in serum insulin. (+info)
Restricted feed intake during fattening reduces intramuscular lipid deposition without modifying muscle fiber characteristics in rabbits.
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The present study was conducted to determine the effects of feed restriction during fattening on muscle fiber characteristics and intramuscular lipid traits. From 11 wk of age onward, rabbits were given free access to feed (control group), or received 70% of the control feed intake (restricted group). At the same weight at slaughter, restricted-fed rabbits were 3 wk older than controls (18 vs. 15 wk). The longissimus lumborum (LL, white loin), biceps femoris (BF, white thigh) and semimembranosus proprius (SMP, red thigh) muscles were then removed, and biochemical and histochemical assays were performed. In the three muscles, there was no effect of feed restriction on mean fiber size or percentage of the different fiber types. Restricted vs. control feeding resulted in a significant reduction (P<0.001) in total lipid content in all three muscles. This reduction was paralleled by a decline (P<0.001) in the activities of the malic enzyme and glucose-6 phosphate dehydrogenase (G6PDH), generating NADPH for the support of fatty acid synthesis. The diet-induced variations in lipid concentration and enzyme activities were larger (P<0.05) in the pure oxidative SMP muscle than in the predominantly fast-twitch glycolytic LL and BF muscles. Whatever feeding status, the ratio of malic enzyme to G6PDH activities was sharply lower (P<0.001) in SMP than in BF and LL muscles (averaging 1.5 vs. 9 and 15, respectively). These data indicate that nutritional status regulates intramuscular lipid deposition, without changing fiber-type composition. Further studies are necessary to determine the role of G6PDH in the lipogenic process of oxidative vs. glycolytic muscles. (+info)
Very-low-density lipoprotein binding to the apolipoprotein E receptor 2 is enhanced by lipoprotein lipase, and does not require apolipoprotein E.
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The apolipoprotein (apo)E receptor 2 (apoER2) is a recently cloned member of the low-density lipoprotein (LDL) receptor (LDLR) family, showing a high homology with both the LDLR and the very-low-density lipoprotein (VLDL) receptor (VLDLR). In the present study, the binding characteristics of the apoER2 with respect to apoE and lipoprotein lipase (LPL) were investigated. VLDL was isolated from both apoE-deficient mice and mice expressing the human APOE2 (Arg(158)-->Cys) and APOE3-Leiden isoforms on an Apoe(-/-),Ldlr(-/-) double knock-out background. apoE-rich rabbit beta-VLDL was used as a positive control for binding. Binding experiments performed with Chinese hamster ovary cells expressing the human apoER2 showed that the receptor was able to bind VLDL containing either of the apoE isoforms, as well as the apoE-deficient VLDL. Hence, in contrast with the VLDLR, the apoER2 is not strictly dependent on apoE for VLDL binding. Since LPL has been shown to enhance the binding of lipoproteins to several members of the LDLR family, including the LDLR-related protein, VLDL receptor, gp330 and the LDLR itself, VLDL binding experiments were performed in the presence of LPL. Addition of LPL resulted in a significant increase in apoER2 binding for all VLDL fractions used in this study. In conclusion, lipoprotein binding of VLDL to the apoER2 is enhanced in the presence of LPL, and is not restricted to apoE-containing lipoproteins. (+info)
6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase gene expression is regulated by diet composition and ration size in liver of gilthead sea bream, Sparus aurata.
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Modulation of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (6PF-2-K/Fru-2,6-P(2)ase) gene expression by diet composition and ration size was studied in the liver of gilthead sea bream, Sparus aurata. From five different types of diet supplied to fish, those with either high carbohydrate/low protein or high carbohydrate/low lipid content stimulated 6PF-2-K/Fru-2,6-P(2)ase expression at the levels of mRNA, immunodetectable protein and kinase activity as well as promoting higher fructose-2,6-bisphosphate (Fru-2,6-P(2)) values. The expression of the bifunctional enzyme and Fru-2,6-P(2) levels showed also direct dependence on the quantity of diet supplied. These findings demonstrate for the first time nutritional regulation of 6PF-2-K/Fru-2,6-P(2)ase at mRNA level by diet composition and ration size and suggest that the carnivorous fish S. aurata can adapt its metabolism, by stimulation of liver glycolysis, to partial substitution of protein by carbohydrate in the diet. In addition, the expression of 6PF-2-K/Fru-2,6-P(2)ase can be used as an indicator of nutritional condition. (+info)
Leptin-specific patterns of gene expression in white adipose tissue.
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Leptin is a hormone that regulates body weight by decreasing food intake and increasing energy expenditure. ob/ob mice carry leptin mutations and are obese and hyperphagic. Leptin administration to lean and ob/ob mice activates a novel metabolic program that depletes adipose tissue. Although this response is physiologically distinct from that evident after food restriction, the molecular nature of these differences is as yet unknown. Expression monitoring of 6500 genes using oligonucleotide microarrays in wild-type, ob/ob, and transgenic mice expressing low levels of leptin revealed that differences in ambient leptin levels have dramatic effects on the phenotype of white adipose tissue. These data identified a large number of genes that are differentially expressed in ob/ob mice. To delineate the components of the transcriptional program specifically affected by leptin, the level of the same 6500 genes was monitored in wild-type and ob/ob mice at various times after leptin treatment or food restriction. A novel application of k-means clustering identified 8 clusters of adipose tissue genes whose expression was different between leptin treatment and food restriction in ob/ob mice and 10 such clusters in wild-type experiments. One of the clusters was repressed specifically by leptin in both wild-type and ob/ob mice and included several genes known to be regulated by SREBP-1/ADD1. Further studies confirmed that leptin decreases the levels of SREBP-1/ADD1 RNA and transcriptionally active SREBP-1/ADD1 protein in white adipose tissue. Future studies of the molecular basis for the apparent coordinate regulation of the other clusters of leptin-regulated genes may reveal additional mechanisms by which leptin exerts its weight-reducing effects. (+info)
Effects of energy intake, implantation, and subcutaneous fat end point on feedlot steer performance and carcass composition.
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The purpose of this experiment was to evaluate the effects of energy intake, implantation, and fat end point on feedlot performance and carcass composition of steers. Three hundred eighty-four yearling crossbred steers (368 +/- 23.1 kg) were allotted in a completely randomized design. Treatments were arranged in a 2 x 3 x 2 factorial experiment. Main effect factors were two levels of intake, three implant strategies, and two compositional fat end points at slaughter. The levels of intake were ad libitum (AL) and restricted (RS) intake (90% ad libitum). The three implant strategies were Revalor-S (REV) (120 mg trenbolone acetate, 24 mg estradiol), Synovex-Plus (SYN) (200 mg trenbolone acetate, 28 mg estradiol benzoate), and no implant (control). The compositional target end points were 1.0 and 1.4 cm s.c. fat cover over the 12th and 13th rib. Restricted-intake steers consumed 9.2% less (P < .01) DM than AL steers. Ad libitum-intake steers gained weight 15.5% more rapidly (P < .01) than RS-intake steers. Steers implanted with REV tended (P < .07) to gain faster than SYN steers, who in turn gained 15.2% more (P < .01) than control steers. Ad libitum-intake steers were 4.8% more (P < .01) efficient than RS steers. Steers fed to a targeted 1.4 cm s.c. backfat cover were 2.9% less (P < .05) efficient than steers fed to 1.0 cm, and steers implanted with either REV or SYN had similar (P = .47) feed efficiencies, whereas control steers had lower (P < .01) feed efficiencies. Steers fed to a targeted compositional fat end point of 1.4 cm had 1.3% higher (P < .01) dressing percentage (DP) than steers fed to 1.0 cm. Control and SYN steers had similar (P = .13) DP; however, REV steers had 6.1% greater (P < .01) DP than SYN steers. Steers fed to 1.4 cm s.c. fat end point had higher (P < .01) numerical yield grades than steers fed to 1.0 cm (3.34 vs 2.71). There was an interaction (P < .01) for intake level and implant for marbling score. Marbling scores were lower (P < .05) for RS x SYN and AL x REV than in other treatments. Steers on the RS x REV treatment were intermediate in marbling to all treatments except AL control, which was higher (P < .01) than RS x SYN, AL x REV, and RS x REV. No interaction for dry matter intake level and anabolic implants was observed for growth performance. The depression in carcass quality resulting from implanting is reduced as backfat increases from 1.0 to 1.4 cm at slaughter. (+info)
Effect of feed restriction on adipose tissue transcript concentrations in genetically lean and obese pigs.
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To determine possible genetic influences on the steady-state concentrations of several key transcription factor transcripts and the transcript concentrations for adipocyte-characteristic proteins, young, genetically obese and lean pigs were given ad libitum access or feed or were restrictively fed at 50% of ad libitum intake for 5 wk. Obese pigs were smaller and fatter than lean pigs, whether intake was ad libitum or restrictive. Plasma protein, albumin, and cholesterol concentrations were greater in obese than in lean pigs. Plasma NEFA, blood urea nitrogen, triacylglycerols, and postprandial glucose and insulin concentrations were less (P < .02) in pigs fed restrictively than in pigs with ad libitum access to feed, regardless of genetic group. The adipose tissue glucose transporter 4, fatty acid synthase, and leptin transcript concentrations were greater (P < .05) in obese than in lean pigs. The CCAAT/enhancer binding proteins beta and alpha, adipocyte fatty acid binding protein, hormone-sensitive lipase, and the beta1-adrenergic receptor transcript concentrations tended (P < . 10) to be greater in adipose tissue from obese than in that from lean pigs. Several other transcripts were numerically greater in obese than in lean pigs. The data collectively suggest that messenger RNA concentration for several adipose tissue proteins is a contributing factor to the excess fat deposition in these obese pigs. Restricted feeding did not change the concentration of any transcript except that for adipocyte fatty acid binding protein, which was reduced. The accretion of fat was markedly reduced in the restrictively fed pigs, but this diminution does not seem to be regulated by modulation of messenger RNA concentration. (+info)