“…Here, caged chickens and females had higher lipid content in breast muscle than the penned ones and males. In a confined system with less area for activity, the oestrogen secreted by ovary could increase lipid deposition among myofibres (Choi et al 2012;Oosthuyse and Bosch, 2012). This result was consistent with higher intramuscular fat in barrows than in gilts (Correa et al 2006).…”
This study evaluated the effects of housing system (cage versus pen), sex and line cross (EMY1 and EMY2) on meat quality in meat-type chickens. Chickens (n ¼ 640) from each line cross (males: females ¼ 1:1) were housed in batteries from d 1 to 28. Then, half of them were transferred to indoor floor pens, and the others were raised in single cages. Meat quality traits of breast fillets were measured at 91 d of age. Percent lipid and histidine were higher, whereas % total protein and myofibre density (MDS) were lower in caged than penned chickens. Cross EMY1 had higher MDS, but lower lipid % and myofibre diameters (MDM) than EMY2 (p < .05). Males had redder and brighter muscles and higher MDM and contents of glycine and proline than the females (p < .05). Penned females had smaller MDM and higher MDS than their caged counterparts (p < .05). Generally, housing systems alone, or interacting with sex and genetic line, affected yellowness, myofibre characteristics, % protein, % lipid, myofibre density, and % His of breast muscle.
“…Here, caged chickens and females had higher lipid content in breast muscle than the penned ones and males. In a confined system with less area for activity, the oestrogen secreted by ovary could increase lipid deposition among myofibres (Choi et al 2012;Oosthuyse and Bosch, 2012). This result was consistent with higher intramuscular fat in barrows than in gilts (Correa et al 2006).…”
This study evaluated the effects of housing system (cage versus pen), sex and line cross (EMY1 and EMY2) on meat quality in meat-type chickens. Chickens (n ¼ 640) from each line cross (males: females ¼ 1:1) were housed in batteries from d 1 to 28. Then, half of them were transferred to indoor floor pens, and the others were raised in single cages. Meat quality traits of breast fillets were measured at 91 d of age. Percent lipid and histidine were higher, whereas % total protein and myofibre density (MDS) were lower in caged than penned chickens. Cross EMY1 had higher MDS, but lower lipid % and myofibre diameters (MDM) than EMY2 (p < .05). Males had redder and brighter muscles and higher MDM and contents of glycine and proline than the females (p < .05). Penned females had smaller MDM and higher MDS than their caged counterparts (p < .05). Generally, housing systems alone, or interacting with sex and genetic line, affected yellowness, myofibre characteristics, % protein, % lipid, myofibre density, and % His of breast muscle.
“…The concomitant increase in PPAR target genes involved in lipid synthesis (FAS) or transport (FAT) in lungs of female fetuses of diabetic rats fed the 6% olive-oil-or the 6% safflower-oil-supplemented diets indicates that this increase may contribute to the accumulation of triglycerides and to providing lipid substrates needed for the production of surfactant lipids in these experimental groups (Rehan & Torday 2012). The sex differences observed can be explained by the complex effects of estrogens, which induce profound changes in lipid metabolic pathways and regulate PPARs expression, and of androgens, which induce changes in the expression of multiple genes, including several PPAR coactivators and corepressors (Bresson et al 2010, Benz et al 2012, Oosthuyse & Bosch 2012.…”
Section: Discussionmentioning
confidence: 99%
“…There is strong evidence of diabetes-induced changes in lipid metabolism, sex-dependent changes in lipid metabolic pathways, and of the role of estrogens in lipid metabolism (Kautzky-Willer & Handisurya 2009, Benz et al 2012, Oosthuyse & Bosch 2012. Also estrogen-responsive elements are found in PPARs promoters, and estrogens can regulate PPARs expression and activation (Yoon 2009, Oosthuyse & Bosch 2012.…”
Maternal diabetes impairs fetal lung development. Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors relevant in lipid homeostasis and lung development. This study aims to evaluate the effect of in vivo activation of PPARs on lipid homeostasis in fetal lungs of diabetic rats. To this end, we studied lipid concentrations, expression of lipid metabolizing enzymes and fatty acid composition in fetal lungs of control and diabetic rats i) after injections of the fetuses with Leukotriene B 4 (LTB 4 , PPARa ligand) or 15deoxyD 12,14 prostaglandin J 2 (15dPGJ 2 , PPARg ligand) and ii) fed during pregnancy with 6% olive oil-or 6% safflower oil-supplemented diets, enriched with PPAR ligands were studied. Maternal diabetes increased triglyceride concentrations and decreased expression of lipid-oxidizing enzymes in fetal lungs of diabetic rats, an expression further decreased by LTB 4 and partially restored by 15dPGJ 2 in lungs of male fetuses in the diabetic group. In lungs of female fetuses in the diabetic group, maternal diets enriched with olive oil increased triglyceride concentrations and fatty acid synthase expression, while those enriched with safflower oil increased triglyceride concentrations and fatty acid transporter expression. Both olive oil-and safflower oil-supplemented diets decreased cholesterol and cholesteryl ester concentrations and increased the expression of the reverse cholesterol transporter ATP-binding cassette A1 in fetal lungs of female fetuses of diabetic rats. In fetal lungs of control and diabetic rats, the proportion of polyunsaturated fatty acids increased with the maternal diets enriched with olive and safflower oils. Our results revealed important changes in lipid metabolism in fetal lungs of diabetic rats, and in the ability of PPAR ligands to modulate the composition of lipid species relevant in the lung during the perinatal period.
“…Alternatively, because EBF2 and PRDM16 have both been shown to be sufficient to induce BAT differentiation and the "beiging" of white fat, and Ppar␥ is crucial for adipogenesis, further studies to address the role of this transcriptional network (31) and its interaction with cellular cholesterol metabolism in the modulation of SC-to-BAT differentiation is warranted. Additionally, gender-specific expression of cholesterol metabolism via estrogen-sensitive regulation of SRBI and other cholesterol homeostatic proteins has been reported in the literature (32)(33)(34)(35)(36), providing a possible mechanism for the exaggerated phenotype that we have reported previously in our female DKO model (12, 13); however, this requires further exploration to identify a causal linkage.…”
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