Muscle Development Of Offspring Research Articles

Maternal Supplementation of Collagen Peptide Chelated Trace Elements Enhances Skeletal Muscle Development in Chicks.

Maternal nutrition plays an important role in regulating the growth and development of offspring. Collagen peptide chelated trace elements (PTE), as a new additive, have been proven to have a positive maternal effect on the intestinal health of offspring, but its effect on the growth anddevelopment is still unclear. This study aimed to investigate the effect of maternal PTE supplementation on the skeletal muscle development of offspring. A total of 270 breeder hens were randomly divided into 3 groups, and fed basal diet (CON), basal diet + 500mg/kg PTE (L-PTE), and 1000mg/kg PTE (H-PTE) for 8weeks. A total of 180 eggs were collected from each group for incubation, and then the hatched male chicks (6 replicates, 12 chicks/replicate) were allocated according to maternal treatment for a 14-day feeding experiment. The results showed that maternal PTE supplementation significantly increased the deposition of iron (Fe), zinc (Zn), and manganese (Mn) in the egg yolk (P < 0.05). In comparison with the CON group, the body weight (days 1 and 14), breast muscle weight (day 14), and muscle fiber density (day 14) of broilers were increased in the L-PTE group (P < 0.05). The serum creatinine (CREA) levels in 1-day-old broilers were reduced in the L-PTE group and H-PTE group(P < 0.05). Additionally, maternal PTE supplementation could upregulate the relative expression level of catalase (CAT) mRNA in breast muscle (P < 0.05). The relative mRNA levels of hemeoxygenase-1 (HO-1) and superoxide dismutase 1(SOD1) in the H-PTE group were significantly upregulated (P < 0.05). Moreover, PTE treatment upregulated the mRNA expression of skeletal muscle development-related genes (Pax7 and MyoG) and the IGF signaling pathway (mTOR, IGF-1R, and IGF-2R) (P < 0.05). In conclusion, maternal PTE supplementation may improve the growth performance and skeletal muscle development of offspring by activating the IGF signaling pathway.

N-Acetylcysteine assists muscle development in offspring of mice subjected to maternal heat stress during pregnancy.

Heat stress (HS) has been shown to affect reproductive performance and muscle development negatively in animals. N-Acetylcysteine (NAC) plays a pivotal role in enhancing the antioxidant performance in animals as a recognized antioxidant. The present study assesses the potential of NAC to modulate the reproductive performance and antioxidant function in pregnant mice exposed to HS. The role of NAC in muscle development of offspring mice was also explored. The results showed that NAC supplementation from day 12 to day 18 of gestation increased the number of litters and enhanced the antioxidant function in pregnant mice under HS exposure. It improved the weight and body condition significantly in the offspring mice (P < 0.05). The alleviation of HS-induced muscle impairment with NAC was consistent with the alleviation of apoptosis, the enrichment of the proliferation and differentiation in the offspring mice muscle. N-Acetylcysteine also reversed HS-induced reduction in the cross-sectional area of the leg muscle and increased the proportion of myosin heavy chain IIx (MYHCIIx) in the muscle fiber. The results of the present study support the use of NAC at a dose of 100 mg kg-1 body weight as supplement for protecting the offspring derived from pregnant mice exposed to HS from muscle impairment by accelerating proliferation and differentiation. © 2024 Society of Chemical Industry.

The effect of chronic, non-pathogenic maternal immune activation on offspring postnatal muscle and immune outcomes.

The objective was to determine the effects of maternal inflammation on offspring muscle development and postnatal innate immune response. Sixteen first-parity gilts were randomly allotted to repeated intravenous injections with lipopolysaccharide (LPS; n=8, treatment code INFLAM) or comparable volume of phosphate buffered saline (CON, n=8). Injections took place every other day from gestational day (GD) 70 to GD 84 with an initial dose of 10μg LPS/kg body weight (BW) increasing by 12% each time to prevent endotoxin tolerance. On GD 70, 76, and 84, blood was collected at 0 and 4h postinjection via jugular or ear venipuncture to determine tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β concentrations. After farrowing, litter mortality was recorded, and the pig closest to litter BW average was used for dissection and muscle fiber characterization. On weaning (postnatal day [PND] 21), pigs were weighed individually and 2 barrows closest to litter BW average were selected for another study. The third barrow closest to litter BW average was selected for the postnatal LPS challenge. On PND 52, pigs were given 5μg LPS/kg BW via intraperitoneal injection, and blood was collected at 0, 4, and 8h postinjection to determine TNF-α concentration. INFLAM gilt TNF-α concentration increased (P<0.01) 4h postinjection compared to 0h postinjection, while CON gilt TNF-α concentration did not differ between time points. INFLAM gilt IL-6 and IL-1β concentrations increased (P=0.03) 4h postinjection compared to 0h postinjection on GD 70, but did not differ between time points on GD 76 and 84. There were no differences between INFLAM and CON gilts litter mortality outcomes (P≥0.13), but INFLAM pigs were smaller (P=0.04) at birth and tended (P=0.09) to be smaller at weaning. Muscle and organ weights did not differ (P≥0.17) between treatments, with the exception of semitendinosus, which was smaller (P<0.01) in INFLAM pigs. INFLAM pigs tended (P=0.06) to have larger type I fibers. INFLAM pig TNF-α concentration did not differ across time, while CON pig TNF-α concentration peaked (P=0.01) 4h postinjection. TNF-α concentration did not differ between treatments at 0 and 8h postinjection, but CON pigs had increased (P=0.01) TNF-α compared to INFLAM pigs 4h postinjection. Overall, maternal immune activation did not alter pig muscle development, but resulted in suppressed innate immune activation.

PSX-A-7 The Effect of Chronic Maternal Lipopolysaccharide Exposure During Late Gestation on Offspring Muscle Development

Abstract The objective of this study was to determine the effect of chronic inflammation during late gestation on offspring muscle development. Starting at gestational day (GD) 70, first-parity gilts were administered either lipopolysaccharide (LPS, n=7) or saline (CON, n=8) via jugular venipuncture every other day until GD 84. LPS was initially given at 10 µg/kg BW and was increased by 12% each instance of administration. Volume of PBS was increased accordingly. Rectal temperatures of gilts were collected at 0, 2, 3, and 4-h post injection. Gilts farrowed naturally at GD 114 (±2). At postnatal day (PND) 3, the pig closest to the average litter weight was euthanized, and the longissimus dorsi, psoas major, semitendinosus, heart, lungs, liver, and kidneys dissected and weighed. The semitendinosus was frozen in liquid N cooled-methylbutane and sectioned for muscle fiber typing analysis. Data were analyzed as a one-way ANOVA with cohort as a random effect and significance considered at (P ≤ 0.05). Gilts exposed to LPS had a 1.3°C increase in rectal temperature at 3 and 4-h post injection (P &amp;lt; 0.05), indicating successful induction of an inflammatory response. LPS exposure reduced (P = 0.04) the weight of piglets born alive and tended to reduce (P =0.09) the weight of piglets weaned, but did not alter the percent of pigs born alive or survival during the suckling period (P ≥ 0.29). Semitendinosus weight was also reduced (P &amp;lt; 0.01) in LPS pigs, and tended to be reduced (P =0.09) as a percentage of whole-body weight. However, there were no differences between treatments in any other tissues. Further, maternal LPS exposure did not alter fiber type proportions, average fiber area, or estimated number of fibers (P ≥ 0.17). Overall, these data indicate that chronic maternal LPS exposure during late gestation did not reduce offspring muscle fiber formation.

PSIII-A-11 Effects of Maternal Nutrition and Selenium Status on Postnatal Muscle Growth and Meat Quality

Abstract To investigate the effects of maternal nutritional plane and selenium (Se) level on offspring muscle development in first parity ewes, Rambouillet ewes (n = 84) were stratified by BW and randomized to receive diets formulated to contain adequate Se (ASe) or high Se (HSe) initiated at breeding. On d 40 of gestation, ewes were assigned randomly within Se treatments supply 60% (RES), 100% (CON), or 140% (HI) of NRC requirements. Offspring were slaughtered at 180 ± 2.2 d of age. Psoas major (PM), longissimuss dorsi (LD), and semimembranosus (SM) samples were snap frozen and analyzed for fiber diameter and type, celluarity, calpain 1 autolysis, and calpastatin expression. Within the PM RNA was increased (P=0.04) in HSe vs. ASe and CON vs. HI. Protein was greater (P=0.05) in ASe than HSe within HI. RES had greater (P=0.09) protein than CON. Calpain 1 had more autolysis in HSe vs. ASe (P≤0.03) in CON and HI. Calpastatin with lower molecular weights was greater (P≤0.01) in the Ase than HSe from CON. Within the SM, ASe had greater (P≤0.05) DNA and RNA concentrations than HSe within HI. Calpastatin immunoreactivity was less (P=0.04) for RES-ASe than all treatments except CON-HSe. Within the LD, calpain 1 had more (P≤0.01) autolytic degradation in CON-ASe than other treatments. Maternal diet did not influence fiber type or diameter. The influence of treatments on skeletal muscle cellularity and calpain system activation is not consistent between muscle types. The PM was most influenced by selenium in the HI group. Conversely, the LD showed more activation of calpain in the CON-ASe. Maternal diet and selenium possibly changed muscle development in offspring which could result in altered quality and yield of lamb produced.

The Effects of Maternal Intake of EPA and DHA Enriched Diet During Pregnancy and Lactation on Offspring's Muscle Development and Energy Homeostasis.

EPA and DHA are n-3 long-chain polyunsaturated fatty acids with a diversity of health benefits on offspring. The objective of this study was to test the in vivo effect of maternal ingestion of EPA and DHA on fetal and offspring muscle development and energy balance. Two groups of female C57BL/6 mice were fed EPA and DHA enriched diet (FA) and diet devoid of EPA and DHA (CON) respectively throughout the entire period of gestation and lactation. Embryos at E13 and offspring at age of D1 and D21 were selected for sample collection and processing. No change in birth number and body weight were observed between groups at D1 and D21. Transient increase in the expression levels of myogenesis regulating genes was detected at D1 (p < 0.05) in FA group. Most of the expression of muscle protein synthesis regulating genes were comparable (p > 0.05) between FA and CON groups at D1 and D21. The significant increase in MHC4, and IGF-1 was not linked to increased muscle mass. A persistent increase in ISR expression (p < 0.05) but not in GLUT-4 (p > 0.05) was detected in offspring. Up-regulation of adipogenesis regulating genes was accompanied by increasing intramuscular fat accumulation in the offspring of FA group. Considerable increase in transcripts of genes regulating lipid catabolism and thermogenesis in liver (p < 0.05) was noticed in FA group at D21; whereas, only the levels of carnitine palmitoyl transferase 1A (Cpt1α) and Enoyl-CoA Hydratase And 3-Hydroxyacyl CoA Dehydrogenase (Ehhadh) increased at D1. Similarly, genes regulating lipolysis were highly expressed at D21 in FA group. EPA and DHA treatment promoted BAT development and activity by increasing the expression of BAT signature genes (p < 0.05). Also, maternal intake of EPA and DHA enriched diet enhanced browning of sWAT. Taken together, maternal ingestion of EPA/DHA may be suggested as a therapeutic option to improve body composition and counteract childhood obesity- related metabolic disorders and confer lifelong positive metabolic impact on offspring.

Maternal Exercise Before and During Pregnancy Facilitates Embryonic Myogenesis by Enhancing Thyroid Hormone Signaling.

Background: Maternal exercise (ME) improves fetal and offspring muscle development, but mechanisms remain to be established. Since the thyroid hormone (TH) is critical for cell differentiation during embryonic development, we hypothesized that ME elevates TH receptor (THR) signaling in embryos, which promotes embryonic myogenesis. Methods: Female mice were exercised daily on a treadmill or received a daily TH, triiodothyronine (T3) injection. Embryos (embryonic day 12.5 [E12.5]) and P19 cells were used for studying effects of TH on embryonic myogenesis. TH levels in serum and embryos after ME or T3I were analyzed. Expression of TH signaling related genes and myogenic genes was assessed. THRα binding to the promoters of myogenic genes was investigated by chromatin immunoprecipitation-qantitative polymerase chain reaction (ChIP-qPCR). A CRISPR/CAS9 plasmid was utilized to knock out THRα in P19 cells. Results: ME elevated TH levels in both maternal circulation and embryos, which were correlated with enhanced TH signaling and myogenesis. At E12.5, both myogenic determinants (Pax3, Pax7) and myogenic regulatory factors (Myf5, Myod) were upregulated in ME embryos. ME increased THRα content and elevated messenger RNA (mRNA) expression of TH transporter Slc16a2 and deiodinase Dio2. In addition, the THRα binding to the promoters of Pax3/7 was increased. In P19 embryoid bodies, T3 promoted myogenic differentiation, which was abolished by ablating THRα. Furthermore, maternal daily injection of T3 at a level matching exercised mothers promoted embryonic myogenesis. Conclusions: ME promotes TH delivery to the embryos and enhances embryonic myogenesis, which is partially mediated by enhanced TH signaling in ME embryos.

Maternal Metformin Treatment during Gestation and Lactation Improves Skeletal Muscle Development in Offspring of Rat Dams Fed High-Fat Diet.

Maternal high-fat (HF) diet is associated with offspring metabolic disorder. This study intended to determine whether maternal metformin (MT) administration during gestation and lactation prevents the effect of maternal HF diet on offspring’s skeletal muscle (SM) development and metabolism. Pregnant Sprague-Dawley rats were divided into four groups according to maternal diet {CHOW (11.8% fat) or HF (60% fat)} and MT administration {control (CT) or MT (300 mg/kg/day)} during gestation and lactation: CH-CT, CH-MT, HF-CT, HF-MT. All offspring were weaned on CHOW diet. SM was collected at weaning and 18 weeks in offspring. Maternal metformin reduced plasma insulin, leptin, triglyceride and cholesterol levels in male and female offspring. Maternal metformin increased MyoD expression but decreased Ppargc1a, Drp1 and Mfn2 expression in SM of adult male and female offspring. Decreased MRF4 expression in SM, muscle dysfunction and mitochondrial vacuolization were observed in weaned HF-CT males, while maternal metformin normalized them. Maternal metformin increased AMPK phosphorylation and decreased 4E-BP1 phosphorylation in SM of male and female offspring. Our data demonstrate that maternal metformin during gestation and lactation can potentially overcome the negative effects of perinatal exposure to HF diet in offspring, by altering their myogenesis, mitochondrial biogenesis and dynamics through AMPK/mTOR pathways in SM.

The Physiological and Metabolic Effects of Maternal Intake of EPA and DHA during Pregnancy and Lactation on Offspring's Muscle Development and Energy Homeostasis

EPA and DHA are long-chain fatty acids with health benefits on offspring underpinning the accumulative recommendations for their prenatal ingestion. Recent in vivo studies have emerged indicating a positive correlation of EPA and DHA with fetal BAT development, while other in vitro trials demonstrated their negative implication in promoting fetal myoblast reprogramming into adipoblasts. Therefore, the objective of this study was to test the effect of maternal EPA and DHA on fetal muscle development and energy balance. Two groups of Female C57BL/6 mice were assigned to different diets throughout the entire period of gestation and lactation; the first group was fed EPA and DHA enriched diet (FA); whereas, the other was fed a diet devoid of n-3 PUFA (CON). Embryos at day 13 of gestation and offspring at age of 1 and 21day were selected for sample collection and processing. No change in little number and body weight were observed between groups in newborns at day1, but a tendency to weigh loss in the FA group was detected after weaning. Transient increase in the expression levels of MYOD1, MYOG, MRF4, and MHC4 were observed at day 1 post-parturition (P<0.05). Except of IGF-1 P<0.05, the expression levels of genes regulating muscle protein synthesis and catabolism were comparable (P>0.05) between groups at day 1 and 21. Persistent increase in ISR expression (P<0.05) but not in GLUT-4 (P>0.05) were detected in day 1 and 21 age offspring. An increase in the expression of PPARγ and AP2 but not C/EBPα (P<0.05) at day 1 were observed. The three key regulators of basal adipogenesis were up-regulated in weaned mice (P<0.05). Up-regulation of PPARγ, AP2, and C/EBPα levels were accompanied by increasing intramuscular fat accumulation in day 1 and 21 samples. Considerable increase in the transcripts of genes regulating lipid catabolism and thermogenesis in liver including Cpt1α,Ehhadh, Mcad, Lcad, Acadvl, slc22a5, slc25a20, and Pparα (P<0.05) was noticed in (FA) group after 21 day of treatment; whereas, only the transcripts of Cpt1α andEhhadh increased in day1 neonates’ livers . Similarly, genes regulating lipolysis (ATGL and HSL, MGL and LPL) were up-regulated at day 21 of treatment only in (FO) group (P<0.05) while EPA and DHA maternal intake does not affect the expression of lipogenesis regulating genes (Fasn and Srebp1c) (P>0.05) in day 1 and 21 offspring. EPA and DHA treatment promoted BAT development and activity through increasing the expression of BAT signature genes including (UCP1, Cidea, Prdm16, Pgc1α, Dio2, Zic1, Fgf21, P2rx5, and PPARα(P<0.05). Also, maternal intake of EPA/ DHA enriched diet enhanced browning of sWAT by stimulating the expression of beige markers such as UCP1, Shox2, Tmem26, and PAT2 and thermogenesis regulating genes (PPARα, PGC1α, Cox7α1, and Cox8β) (P<0.05). Taken together, maternal ingestion of EPA and DHA may be suggested as a therapeutic option to encounter many pathophysiological disorders, mainly childhood obesity, and confer long-lasting metabolic benefits on offspring.

Sex‐Specific Alterations on Muscle Plasticity and Myogenesis in Offspring Rats from Vitamin D Deficient Mothers

ObjectiveTo analyze the impact of maternal Vitamin D deficiency (VDD) on offspring muscle development in adulthood of male and female rats.MethodsTwelve 5‐week‐old female Wistar Hannover rats were fed either a Vit. D3+ diet (AIN93G with 1000 IU vitamin D3/kg diet) or Vit. D3− diet (AIN93G without vitamin D3) for six weeks and then bred to male rats. Mothers were maintained on the diets throughout gestation and lactation. At weaning, male and female offsprings were separated in four groups: male and female offspring control (M‐CTRL and F‐CTRL, respectively) pups of dams with Vit. D3+ diet; male and female offspring VDD (M‐VDD and F‐VDD, respectively) pups of dams with Vit. D3− diet. Offspring received a standard diet (Nuvilab) until 180 days of age, at which point tissues were harvested for analysis. *P≤0,05 (CEUA 052/2018).ResultsBoth male and female VDD groups showed a reduction in the calcidiol serum concentration (23±1 vs 40±2 ng/ml in M‐CTRL and 23±2.2 ng/ml vs 36.6±0.9 ng/ml in F‐CTRL) without affecting Ca+2 serum. At weaning, M‐VDD weighed less than M‐CTRL rats but recovered weight in the 60 days post weaning and acquired a greater body weight accompanied by a higher mass of white and brown adipose tissue at 180 days. Extensor digitorum longus (EDL) muscles from the M‐VDD showed a decrease (20 %; p&lt;0.05) in the number of total fibers and an increase in the cross sectional area of IIB (17 %), IIA (19 %) and IIAX (21%; p&lt;0.05) fibers. VDD also deregulated myogenesis as indicated by the higher levels of MyoD (43%; p&lt;0.05) and Myogenin (160%; p&lt;0.05) and in the number of satellite cells (128.8±14 vs 91±7.6 nuclei Pax7+ in the MO‐CTRL). To further investigate the signaling pathways involved in the muscle hypertrophy effect in the M‐VDD group, p‐IGF‐1/insulin receptor levels, and different insulin downstream targets related to protein synthesis including Ser 473p‐Akt, Ser 21/9 p‐GSK‐3β and Ser 209p‐eIF4e were measured. VDD increased all these parameters and in parallel increased plasma insulin and muscle IGF‐1 mRNA levels, but did not affect mTOR signaling. These changes were not found in Soleus from the M‐VDD group and in both EDL and Soleus from the female offspring.ConclusionMaternal VDD selectively affect the development of glycolytic muscle in male offspring characterized by hypoplasia, hypertrophy and deregulated myogenesis. The muscle hypertrophy is a compensatory mechanism probably due to the greater insulin sensitivity and activation of the Akt pathway. Muscles from female offspring seem to be protected from this metabolic disturbance showing a clear sex‐specific effect induced by maternal VDD.Support or Funding InformationFAPESP (19/06517‐1; 18/10089‐2)

Effect of dietary L-carnitine supplementation to sows during gestation and/or lactation on sow productivity, muscle maturation and lifetime growth in progeny from large litters.

Genetic selection for increased sow prolificacy has resulted in decreased mean piglet birth-weight. This study aimed to investigate the effect of L-carnitine (CAR) supplementation to sows during gestation and/or lactation on sow productivity, semitendinosus muscle (STM) maturity, and lifetime growth in progeny. Sixty-four sows were randomly assigned to one of four dietary treatments at breeding until weaning; CONTROL (0mg CAR/d), GEST (125mg CAR/d during gestation), LACT (250mg CAR/d during lactation), and BOTH (125mg CAR/d during gestation & 250mg CAR/d during lactation). The total number of piglets born per litter was greater for sows supplemented with CAR during gestation (17.3 v 15.8 ± 0.52; P<0.05). Piglet birth-weight (total and live) was unaffected by sow treatment (P>0.05). Total myofibre number (P=0.08) and the expression level of selected myosin heavy chain genes in the STM (P<0.05) was greater in piglets of sows supplemented with CAR during gestation. Pigs from sows supplemented with CAR during gestation had lighter carcasses at slaughter than pigs from non-supplemented sows during gestation (83.8 v 86.7 ± 0.86kg; P<0.05). In conclusion, CAR supplementation during gestation increased litter size at birth without compromising piglet birth-weight. Results also showed that the STM of piglets born to sows supplemented with CAR during gestation was more developed at birth. However, carcass weight at slaughter was reduced in progeny of sows supplemented with CAR during gestation. The CAR supplementation strategy applied during gestation in this study could be utilized by commercial pork producers to increase sow litter size and improve offspring muscle development.

Poor maternal nutrition during gestation in sheep alters prenatal muscle growth and development in offspring.

Poor maternal nutrition during gestation can have immediate and life-long negative effects on offspring growth and health. In livestock, this leads to reduced product quality and increased costs of production. Based on previous evidence that both restricted- and overfeeding during gestation decrease offspring muscle growth and alter metabolism postnatally, we hypothesized that poor maternal nutrition during gestation would reduce the growth and development of offspring muscle prenatally, reduce the number of myogenic progenitor cells, and result in changes in the global expression of genes involved in prenatal muscle development and function. Ewes were fed a control (100% NRC)-, restricted (60% NRC)-, or overfed (140% NRC) diet beginning on day 30 of gestation until days 45, 90, and 135 of gestation or until parturition. At each time point fetuses and offspring (referred to as CON, RES, and OVER) were euthanized and longissimus dorsi (LM), semitendinosus (STN), and triceps brachii (TB) were collected at each time point for histological and RNA-Seq analysis. In fetuses and offspring, we did not observe an effect of diet on cross-sectional area (CSA), but CSA increased over time (P < 0.05). At day 90, RES and OVER had reduced secondary:primary muscle fiber ratios in LM (P < 0.05), but not in STN and TB. However, in STN and TB percent PAX7-positive cells were decreased compared with CON (P < 0.05). Maternal diet altered LM mRNA expression of 20 genes (7 genes downregulated in OVER and 2 downregulated in RES compared with CON; 5 downregulated in OVER compared with RES; false discovery rate (FDR)-adj. P < 0.05). A diet by time interaction was not observed for any genes in the RNA-Seq analysis; however, 2,205 genes were differentially expressed over time between days 90 and 135 and birth (FDR-adj. P < 0.05). Specifically, consistent with increased protein accretion, changes in muscle function, and increased metabolic activity during myogenesis, changes in genes involved in cell cycle, metabolic processes, and protein synthesis were observed during fetal myogenesis. In conclusion, poor maternal nutrition during gestation contributes to altered offspring muscle growth during early fetal development which persists throughout the fetal stage. Based on muscle-type-specific effects of maternal diet, it is important to evaluate more than one type of muscle to fully elucidate the effects of maternal diet on offspring muscle development.

The effects of vitamin A supplementation during late-stage pregnancy on longissimus dorsi muscle tissue development, birth traits, and growth performance in postnatal Korean native calves.

ObjectiveThis study investigated the effects of vitamin A (VA) supplementation during late-stage pregnancy on longissimus dorsi muscle tissue development, birth traits, and growth performance of postnatal Korean native calves.MethodsIn the preliminary experiment, twenty-six pregnant cattle (initial body weight [BW] = 319 kg (standard deviation [SD] = 30.1; 1st parity) were randomly assigned to the control and treatment groups. The treatment group received VA supplementation at 24,000 IU/d from gestational day 225 until delivery. In the main experiment, twelve pregnant cattle (initial BW = 317 kg [SD = 31.3]; 1st parity) were treated with VA supplementation at 24,000 IU/d (gestational days 150 to 225) and at 78,000 IU/d (gestational day 225 until delivery). Serum VA levels were analyzed in pregnant cattle, and the growth performance, gene expression, and serum VA levels were analyzed in the offspring.ResultsSerum VA levels in pregnant cattle decreased the late gestation in both experiments (p<0.001). In the main experiment, pregnant cattle at parturition and offspring at birth in the treatment group had higher serum VA levels than those in the control group (p<0.05). In the treatment groups, an increased birth weight was observed in the main experimental group (p = 0.022), and a tendency (p = 0.088) toward an increased birth weight was observed in the preliminary experimental group. However, no differences were observed in the feed intake, average daily gain, gain-to-feed ratio, or BW of 31-day-old calves. Gene expression was analyzed in longissimus dorsi muscles of 31-day-old calves. VA supplementation in pregnant cattle stimulated postnatal muscle development in offspring by elevating myogenic factor 5 (MYF5), MYF6, and myoblast determination levels (p<0.05). Moreover, preadipocyte-related marker genes such as extracellular signal-regulated kinase 2 and krüppel-like factor 2 were higher in the treatment group than in the control group (p<0.05).ConclusionVA supplementation (78,000 IU/d) in late-stage pregnant cattle maintained serum VA levels. In addition, 78,000 IU/d VA supplementation increased the birth weight and expression of genes related to muscle and preadipocyte development in offspring. Overall, 78,000 IU/d VA supplementation in pregnant cattle is beneficial to newborn calves.

PSII-23 Concurrent supplementation of n-3 polyunsaturated fatty acids impairs C2C12 from the acquisition of functional brown adipocyte phenotype by negatively affecting the mitochondrial thermogenesis

Abstract Regarding the beneficial roles in fetal neurodevelopment, n-3 polyunsaturated fatty acids (PUFAs) are wildly used as dietary supplements during pregnancy. However, it may affect fetal and offspring muscle development and energy balance by changing the levels of key proteins controlling lipid metabolism and energy utilization. Regulation of energy balance in vivo is a topic of great interest and prominent goal for many studies. In this study, we focus on the effect of EPA and DHA on C2C12 brown adipogenic capacity. We demonstrated that the differentiation route of C2C12 into brown adipocytes was compromised by PUFA treatment through reducing their thermogenesis independent of UCP1 gene. This effect might be in part due to down-regulation of the expression of some brown adipocytes specific genes such as CP-3, DIO2, and PGC1α. Moreover, members of complex ІV (COX7a1 and COX8b) and complex V (ATP5j2) regulating ECT function were reduced in PUFA treated group. Also, mitochondrial biogenesis related genes including PGC1α, PGC1β, TFAM, and ERR-a were significantly suppressed by PUFA treatment. The mass spectrometric evaluation exhibited a strong correlation between PUFA treatment and the decreasing of levels of the proteins regulate Krebs cycle and ETC, such as ATP synthase α and β (F1F0 complex), citrate synthase, succinate CO-A, aconitate hydratase, and cytochrome c. Genomic and proteomic changes were accompanied by mitochondrial dysfunction represented by reducing oxygen consumption rate, ATP production, and proton leak (All statistically different at P &amp;lt; 0.05). In line with that, our results demonstrated an increase in lipid droplets size and number. EPA and DHA associated inhibition of the acquisition of functional brown adipocytes might negatively affect factor in the neonatal thermoregulation but potentially increase the intramuscular adipogenesis.

PSIV-8 Effects of restricted maternal nutrition and re-alimentation on fetal muscle development from mid to late gestation in sheep

Abstract Inadequate maternal nutrition during gestation negatively impacts offspring muscle development, which may be attenuated by re-alimentation. We hypothesized that restricted maternal nutrition would alter fetal muscle fiber cross-sectional area (CSA) and the percent of Pax7(+) progenitor cells. To test this, 48 primiparous ewes, pregnant with singletons, were fed 100% of NRC requirements (CON) between days 25 and 50 of gestation. At day 50 of gestation, seven ewes were euthanized for fetal sample collection. The remaining ewes were fed either CON or 60% NRC requirements (RES). At day 90 of gestation, seven ewes per diet were euthanized for fetal sample collection. The remaining ewes were maintained on their current diet (CON-CON, RES-RES) or switched to the alternate diet (CON-RES, RES-CON). At day 130 of gestation, all ewes (n = 6 or 7 ewes/diet) were euthanized, and fetal samples were collected. On days 90 and 130, fetal longissimus (LM) and triceps brachii (TB) were collected and immunostained for enumeration of Pax7(+) cells and muscle fiber CSA. The percent of Pax7(+) cells was determined by dividing the number of Pax7(+) cells by the total number of cells. At day 90 of gestation, the percent of Pax7(+) cells was less (P &amp;lt; 0.01) in the TB of RES compared with CON. At day 130, fiber CSA was greater (P &amp;lt; 0.04) in RES-CON compared with CON-CON, CON-RES, and RES-CON in the TB, and was greater (P &amp;lt; 0.02) in RES-CON compared with RES-RES and CON-RES in the LM. An effect of maternal nutrition was not observed for the percent of Pax7(+) cells in the LM, or for CSA at day 90 in either muscle. Thus, restricted maternal nutrition during early to mid-gestation alters the percent of Pax7(+) cells at mid-gestation in a muscle specific manner. Re-alimentation during late gestation increased fiber CSA, demonstrating that re-alimentation alters fetal muscle development.

Effects of maternal dietary supplementation of phytosterol esters during gestation on muscle development of offspring in mice

The development of muscle in the embryo, which is crucial for postnatal skeletal muscle growth, has been investigated widely. Much has been learned during the past several decades about the role of maternal nutrition in the outcome of pregnancy. Protein and carbohydrate levels during pregnancy have been shown to be important in the development of offspring, especially muscle development. However, the maternal effects of steroids were still not clear. Phytosterol esters (PEs) are produced by the esterification of phytosterols and fatty acids and have many beneficial functions, such as anti-inflammation and hypolipemic functions. Through the effect of regulation on lipid metabolism, can pregnant mice fed with PEs show any programming effect on the muscle development of offspring? In our study, PEs were supplied to the maternal diet, and changes in maternal lipid metabolism and the development of offspring skeletal muscle were detected. As a result, the amniotic fluid total bile acid (TBA) and total cholesterol (TC) levels were decreased; the growth of offspring was significantly faster than that of the control group until 6 weeks of age. Adult offspring had a higher lean mass index and grip strength. In skeletal muscle, the proportion of myosin heavy chain (MHC) 1 was significantly decreased, while the proportion of MHC 2 b was increased. In conclusion, maternal PEs significantly reduced sterols in the amniotic fluid, while skeletal muscle development was promoted in the offspring.

498 Implications of maternal infection and inflammation for offspring muscle development.

498 Implications of maternal infection and inflammation for offspring muscle development.

Transcriptomics-Related Mechanisms of Supplementing Laying Broiler Breeder Hens with Dietary Daidzein to Improve the Immune Function and Growth Performance of Offspring.

Daidzein (DA) is an isoflavone that is primarily extracted from soy plants. This study evaluated the effects of supplementing laying broiler breeder hens with dietary DA on the immune function and growth performance of their offspring and the underlying mechanism. A total of 720 breeders were divided into three treatment groups that were fed either a control diet (CON), a DA-low-supplemented diet (DLS, CON+20 mg/kg DA), or a DA-high-supplemented diet (DHS, CON+100 mg/kg DA) for 8 weeks, and eggs were collected for hatching during the final week. The broiler offspring received a basal diet for 42 days, and blood, livers, and immune organs were collected at 21 and 42 days of age. DLS treatment promoted embryonic development and increased growth hormone levels, body weight, feed intake, and carcass traits on days 21 and 42 of broilers. Additionally, the IgA and IgG concentrations, antibody titers, and antioxidant capacity of broilers were increased at 21 days of age, and B lymphocyte differentiation was increased at 42 days. Besides, DLS treatment upregulated the expression of genes related to embryonic and muscle development in offspring and regulated mitogen-activated protein kinase (MAPK), transforming growth factor beta (TGF-β), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and Toll-like receptor signaling. DHS treatment decreased the percentage of abdominal fat in the broilers at 42 days, but it did not significantly affect embryonic development, growth performance, or IgA and IgG concentrations. In summary, providing dietary DA supplementation at 20 mg/kg to broiler breeders can improve their immune function and growth performance.

Sex-Specific Muscular Maturation Responses Following Prenatal Exposure to Methylation-Related Micronutrients in Pigs.

Supplementation of micronutrients involved in DNA methylation, particularly during pregnancy, is recommended because of its impacts on human health, but further evidence is needed regarding the effects of over-supplementation and differences between sexes. Here, a porcine model was used to assess effects of maternal supplementation with one-carbon-cycle compounds during prenatal and postnatal stages on offspring muscle development. Sows received either a standard diet (CON) or a standard diet supplemented with folate, B6, B12, methionine, choline, and zinc (MET) throughout gestation. Myogenesis-, growth-, and nutrient utilization-related transcript expression was assessed using quantitative PCR. Organismal phenotype and gene expression effects differed significantly between males and females. Male MET-offspring showed increased fetal weight during late pregnancy but decreased live weight postnatally, with compensatory transcriptional responses comprising myogenic key drivers (Pax7, MyoD1, myogenin). In contrast, female weights were unaffected by diet, and mRNA abundances corresponded to a phenotype of cellular reorganization via FABP3, FABP4, SPP1 and Insulin-like Growth Factor-signaling. These findings in an animal model suggest that supplementation during pregnancy with methylation-related micronutrients can promote sex-specific myogenic maturation processes related to organismal growth and muscle metabolism. The usage of maternal dietary supplements should be more carefully considered regarding its ability to promote fetal and postnatal health.

Improving maternal vitamin D status promotes prenatal and postnatal skeletal muscle development of pig offspring

ObjectiveVitamin D deficiency is a worldwide problem. Although vitamin D has been implicated in muscle development, little is known about the effects of maternal vitamin D status on the muscle development of offspring. The aim of this study was to evaluate the effects of improving maternal vitamin D status by dietary 25-hydroxyvitamin D3 (25 OHD3) supplementation on prenatal and postnatal skeletal muscle development of offspring, using pigs as the model. MethodsTwenty gilts were allocated to a normal vitamin D (ND) dietary group with 50 μg/kg vitamin D3 or a high-vitamin D (HD) group with an additional 50 μg/kg 25 OHD3 from mating to weaning. Muscle samples were obtained from piglets at birth and weaning. ResultsSerum 25 OHD concentrations were significantly increased in gilts and newborn piglets in the HD group compared with those in the ND group (P < 0.01). Maternal HD significantly increased numbers of muscle fiber in the longissimus dorsi (LM) of newborn piglets (+23.53%; P < 0.01) and weaning piglets (+27.47%; P < 0.05). Meanwhile, maternal HD had significant effects on cross-sectional areas of muscle fiber in psoas major (PM; +12.82%; P < 0.05) and LM (+22.62%; P < 0.05) of weaning piglets. Reverse transcription polymerase chain reaction revealed that PM and LM of piglets from the HD group had higher IGF2, IGF2 R, MyOD1, and myogenin mRNA expressions, but lower MyHC Ι and myostatin mRNA expressions than those of the ND piglets (P < 0.05). ConclusionThese results suggest that improving maternal vitamin D status by dietary supplementation with 25 OHD3 can promote prenatal and postnatal skeletal muscle development of pig offspring by modulating the expressions of muscle transcription factors.