BackgroundMaternal over and restricted nutrition has negative consequences on the muscle of offspring by reducing muscle fiber number and altering regulators of muscle growth. To determine if over and restricted maternal nutrition affected muscle growth and gene and protein expression in offspring, 36 pregnant ewes were fed 60%, 100% or 140% of National Research Council requirements from d 31 ± 1.3 of gestation until parturition. Lambs from control-fed (CON), restricted-fed (RES) or over-fed (OVER) ewes were necropsied within 1 d of birth (n = 18) or maintained on a control diet for 3 mo (n = 15). Semitendinosus muscle was collected for immunohistochemistry, and protein and gene expression analysis.ResultsCompared with CON, muscle fiber cross-sectional area (CSA) increased in RES (58%) and OVER (47%) lambs at 1 d of age (P < 0.01); however at 3 mo, CSA decreased 15% and 17% compared with CON, respectively (P < 0.01). Compared with CON, muscle lipid content was increased in OVER (212.4%) and RES (92.5%) at d 1 (P < 0.0001). Muscle lipid content was increased 36.1% in OVER and decreased 23.6% in RES compared with CON at 3 mo (P < 0.0001). At d 1, myostatin mRNA abundance in whole muscle tended to be greater in OVER (P = 0.07) than CON. Follistatin mRNA abundance increased in OVER (P = 0.04) and tended to increase in RES (P = 0.06) compared with CON at d 1. However, there was no difference in myostatin or follistatin protein expression (P > 0.3). Phosphorylated Akt (ser473) was increased in RES at 3 mo compared with CON (P = 0.006).ConclusionsIn conclusion, maternal over and restricted nutrient intake alters muscle lipid content and growth of offspring, possibly through altered gene and protein expression.
Poor maternal nutrition inhibits muscle development and postnatal muscle growth. Satellite cells are myogenic precursor cells that contribute to postnatal muscle growth, and their activity can be evaluated by the expression of several transcription factors. Pairedbox (Pax)7 is expressed in quiescent and active satellite cells. MyoD is expressed in activated and proliferating satellite cells and myogenin is expressed in terminally differentiating cells. Disruption in the expression pattern or timing of expression of myogenic regulatory factors negatively affects muscle development and growth. We hypothesized that poor maternal nutrition during gestation would alter the in vitro temporal expression of MyoD and myogenin in satellite cells from offspring at birth and 3 months of age. Ewes were fed 100% or 60% of NRC requirements from day 31 ± 1.3 of gestation. Lambs from control-fed (CON) or restricted-fed (RES) ewes were euthanized within 24 h of birth (birth; n = 5) or were fed a control diet until 3 months of age ( n = 5). Satellite cells isolated from the semitendinosus muscle were used for gene expression analysis or cultured for 24, 48 or 72 h and immunostained for Pax7, MyoD or myogenin. Fusion index was calculated from a subset of cells allowed to differentiate. Compared with CON, temporal expression of MyoD and myogenin was altered in cultured satellite cells isolated from RES lambs at birth. The percent of cells expressing MyoD was greater in RES than CON ( P = 0.03) after 24 h in culture. After 48 h of culture, there was a greater percent of cells expressing myogenin in RES compared with CON ( P < 0.001). After 72 h of culture the percent of satellite cells expressing myogenin in RES was less than CON ( P < 0.01). There were no differences in the gene expression of Pax7, Myf5 or MyoD in isolated satellite cells at birth ( P > 0.05). In satellite cells from RES lambs at 3 months of age, the percent of cells expressing MyoD and myogenin were greater than CON after 72 h in culture ( P < 0.05). Fusion index was reduced in RES lambs at 3 months of age compared with CON ( P < 0.001). Restricted nutrition during gestation alters the temporal expression of myogenic regulatory factors in satellite cells of the offspring, which may reduce the pool of myoblasts, decrease myoblast fusion and contribute to the poor postnatal muscle growth previously observed in these animals.
Hypothesis: Animals with cochlear implantation-induced hearing loss will have a lower endocochlear potential (EP) and decreased strial vascular density. Background: The cause of residual hearing loss following cochlear implantation remains poorly understood. Recent work from our lab has shown a correlation between vascular changes in the cochlear lateral wall and postimplantation hearing loss, suggesting a role of the stria vascularis and EP. Methods: Fourteen young, normal-hearing male albino guinea pigs underwent cochlear implantation using either a cochleostomy (CI-c, n = 9) or an extended round window (CI-eRW, n = 5) approach. Hearing sensitivity was assessed pre- and postoperatively using auditory brainstem response thresholds. Three weeks after implantation, EP measurements were obtained from the first and second turns. Hair cell counts and stria vascularis capillary density measurements were also obtained. Results: The implanted group experienced significant threshold elevations at 8 to 24 kHz (mean threshold shift 9.1 ± 1.1 dB), with a more robust threshold shift observed in the CI-eRW group compared to the CI-c group. Implanted animals had a significantly lower first turn EP (81.4 ± 5.1 mV) compared with controls (87.9 ± 6.1 mV). No differences were observed in the second turn (75.8 ± 12.0 mV for implanted animals compared to 76.5 ± 7.0 mV for controls). There were no significant correlations between turn-specific threshold shifts, EP measurements, or strial blood vessel density. Conclusions: Reliable EP measurements can be obtained in chronically implanted guinea pigs. Hearing loss after implantation is not explained by changes in strial vascular density or reductions in EP.
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