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Abigail L Fowden - One of the best experts on this subject based on the ideXlab platform.

  • development and thyroid hormone dependence of skeletal muscle Mitochondrial Function towards birth
    The Journal of Physiology, 2020
    Co-Authors: Katie L Davies, Emily J Camm, E V Atkinson, T Lopez, Alison J. Forhead, Andrew J. Murray, Abigail L Fowden
    Abstract:

    KEY POINTS Skeletal muscle energy requirements increase at birth but little is known regarding the development of mitochondria that provide most of the cellular energy as ATP. Thyroid hormones are known regulators of adult metabolism and are important in driving several aspects of fetal development, including muscle fibre differentiation. Mitochondrial density and the abundance of Mitochondrial membrane proteins in skeletal muscle increased during late gestation. However, Mitochondrial Functional capacity, measured as oxygen consumption rate, increased primarily after birth. Fetal hypothyroidism resulted in significant reductions in Mitochondrial Function and density in skeletal muscle before birth. Mitochondrial Function matures towards birth and is dependent on the presence of thyroid hormones, with potential implications for the health of pre-term and hypothyroid infants. ABSTRACT Birth is a significant metabolic challenge with exposure to a pro-oxidant environment and the increased energy demands for neonatal survival. This study investigated the development of Mitochondrial density and activity in ovine biceps femoris skeletal muscle during the perinatal period and examined the role of thyroid hormones in these processes. Muscle capacity for oxidative phosphorylation increased primarily after birth but was accompanied by prepartum increases in Mitochondrial density and the abundance of electron transfer system (ETS) complexes I-IV and ATP-synthase as well as by neonatal upregulation of uncoupling proteins. This temporal disparity between prepartum maturation and neonatal upregulation of Mitochondrial oxidative capacity may protect against oxidative stress associated with birth while ensuring energy availability to the neonate. Fetal thyroid hormone deficiency reduced oxidative phosphorylation and prevented the prepartum upregulation of Mitochondrial density and ETS proteins in fetal skeletal muscle. Overall, the data show that Mitochondrial Function matures over the perinatal period and is dependent on thyroid hormones, with potential consequences for neonatal viability and adult metabolic health.

  • development and thyroid hormone dependence of skeletal muscle Mitochondrial Function towards birth
    The Journal of Physiology, 2020
    Co-Authors: Katie L Davies, Emily J Camm, E V Atkinson, T Lopez, Alison J. Forhead, Andrew J. Murray, Abigail L Fowden
    Abstract:

    KEY POINTS: Skeletal muscle energy requirements increase at birth but little is known about the development of mitochondria that provide most of the cellular energy as ATP. Thyroid hormones are known regulators of adult metabolism and are important in driving several aspects of fetal development, including muscle fibre differentiation. Mitochondrial density and abundance of Mitochondrial membrane proteins in skeletal muscle increased during late gestation. However, Mitochondrial Functional capacity, measured as oxygen consumption rate, increased primarily after birth. Fetal hypothyroidism resulted in significant reductions in Mitochondrial Function and density in skeletal muscle before birth. Mitochondrial Function matures towards birth and is dependent on the presence of thyroid hormones with potential implications for the health of pre-term and hypothyroid infants. ABSTRACT: Birth is a significant metabolic challenge with exposure to a pro-oxidant environment and the increased energy demands for neonatal survival. This study investigated the development of Mitochondrial density and activity in ovine biceps femoris skeletal muscle during the perinatal period and examined the role of thyroid hormones in these processes. Muscle capacity for oxidative phosphorylation increased primarily after birth but was accompanied by prepartum increases in Mitochondrial density and the abundance of electron transfer system (ETS) complexes I-IV and ATP-synthase as well as by neonatal upregulation of uncoupling proteins. This temporal disparity between prepartum maturation and neonatal upregulation of Mitochondrial oxidative capacity may protect against oxidative stress associated with birth while ensuring energy availability to the neonate. Fetal thyroid hormone deficiency reduced oxidative phosphorylation and prevented the prepartum upregulation of Mitochondrial density and ETS proteins in fetal skeletal muscle. Overall, the data show that Mitochondrial Function matures over the perinatal period and is dependent on thyroid hormones, with potential consequences for neonatal viability and adult metabolic health.

Alison J. Forhead - One of the best experts on this subject based on the ideXlab platform.

  • development and thyroid hormone dependence of skeletal muscle Mitochondrial Function towards birth
    The Journal of Physiology, 2020
    Co-Authors: Katie L Davies, Emily J Camm, E V Atkinson, T Lopez, Alison J. Forhead, Andrew J. Murray, Abigail L Fowden
    Abstract:

    KEY POINTS Skeletal muscle energy requirements increase at birth but little is known regarding the development of mitochondria that provide most of the cellular energy as ATP. Thyroid hormones are known regulators of adult metabolism and are important in driving several aspects of fetal development, including muscle fibre differentiation. Mitochondrial density and the abundance of Mitochondrial membrane proteins in skeletal muscle increased during late gestation. However, Mitochondrial Functional capacity, measured as oxygen consumption rate, increased primarily after birth. Fetal hypothyroidism resulted in significant reductions in Mitochondrial Function and density in skeletal muscle before birth. Mitochondrial Function matures towards birth and is dependent on the presence of thyroid hormones, with potential implications for the health of pre-term and hypothyroid infants. ABSTRACT Birth is a significant metabolic challenge with exposure to a pro-oxidant environment and the increased energy demands for neonatal survival. This study investigated the development of Mitochondrial density and activity in ovine biceps femoris skeletal muscle during the perinatal period and examined the role of thyroid hormones in these processes. Muscle capacity for oxidative phosphorylation increased primarily after birth but was accompanied by prepartum increases in Mitochondrial density and the abundance of electron transfer system (ETS) complexes I-IV and ATP-synthase as well as by neonatal upregulation of uncoupling proteins. This temporal disparity between prepartum maturation and neonatal upregulation of Mitochondrial oxidative capacity may protect against oxidative stress associated with birth while ensuring energy availability to the neonate. Fetal thyroid hormone deficiency reduced oxidative phosphorylation and prevented the prepartum upregulation of Mitochondrial density and ETS proteins in fetal skeletal muscle. Overall, the data show that Mitochondrial Function matures over the perinatal period and is dependent on thyroid hormones, with potential consequences for neonatal viability and adult metabolic health.

  • development and thyroid hormone dependence of skeletal muscle Mitochondrial Function towards birth
    The Journal of Physiology, 2020
    Co-Authors: Katie L Davies, Emily J Camm, E V Atkinson, T Lopez, Alison J. Forhead, Andrew J. Murray, Abigail L Fowden
    Abstract:

    KEY POINTS: Skeletal muscle energy requirements increase at birth but little is known about the development of mitochondria that provide most of the cellular energy as ATP. Thyroid hormones are known regulators of adult metabolism and are important in driving several aspects of fetal development, including muscle fibre differentiation. Mitochondrial density and abundance of Mitochondrial membrane proteins in skeletal muscle increased during late gestation. However, Mitochondrial Functional capacity, measured as oxygen consumption rate, increased primarily after birth. Fetal hypothyroidism resulted in significant reductions in Mitochondrial Function and density in skeletal muscle before birth. Mitochondrial Function matures towards birth and is dependent on the presence of thyroid hormones with potential implications for the health of pre-term and hypothyroid infants. ABSTRACT: Birth is a significant metabolic challenge with exposure to a pro-oxidant environment and the increased energy demands for neonatal survival. This study investigated the development of Mitochondrial density and activity in ovine biceps femoris skeletal muscle during the perinatal period and examined the role of thyroid hormones in these processes. Muscle capacity for oxidative phosphorylation increased primarily after birth but was accompanied by prepartum increases in Mitochondrial density and the abundance of electron transfer system (ETS) complexes I-IV and ATP-synthase as well as by neonatal upregulation of uncoupling proteins. This temporal disparity between prepartum maturation and neonatal upregulation of Mitochondrial oxidative capacity may protect against oxidative stress associated with birth while ensuring energy availability to the neonate. Fetal thyroid hormone deficiency reduced oxidative phosphorylation and prevented the prepartum upregulation of Mitochondrial density and ETS proteins in fetal skeletal muscle. Overall, the data show that Mitochondrial Function matures over the perinatal period and is dependent on thyroid hormones, with potential consequences for neonatal viability and adult metabolic health.

Katie L Davies - One of the best experts on this subject based on the ideXlab platform.

  • development and thyroid hormone dependence of skeletal muscle Mitochondrial Function towards birth
    The Journal of Physiology, 2020
    Co-Authors: Katie L Davies, Emily J Camm, E V Atkinson, T Lopez, Alison J. Forhead, Andrew J. Murray, Abigail L Fowden
    Abstract:

    KEY POINTS Skeletal muscle energy requirements increase at birth but little is known regarding the development of mitochondria that provide most of the cellular energy as ATP. Thyroid hormones are known regulators of adult metabolism and are important in driving several aspects of fetal development, including muscle fibre differentiation. Mitochondrial density and the abundance of Mitochondrial membrane proteins in skeletal muscle increased during late gestation. However, Mitochondrial Functional capacity, measured as oxygen consumption rate, increased primarily after birth. Fetal hypothyroidism resulted in significant reductions in Mitochondrial Function and density in skeletal muscle before birth. Mitochondrial Function matures towards birth and is dependent on the presence of thyroid hormones, with potential implications for the health of pre-term and hypothyroid infants. ABSTRACT Birth is a significant metabolic challenge with exposure to a pro-oxidant environment and the increased energy demands for neonatal survival. This study investigated the development of Mitochondrial density and activity in ovine biceps femoris skeletal muscle during the perinatal period and examined the role of thyroid hormones in these processes. Muscle capacity for oxidative phosphorylation increased primarily after birth but was accompanied by prepartum increases in Mitochondrial density and the abundance of electron transfer system (ETS) complexes I-IV and ATP-synthase as well as by neonatal upregulation of uncoupling proteins. This temporal disparity between prepartum maturation and neonatal upregulation of Mitochondrial oxidative capacity may protect against oxidative stress associated with birth while ensuring energy availability to the neonate. Fetal thyroid hormone deficiency reduced oxidative phosphorylation and prevented the prepartum upregulation of Mitochondrial density and ETS proteins in fetal skeletal muscle. Overall, the data show that Mitochondrial Function matures over the perinatal period and is dependent on thyroid hormones, with potential consequences for neonatal viability and adult metabolic health.

  • development and thyroid hormone dependence of skeletal muscle Mitochondrial Function towards birth
    The Journal of Physiology, 2020
    Co-Authors: Katie L Davies, Emily J Camm, E V Atkinson, T Lopez, Alison J. Forhead, Andrew J. Murray, Abigail L Fowden
    Abstract:

    KEY POINTS: Skeletal muscle energy requirements increase at birth but little is known about the development of mitochondria that provide most of the cellular energy as ATP. Thyroid hormones are known regulators of adult metabolism and are important in driving several aspects of fetal development, including muscle fibre differentiation. Mitochondrial density and abundance of Mitochondrial membrane proteins in skeletal muscle increased during late gestation. However, Mitochondrial Functional capacity, measured as oxygen consumption rate, increased primarily after birth. Fetal hypothyroidism resulted in significant reductions in Mitochondrial Function and density in skeletal muscle before birth. Mitochondrial Function matures towards birth and is dependent on the presence of thyroid hormones with potential implications for the health of pre-term and hypothyroid infants. ABSTRACT: Birth is a significant metabolic challenge with exposure to a pro-oxidant environment and the increased energy demands for neonatal survival. This study investigated the development of Mitochondrial density and activity in ovine biceps femoris skeletal muscle during the perinatal period and examined the role of thyroid hormones in these processes. Muscle capacity for oxidative phosphorylation increased primarily after birth but was accompanied by prepartum increases in Mitochondrial density and the abundance of electron transfer system (ETS) complexes I-IV and ATP-synthase as well as by neonatal upregulation of uncoupling proteins. This temporal disparity between prepartum maturation and neonatal upregulation of Mitochondrial oxidative capacity may protect against oxidative stress associated with birth while ensuring energy availability to the neonate. Fetal thyroid hormone deficiency reduced oxidative phosphorylation and prevented the prepartum upregulation of Mitochondrial density and ETS proteins in fetal skeletal muscle. Overall, the data show that Mitochondrial Function matures over the perinatal period and is dependent on thyroid hormones, with potential consequences for neonatal viability and adult metabolic health.

Maurine Neiman - One of the best experts on this subject based on the ideXlab platform.

  • Genetic Variation for Mitochondrial Function in the New Zealand Freshwater Snail Potamopyrgus antipodarum.
    Journal of Heredity, 2017
    Co-Authors: Joel Sharbrough, Jennifer L. Cruise, Megan Beetch, Nicole M Enright, Maurine Neiman
    Abstract:

    The proteins responsible for Mitochondrial Function are encoded by 2 different genomes with distinct inheritance regimes, rendering rigorous inference of genotype-phenotype connections intractable for all but a few model systems. Asexual organisms provide a powerful means to address these challenges because offspring produced without recombination inherit both nuclear and Mitochondrial genomes from a single parent. As such, these offspring inherit mitonuclear genotypes that are identical to the mitonuclear genotypes of their parents and siblings but different from those of other asexual lineages. Here, we compared Mitochondrial Function across distinct asexual lineages of Potamopyrgus antipodarum, a New Zealand freshwater snail model for understanding the evolutionary consequences of asexuality. Our analyses revealed substantial phenotypic variation across asexual lineages at 3 levels of biological organization: mitogenomic, organellar, and organismal. These data demonstrate that different asexual lineages have different Mitochondrial Function phenotypes, likely reflecting heritable variation (i.e., the raw material for evolution) for Mitochondrial Function in P. antipodarum. The discovery of this variation combined with the methods developed here sets the stage to use P. antipodarum to study central evolutionary questions involving Mitochondrial Function, including whether Mitochondrial mutation accumulation influences the maintenance of sexual reproduction in natural populations.

T Lopez - One of the best experts on this subject based on the ideXlab platform.

  • development and thyroid hormone dependence of skeletal muscle Mitochondrial Function towards birth
    The Journal of Physiology, 2020
    Co-Authors: Katie L Davies, Emily J Camm, E V Atkinson, T Lopez, Alison J. Forhead, Andrew J. Murray, Abigail L Fowden
    Abstract:

    KEY POINTS Skeletal muscle energy requirements increase at birth but little is known regarding the development of mitochondria that provide most of the cellular energy as ATP. Thyroid hormones are known regulators of adult metabolism and are important in driving several aspects of fetal development, including muscle fibre differentiation. Mitochondrial density and the abundance of Mitochondrial membrane proteins in skeletal muscle increased during late gestation. However, Mitochondrial Functional capacity, measured as oxygen consumption rate, increased primarily after birth. Fetal hypothyroidism resulted in significant reductions in Mitochondrial Function and density in skeletal muscle before birth. Mitochondrial Function matures towards birth and is dependent on the presence of thyroid hormones, with potential implications for the health of pre-term and hypothyroid infants. ABSTRACT Birth is a significant metabolic challenge with exposure to a pro-oxidant environment and the increased energy demands for neonatal survival. This study investigated the development of Mitochondrial density and activity in ovine biceps femoris skeletal muscle during the perinatal period and examined the role of thyroid hormones in these processes. Muscle capacity for oxidative phosphorylation increased primarily after birth but was accompanied by prepartum increases in Mitochondrial density and the abundance of electron transfer system (ETS) complexes I-IV and ATP-synthase as well as by neonatal upregulation of uncoupling proteins. This temporal disparity between prepartum maturation and neonatal upregulation of Mitochondrial oxidative capacity may protect against oxidative stress associated with birth while ensuring energy availability to the neonate. Fetal thyroid hormone deficiency reduced oxidative phosphorylation and prevented the prepartum upregulation of Mitochondrial density and ETS proteins in fetal skeletal muscle. Overall, the data show that Mitochondrial Function matures over the perinatal period and is dependent on thyroid hormones, with potential consequences for neonatal viability and adult metabolic health.

  • development and thyroid hormone dependence of skeletal muscle Mitochondrial Function towards birth
    The Journal of Physiology, 2020
    Co-Authors: Katie L Davies, Emily J Camm, E V Atkinson, T Lopez, Alison J. Forhead, Andrew J. Murray, Abigail L Fowden
    Abstract:

    KEY POINTS: Skeletal muscle energy requirements increase at birth but little is known about the development of mitochondria that provide most of the cellular energy as ATP. Thyroid hormones are known regulators of adult metabolism and are important in driving several aspects of fetal development, including muscle fibre differentiation. Mitochondrial density and abundance of Mitochondrial membrane proteins in skeletal muscle increased during late gestation. However, Mitochondrial Functional capacity, measured as oxygen consumption rate, increased primarily after birth. Fetal hypothyroidism resulted in significant reductions in Mitochondrial Function and density in skeletal muscle before birth. Mitochondrial Function matures towards birth and is dependent on the presence of thyroid hormones with potential implications for the health of pre-term and hypothyroid infants. ABSTRACT: Birth is a significant metabolic challenge with exposure to a pro-oxidant environment and the increased energy demands for neonatal survival. This study investigated the development of Mitochondrial density and activity in ovine biceps femoris skeletal muscle during the perinatal period and examined the role of thyroid hormones in these processes. Muscle capacity for oxidative phosphorylation increased primarily after birth but was accompanied by prepartum increases in Mitochondrial density and the abundance of electron transfer system (ETS) complexes I-IV and ATP-synthase as well as by neonatal upregulation of uncoupling proteins. This temporal disparity between prepartum maturation and neonatal upregulation of Mitochondrial oxidative capacity may protect against oxidative stress associated with birth while ensuring energy availability to the neonate. Fetal thyroid hormone deficiency reduced oxidative phosphorylation and prevented the prepartum upregulation of Mitochondrial density and ETS proteins in fetal skeletal muscle. Overall, the data show that Mitochondrial Function matures over the perinatal period and is dependent on thyroid hormones, with potential consequences for neonatal viability and adult metabolic health.