Maternal vitamin D deficiency affects the morphology and function of glycolytic muscle in adult offspring rats

Background Fetal stage is a critical developmental window for the skeletal muscle, but little information is available about the impact of maternal vitamin D (Vit. D) deficiency (VDD) on offspring lean mass development in the adult life of male and female animals. Methods Female rats (Wistar Hannove...

Full description

Saved in:
Bibliographic Details
Published inJournal of cachexia, sarcopenia and muscle Vol. 13; no. 4; pp. 2175 - 2187
Main Authors Reis, Natany G., Assis, Ana P., Lautherbach, Natália, Gonçalves, Dawit A., Silveira, Wilian A., Morgan, Henrique J.N., Valentim, Rafael R., Almeida, Lucas F., Heck, Lilian C., Zanon, Neusa M., Koike, Tatiana E., Santos, Audrei R., Miyabara, Elen H., Kettelhut, Isis C., Navegantes, Luiz C.
Format Journal Article
LanguageEnglish
Published Germany John Wiley & Sons, Inc 01.08.2022
John Wiley and Sons Inc
Wiley
Subjects
Online AccessGet full text

Cover

Loading…
Abstract Background Fetal stage is a critical developmental window for the skeletal muscle, but little information is available about the impact of maternal vitamin D (Vit. D) deficiency (VDD) on offspring lean mass development in the adult life of male and female animals. Methods Female rats (Wistar Hannover) were fed either a control (1000 IU Vit. D3/kg) or a VDD diet (0 IU Vit. D3/kg) for 6 weeks and during gestation and lactation. At weaning, male and female offspring were randomly separated and received a standard diet up to 180 days old. Results Vitamin D deficiency induced muscle atrophy in the male (M‐VDD) offspring at the end of weaning, an effect that was reverted along the time. Following 180 days, fast‐twitch skeletal muscles [extensor digitorum longus (EDL)] from the M‐VDD showed a decrease (20%; P < 0.05) in the number of total fibres but an increase in the cross‐sectional area of IIB (17%; P < 0.05), IIA (19%; P < 0.05) and IIAX (21%; P < 0.05) fibres. The fibre hypertrophy was associated with the higher protein levels of MyoD (73%; P < 0.05) and myogenin (55% %; P < 0.05) and in the number of satellite cells (128.8 ± 14 vs. 91 ± 7.6 nuclei Pax7 + in the M‐CTRL; P < 0.05). M‐VDD increased time to fatigue during ex vivo contractions of EDL muscles and showed an increase in the phosphorylation levels of IGF‐1/insulin receptor and their downstream targets related to anabolic processes and myogenic activation, including Ser 473Akt and Ser 21/9GSK‐3β. In such muscles, maternal VDD induced a compensatory increase in the content of calcitriol (two‐fold; P < 0.05) and CYP27B1 (58%; P < 0.05), a metabolizing enzyme that converts calcidiol to calcitriol. Interestingly, most morphological and biochemical changes found in EDL were not observed in slow‐twitch skeletal muscles (soleus) from the M‐VDD group as well as in both EDL and soleus muscles from the female offspring. Conclusions These data show that maternal VDD selectively affects the development of type‐II muscle fibres in male offspring rats but not in female offspring rats and suggest that the enhancement of their size and fatigue resistance in fast‐twitch skeletal muscle (EDL) is probably due to a compensatory increase in the muscle content of Vit. D in the adult age.
AbstractList BackgroundFetal stage is a critical developmental window for the skeletal muscle, but little information is available about the impact of maternal vitamin D (Vit. D) deficiency (VDD) on offspring lean mass development in the adult life of male and female animals.MethodsFemale rats (Wistar Hannover) were fed either a control (1000 IU Vit. D3/kg) or a VDD diet (0 IU Vit. D3/kg) for 6 weeks and during gestation and lactation. At weaning, male and female offspring were randomly separated and received a standard diet up to 180 days old.ResultsVitamin D deficiency induced muscle atrophy in the male (M-VDD) offspring at the end of weaning, an effect that was reverted along the time. Following 180 days, fast-twitch skeletal muscles [extensor digitorum longus (EDL)] from the M-VDD showed a decrease (20%; P < 0.05) in the number of total fibres but an increase in the cross-sectional area of IIB (17%; P < 0.05), IIA (19%; P < 0.05) and IIAX (21%; P < 0.05) fibres. The fibre hypertrophy was associated with the higher protein levels of MyoD (73%; P < 0.05) and myogenin (55% %; P < 0.05) and in the number of satellite cells (128.8 ± 14 vs. 91 ± 7.6 nuclei Pax7 + in the M-CTRL; P < 0.05). M-VDD increased time to fatigue during ex vivo contractions of EDL muscles and showed an increase in the phosphorylation levels of IGF-1/insulin receptor and their downstream targets related to anabolic processes and myogenic activation, including Ser 473Akt and Ser 21/9GSK-3β. In such muscles, maternal VDD induced a compensatory increase in the content of calcitriol (two-fold; P < 0.05) and CYP27B1 (58%; P < 0.05), a metabolizing enzyme that converts calcidiol to calcitriol. Interestingly, most morphological and biochemical changes found in EDL were not observed in slow-twitch skeletal muscles (soleus) from the M-VDD group as well as in both EDL and soleus muscles from the female offspring.ConclusionsThese data show that maternal VDD selectively affects the development of type-II muscle fibres in male offspring rats but not in female offspring rats and suggest that the enhancement of their size and fatigue resistance in fast-twitch skeletal muscle (EDL) is probably due to a compensatory increase in the muscle content of Vit. D in the adult age.
Abstract Background Fetal stage is a critical developmental window for the skeletal muscle, but little information is available about the impact of maternal vitamin D (Vit. D) deficiency (VDD) on offspring lean mass development in the adult life of male and female animals. Methods Female rats (Wistar Hannover) were fed either a control (1000 IU Vit. D3/kg) or a VDD diet (0 IU Vit. D3/kg) for 6 weeks and during gestation and lactation. At weaning, male and female offspring were randomly separated and received a standard diet up to 180 days old. Results Vitamin D deficiency induced muscle atrophy in the male (M‐VDD) offspring at the end of weaning, an effect that was reverted along the time. Following 180 days, fast‐twitch skeletal muscles [extensor digitorum longus (EDL)] from the M‐VDD showed a decrease (20%; P < 0.05) in the number of total fibres but an increase in the cross‐sectional area of IIB (17%; P < 0.05), IIA (19%; P < 0.05) and IIAX (21%; P < 0.05) fibres. The fibre hypertrophy was associated with the higher protein levels of MyoD (73%; P < 0.05) and myogenin (55% %; P < 0.05) and in the number of satellite cells (128.8 ± 14 vs. 91 ± 7.6 nuclei Pax7 + in the M‐CTRL; P < 0.05). M‐VDD increased time to fatigue during ex vivo contractions of EDL muscles and showed an increase in the phosphorylation levels of IGF‐1/insulin receptor and their downstream targets related to anabolic processes and myogenic activation, including Ser 473Akt and Ser 21/9GSK‐3β. In such muscles, maternal VDD induced a compensatory increase in the content of calcitriol (two‐fold; P < 0.05) and CYP27B1 (58%; P < 0.05), a metabolizing enzyme that converts calcidiol to calcitriol. Interestingly, most morphological and biochemical changes found in EDL were not observed in slow‐twitch skeletal muscles (soleus) from the M‐VDD group as well as in both EDL and soleus muscles from the female offspring. Conclusions These data show that maternal VDD selectively affects the development of type‐II muscle fibres in male offspring rats but not in female offspring rats and suggest that the enhancement of their size and fatigue resistance in fast‐twitch skeletal muscle (EDL) is probably due to a compensatory increase in the muscle content of Vit. D in the adult age.
Background Fetal stage is a critical developmental window for the skeletal muscle, but little information is available about the impact of maternal vitamin D (Vit. D) deficiency (VDD) on offspring lean mass development in the adult life of male and female animals. Methods Female rats (Wistar Hannover) were fed either a control (1000 IU Vit. D3/kg) or a VDD diet (0 IU Vit. D3/kg) for 6 weeks and during gestation and lactation. At weaning, male and female offspring were randomly separated and received a standard diet up to 180 days old. Results Vitamin D deficiency induced muscle atrophy in the male (M‐VDD) offspring at the end of weaning, an effect that was reverted along the time. Following 180 days, fast‐twitch skeletal muscles [extensor digitorum longus (EDL)] from the M‐VDD showed a decrease (20%; P < 0.05) in the number of total fibres but an increase in the cross‐sectional area of IIB (17%; P < 0.05), IIA (19%; P < 0.05) and IIAX (21%; P < 0.05) fibres. The fibre hypertrophy was associated with the higher protein levels of MyoD (73%; P < 0.05) and myogenin (55% %; P < 0.05) and in the number of satellite cells (128.8 ± 14 vs. 91 ± 7.6 nuclei Pax7 + in the M‐CTRL; P < 0.05). M‐VDD increased time to fatigue during ex vivo contractions of EDL muscles and showed an increase in the phosphorylation levels of IGF‐1/insulin receptor and their downstream targets related to anabolic processes and myogenic activation, including Ser 473Akt and Ser 21/9GSK‐3β. In such muscles, maternal VDD induced a compensatory increase in the content of calcitriol (two‐fold; P < 0.05) and CYP27B1 (58%; P < 0.05), a metabolizing enzyme that converts calcidiol to calcitriol. Interestingly, most morphological and biochemical changes found in EDL were not observed in slow‐twitch skeletal muscles (soleus) from the M‐VDD group as well as in both EDL and soleus muscles from the female offspring. Conclusions These data show that maternal VDD selectively affects the development of type‐II muscle fibres in male offspring rats but not in female offspring rats and suggest that the enhancement of their size and fatigue resistance in fast‐twitch skeletal muscle (EDL) is probably due to a compensatory increase in the muscle content of Vit. D in the adult age.
Fetal stage is a critical developmental window for the skeletal muscle, but little information is available about the impact of maternal vitamin D (Vit. D) deficiency (VDD) on offspring lean mass development in the adult life of male and female animals. Female rats (Wistar Hannover) were fed either a control (1000 IU Vit. D3/kg) or a VDD diet (0 IU Vit. D3/kg) for 6 weeks and during gestation and lactation. At weaning, male and female offspring were randomly separated and received a standard diet up to 180 days old. Vitamin D deficiency induced muscle atrophy in the male (M-VDD) offspring at the end of weaning, an effect that was reverted along the time. Following 180 days, fast-twitch skeletal muscles [extensor digitorum longus (EDL)] from the M-VDD showed a decrease (20%; P < 0.05) in the number of total fibres but an increase in the cross-sectional area of IIB (17%; P < 0.05), IIA (19%; P < 0.05) and IIAX (21%; P < 0.05) fibres. The fibre hypertrophy was associated with the higher protein levels of MyoD (73%; P < 0.05) and myogenin (55% %; P < 0.05) and in the number of satellite cells (128.8 ± 14 vs. 91 ± 7.6 nuclei Pax7 + in the M-CTRL; P < 0.05). M-VDD increased time to fatigue during ex vivo contractions of EDL muscles and showed an increase in the phosphorylation levels of IGF-1/insulin receptor and their downstream targets related to anabolic processes and myogenic activation, including Ser Akt and Ser GSK-3β. In such muscles, maternal VDD induced a compensatory increase in the content of calcitriol (two-fold; P < 0.05) and CYP27B1 (58%; P < 0.05), a metabolizing enzyme that converts calcidiol to calcitriol. Interestingly, most morphological and biochemical changes found in EDL were not observed in slow-twitch skeletal muscles (soleus) from the M-VDD group as well as in both EDL and soleus muscles from the female offspring. These data show that maternal VDD selectively affects the development of type-II muscle fibres in male offspring rats but not in female offspring rats and suggest that the enhancement of their size and fatigue resistance in fast-twitch skeletal muscle (EDL) is probably due to a compensatory increase in the muscle content of Vit. D in the adult age.
BACKGROUNDFetal stage is a critical developmental window for the skeletal muscle, but little information is available about the impact of maternal vitamin D (Vit. D) deficiency (VDD) on offspring lean mass development in the adult life of male and female animals. METHODSFemale rats (Wistar Hannover) were fed either a control (1000 IU Vit. D3/kg) or a VDD diet (0 IU Vit. D3/kg) for 6 weeks and during gestation and lactation. At weaning, male and female offspring were randomly separated and received a standard diet up to 180 days old. RESULTSVitamin D deficiency induced muscle atrophy in the male (M-VDD) offspring at the end of weaning, an effect that was reverted along the time. Following 180 days, fast-twitch skeletal muscles [extensor digitorum longus (EDL)] from the M-VDD showed a decrease (20%; P < 0.05) in the number of total fibres but an increase in the cross-sectional area of IIB (17%; P < 0.05), IIA (19%; P < 0.05) and IIAX (21%; P < 0.05) fibres. The fibre hypertrophy was associated with the higher protein levels of MyoD (73%; P < 0.05) and myogenin (55% %; P < 0.05) and in the number of satellite cells (128.8 ± 14 vs. 91 ± 7.6 nuclei Pax7 + in the M-CTRL; P < 0.05). M-VDD increased time to fatigue during ex vivo contractions of EDL muscles and showed an increase in the phosphorylation levels of IGF-1/insulin receptor and their downstream targets related to anabolic processes and myogenic activation, including Ser 473 Akt and Ser 21/9 GSK-3β. In such muscles, maternal VDD induced a compensatory increase in the content of calcitriol (two-fold; P < 0.05) and CYP27B1 (58%; P < 0.05), a metabolizing enzyme that converts calcidiol to calcitriol. Interestingly, most morphological and biochemical changes found in EDL were not observed in slow-twitch skeletal muscles (soleus) from the M-VDD group as well as in both EDL and soleus muscles from the female offspring. CONCLUSIONSThese data show that maternal VDD selectively affects the development of type-II muscle fibres in male offspring rats but not in female offspring rats and suggest that the enhancement of their size and fatigue resistance in fast-twitch skeletal muscle (EDL) is probably due to a compensatory increase in the muscle content of Vit. D in the adult age.
Author Miyabara, Elen H.
Morgan, Henrique J.N.
Zanon, Neusa M.
Assis, Ana P.
Gonçalves, Dawit A.
Heck, Lilian C.
Navegantes, Luiz C.
Koike, Tatiana E.
Almeida, Lucas F.
Reis, Natany G.
Silveira, Wilian A.
Kettelhut, Isis C.
Santos, Audrei R.
Valentim, Rafael R.
Lautherbach, Natália
AuthorAffiliation 4 Institute of Biological and Natural Science Federal University of Triângulo Mineiro Uberaba MG Brazil
2 Department of Biochemistry & Immunology Ribeirão Preto Medical School, University of São Paulo Ribeirão Preto SP Brazil
5 Department of Anatomy Institute of Biomedical Sciences, University of Sao Paulo São Paulo SP Brazil
1 Department of Physiology Ribeirão Preto Medical School, University of São Paulo Ribeirão Preto SP Brazil
3 Exercise Physiology Laboratory, School of Physical Education, Physiotherapy and Occupational Therapy Universidade Federal de Minas Gerais Belo Horizonte MG Brazil
AuthorAffiliation_xml – name: 2 Department of Biochemistry & Immunology Ribeirão Preto Medical School, University of São Paulo Ribeirão Preto SP Brazil
– name: 4 Institute of Biological and Natural Science Federal University of Triângulo Mineiro Uberaba MG Brazil
– name: 5 Department of Anatomy Institute of Biomedical Sciences, University of Sao Paulo São Paulo SP Brazil
– name: 3 Exercise Physiology Laboratory, School of Physical Education, Physiotherapy and Occupational Therapy Universidade Federal de Minas Gerais Belo Horizonte MG Brazil
– name: 1 Department of Physiology Ribeirão Preto Medical School, University of São Paulo Ribeirão Preto SP Brazil
Author_xml – sequence: 1
  givenname: Natany G.
  orcidid: 0000-0003-0391-7255
  surname: Reis
  fullname: Reis, Natany G.
  email: natany.garcia.reis@gmail.com
  organization: Ribeirão Preto Medical School, University of São Paulo
– sequence: 2
  givenname: Ana P.
  orcidid: 0000-0002-5738-9374
  surname: Assis
  fullname: Assis, Ana P.
  organization: Ribeirão Preto Medical School, University of São Paulo
– sequence: 3
  givenname: Natália
  orcidid: 0000-0001-6933-6598
  surname: Lautherbach
  fullname: Lautherbach, Natália
  organization: Ribeirão Preto Medical School, University of São Paulo
– sequence: 4
  givenname: Dawit A.
  orcidid: 0000-0003-2621-3330
  surname: Gonçalves
  fullname: Gonçalves, Dawit A.
  email: dawit@ufmg.br
  organization: Universidade Federal de Minas Gerais
– sequence: 5
  givenname: Wilian A.
  orcidid: 0000-0002-6171-7940
  surname: Silveira
  fullname: Silveira, Wilian A.
  organization: Federal University of Triângulo Mineiro
– sequence: 6
  givenname: Henrique J.N.
  orcidid: 0000-0001-5062-4493
  surname: Morgan
  fullname: Morgan, Henrique J.N.
  organization: Ribeirão Preto Medical School, University of São Paulo
– sequence: 7
  givenname: Rafael R.
  orcidid: 0000-0002-2352-6449
  surname: Valentim
  fullname: Valentim, Rafael R.
  organization: Ribeirão Preto Medical School, University of São Paulo
– sequence: 8
  givenname: Lucas F.
  orcidid: 0000-0002-5731-1219
  surname: Almeida
  fullname: Almeida, Lucas F.
  organization: Ribeirão Preto Medical School, University of São Paulo
– sequence: 9
  givenname: Lilian C.
  surname: Heck
  fullname: Heck, Lilian C.
  organization: Ribeirão Preto Medical School, University of São Paulo
– sequence: 10
  givenname: Neusa M.
  surname: Zanon
  fullname: Zanon, Neusa M.
  organization: Ribeirão Preto Medical School, University of São Paulo
– sequence: 11
  givenname: Tatiana E.
  orcidid: 0000-0002-9423-9965
  surname: Koike
  fullname: Koike, Tatiana E.
  organization: Institute of Biomedical Sciences, University of Sao Paulo
– sequence: 12
  givenname: Audrei R.
  orcidid: 0000-0002-9366-2593
  surname: Santos
  fullname: Santos, Audrei R.
  organization: Institute of Biomedical Sciences, University of Sao Paulo
– sequence: 13
  givenname: Elen H.
  orcidid: 0000-0002-2325-9571
  surname: Miyabara
  fullname: Miyabara, Elen H.
  organization: Institute of Biomedical Sciences, University of Sao Paulo
– sequence: 14
  givenname: Isis C.
  orcidid: 0000-0002-9034-5357
  surname: Kettelhut
  fullname: Kettelhut, Isis C.
  organization: Ribeirão Preto Medical School, University of São Paulo
– sequence: 15
  givenname: Luiz C.
  orcidid: 0000-0002-9870-9469
  surname: Navegantes
  fullname: Navegantes, Luiz C.
  email: navegantes@fmrp.usp.br
  organization: Ribeirão Preto Medical School, University of São Paulo
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35582969$$D View this record in MEDLINE/PubMed
BookMark eNp9kk1vEzEQhleoiJbSCz8AWeKCkFJs7_rrgoTCV1ErDsDZ8nrHiSOvHezdovx7nCZUlAO-2Jp59PiVZp42JzFFaJrnBF8SjOmbjS3jJaFK8kfNGSUKLzjG6uT4ZkqR0-ailA2up-OEM_ykOW0Zk1RxddbEGzNBjiagWz-Z0Uf0Hg3gvPUQ7Q4Z58BOBU1rQGPK23UKaVXLcUBujnbyKaLk0CrsbAq7yVs0zsUGQFVkhjlMtevKNvu4QtlM5Vnz2JlQ4OJ4nzc_Pn74vvy8uP766Wr57nphGZd8QSyhgpnWyR4EcaKTlEMnlLTO1aqw0gpXsykHDrhxbd9SSVtBJSGGStueN1cH75DMRtf_R5N3Ohmv7wopr7TJNW4AbWnPcWcHgZ3pOilMT7HpoFfcCeF6Wl1vD67t3I8wWIhTNuGB9GEn-rVepVutWiUpZVXw6ijI6ecMZdKjLxZCMBHSXDTlnDOGOSMVffkPuknzfjyVEpi1qg56n-j1gbI5lZLB3YchWO-3Qu-3Qt9tRYVf_B3_Hv2zAxUgB-CXD7D7j0p_WX67OUh_A4CIxoM
CitedBy_id crossref_primary_10_3390_nu16060906
crossref_primary_10_3390_ijms25084136
crossref_primary_10_3390_nu14214558
crossref_primary_10_1002_jcsm_13378
Cites_doi 10.1210/endo.132.1.8419119
10.1113/jphysiol.2006.112110
10.1210/en.2013-1938
10.1371/journal.pone.0010164
10.1056/NEJMra070553
10.3389/fped.2019.00022
10.1007/s00223-015-0054-x
10.1096/fj.10-168799
10.1016/j.molmet.2020.101059
10.1098/rsob.200048
10.1002/jcsm.12899
10.1038/cdd.2011.117
10.1371/journal.pone.0085283
10.1210/en.2015-1685
10.1210/en.2014-1016
10.1210/en.2003-0502
10.1210/en.2012-2245
10.1038/249083a0
10.1111/apha.13269
10.1111/febs.12253
10.1042/CS20060265
10.1016/0003-9861(82)90581-1
10.1016/j.nut.2016.03.004
10.1093/jn/123.11.1939
10.1016/j.bbadis.2014.12.006
10.2174/138920106776597621
10.1152/ajpcell.00014.2012
10.1002/mnfr.201300074
10.2527/jas.2013-6565
10.1111/j.1469-185X.1997.tb00016.x
10.1530/JOE-13-0567
10.1016/j.chembiol.2013.12.016
10.1016/j.jsbmb.2017.01.022
10.1095/biolreprod.104.034561
10.1371/journal.pone.0037890
10.1172/JCI113518
10.18632/aging.202669
10.1152/japplphysiol.00194.2021
10.1002/jcp.25388
ContentType Journal Article
Copyright 2022 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders.
2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Copyright_xml – notice: 2022 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders.
– notice: 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
DBID 24P
WIN
NPM
AAYXX
CITATION
3V.
7X7
7XB
8FI
8FJ
8FK
ABUWG
AFKRA
AZQEC
BENPR
CCPQU
DWQXO
FYUFA
GHDGH
K9.
M0S
PIMPY
PQEST
PQQKQ
PQUKI
7X8
5PM
DOA
DOI 10.1002/jcsm.12986
DatabaseName Wiley Online Library Open Access
Wiley Online Library website
PubMed
CrossRef
ProQuest Central (Corporate)
Health & Medical Collection
ProQuest Central (purchase pre-March 2016)
Hospital Premium Collection
Hospital Premium Collection (Alumni Edition)
ProQuest Central (Alumni) (purchase pre-March 2016)
ProQuest Central (Alumni)
ProQuest Central
ProQuest Central Essentials
ProQuest Central
ProQuest One Community College
ProQuest Central Korea
Health Research Premium Collection
Health Research Premium Collection (Alumni)
ProQuest Health & Medical Complete (Alumni)
Health & Medical Collection (Alumni Edition)
Publicly Available Content Database
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Academic
ProQuest One Academic UKI Edition
MEDLINE - Academic
PubMed Central (Full Participant titles)
DOAJ Directory of Open Access Journals
DatabaseTitle PubMed
CrossRef
Publicly Available Content Database
ProQuest Central Essentials
ProQuest One Academic Eastern Edition
ProQuest Health & Medical Complete (Alumni)
ProQuest Central (Alumni Edition)
ProQuest One Community College
ProQuest Hospital Collection
Health Research Premium Collection (Alumni)
ProQuest Hospital Collection (Alumni)
ProQuest Central
ProQuest Health & Medical Complete
Health Research Premium Collection
ProQuest One Academic UKI Edition
Health and Medicine Complete (Alumni Edition)
ProQuest Central Korea
ProQuest One Academic
ProQuest Central (Alumni)
MEDLINE - Academic
DatabaseTitleList Publicly Available Content Database


PubMed
MEDLINE - Academic
Database_xml – sequence: 1
  dbid: DOA
  name: DOAJ Directory of Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
– sequence: 2
  dbid: 24P
  name: Wiley Open Access
  url: https://authorservices.wiley.com/open-science/open-access/browse-journals.html
  sourceTypes: Publisher
– sequence: 3
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 4
  dbid: 7X7
  name: Health & Medical Collection
  url: https://search.proquest.com/healthcomplete
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
DocumentTitleAlternate Maternal vitamin D deficiency and skeletal muscle plasticity
EISSN 2190-6009
EndPage 2187
ExternalDocumentID oai_doaj_org_article_c2b604cd70fa4487ab20a4eb96f77fb2
10_1002_jcsm_12986
35582969
JCSM12986
Genre article
Journal Article
GeographicLocations United States--US
Fiji
GeographicLocations_xml – name: Fiji
– name: United States--US
GrantInformation_xml – fundername: São Paulo Research Foundation (FAPESP)
  funderid: 2018/10089‐2; 2019/06517‐1
– fundername: São Paulo Research Foundation (FAPESP)
  grantid: 2018/10089-2
– fundername: São Paulo Research Foundation (FAPESP)
  grantid: 2019/06517-1
– fundername: ;
  grantid: 2018/10089‐2; 2019/06517‐1
GroupedDBID ---
0R~
1OC
24P
2VQ
4.4
40G
53G
5VS
7X7
8FI
8FJ
AAHHS
AAKDD
AAZKR
ABUWG
ACCFJ
ACXQS
ADBBV
ADINQ
ADKYN
ADPDF
ADRAZ
ADZMN
ADZOD
AEEZP
AENEX
AEQDE
AFGXO
AFKRA
AFPKN
AHBYD
AHSBF
AIWBW
AJBDE
ALIPV
ALMA_UNASSIGNED_HOLDINGS
ALUQN
AMKLP
AOIJS
AVUZU
AZFZN
BAWUL
BCNDV
BENPR
BPHCQ
BVXVI
CCPQU
DIK
EBS
EJD
EMOBN
FYUFA
GROUPED_DOAJ
GX1
H13
HMCUK
HYE
IAO
IHR
INH
KQ8
M48
M~E
O9-
OK1
OVD
OVEED
PIMPY
PQQKQ
PROAC
RPM
RSV
SMD
SOJ
U2A
UKHRP
WIN
ZOVNA
ITC
NPM
AAYXX
CITATION
3V.
7XB
8FK
AZQEC
DWQXO
K9.
PQEST
PQUKI
7X8
5PM
ID FETCH-LOGICAL-c5686-1c1275a3f8be71f74826e4798cffa3f7c8c7faff9fefe6af3b3282372811a28c3
IEDL.DBID RPM
ISSN 2190-5991
IngestDate Tue Oct 22 15:02:39 EDT 2024
Tue Sep 17 20:50:15 EDT 2024
Sat Oct 05 05:18:07 EDT 2024
Tue Nov 05 12:42:19 EST 2024
Fri Dec 06 02:51:52 EST 2024
Wed Oct 16 00:41:34 EDT 2024
Sat Aug 24 00:54:29 EDT 2024
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 4
Keywords Muscle development
Vitamin D
Fetal programming
Skeletal muscle
Hypertrophy
Language English
License Attribution
2022 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders.
This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c5686-1c1275a3f8be71f74826e4798cffa3f7c8c7faff9fefe6af3b3282372811a28c3
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ORCID 0000-0003-2621-3330
0000-0002-9870-9469
0000-0001-6933-6598
0000-0002-2352-6449
0000-0002-2325-9571
0000-0002-9034-5357
0000-0002-9366-2593
0000-0002-9423-9965
0000-0002-5731-1219
0000-0001-5062-4493
0000-0003-0391-7255
0000-0002-5738-9374
0000-0002-6171-7940
OpenAccessLink https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9398225/
PMID 35582969
PQID 2705392982
PQPubID 4370305
PageCount 13
ParticipantIDs doaj_primary_oai_doaj_org_article_c2b604cd70fa4487ab20a4eb96f77fb2
pubmedcentral_primary_oai_pubmedcentral_nih_gov_9398225
proquest_miscellaneous_2666550651
proquest_journals_2705392982
crossref_primary_10_1002_jcsm_12986
pubmed_primary_35582969
wiley_primary_10_1002_jcsm_12986_JCSM12986
PublicationCentury 2000
PublicationDate August 2022
PublicationDateYYYYMMDD 2022-08-01
PublicationDate_xml – month: 08
  year: 2022
  text: August 2022
PublicationDecade 2020
PublicationPlace Germany
PublicationPlace_xml – name: Germany
– name: Heidelberg
– name: Hoboken
PublicationTitle Journal of cachexia, sarcopenia and muscle
PublicationTitleAlternate J Cachexia Sarcopenia Muscle
PublicationYear 2022
Publisher John Wiley & Sons, Inc
John Wiley and Sons Inc
Wiley
Publisher_xml – name: John Wiley & Sons, Inc
– name: John Wiley and Sons Inc
– name: Wiley
References 2019; 7
2020; 42
2015; 97
2006; 7
2013; 91
2016; 32
1974; 249
2019; 226
2012; 19
2015; 1852
2017; 173
2020; 10
2013; 280
2014; 155
2012; 303
2014; 21
1993; 123
2006; 575
2007; 357
2021; 13
2007; 112
1997; 72
2021; 12
2004; 71
2013; 57
2016; 157
2016; 231
2021; 131
2013; 154
1982; 213
2011; 25
2014; 9
2014; 221
2012; 7
1988; 81
2010; 5
2003; 144
1993; 132
e_1_2_8_28_1
e_1_2_8_29_1
e_1_2_8_24_1
e_1_2_8_25_1
e_1_2_8_26_1
e_1_2_8_27_1
e_1_2_8_3_1
e_1_2_8_2_1
e_1_2_8_5_1
e_1_2_8_4_1
e_1_2_8_7_1
e_1_2_8_6_1
e_1_2_8_9_1
e_1_2_8_8_1
e_1_2_8_20_1
e_1_2_8_21_1
e_1_2_8_22_1
e_1_2_8_23_1
e_1_2_8_40_1
e_1_2_8_17_1
e_1_2_8_18_1
e_1_2_8_39_1
e_1_2_8_19_1
e_1_2_8_13_1
e_1_2_8_36_1
e_1_2_8_14_1
e_1_2_8_35_1
e_1_2_8_15_1
e_1_2_8_38_1
e_1_2_8_16_1
e_1_2_8_37_1
e_1_2_8_32_1
e_1_2_8_10_1
e_1_2_8_31_1
e_1_2_8_11_1
e_1_2_8_34_1
e_1_2_8_12_1
e_1_2_8_33_1
e_1_2_8_30_1
References_xml – volume: 7
  year: 2019
  article-title: Sex differences in nutrition, growth, and metabolism in preterm infants
  publication-title: Front Pediatr
– volume: 231
  start-page: 2517
  year: 2016
  end-page: 2528
  article-title: Effects of 1,25(OH)2 D3 and 25(OH)D3 on C2C12 myoblast proliferation, differentiation, and myotube hypertrophy
  publication-title: J Cell Physiol
– volume: 155
  start-page: 3227
  year: 2014
  end-page: 3237
  article-title: The vitamin D receptor (VDR) is expressed in skeletal muscle of male mice and modulates 25‐hydroxyvitamin D (25OHD) uptake in myofibers
  publication-title: Endocrinology
– volume: 112
  start-page: 499
  year: 2007
  end-page: 506
  article-title: Proteasome proteolytic activity in skeletal muscle is increased in patients with sepsis
  publication-title: Clin Sci
– volume: 7
  start-page: 125
  year: 2006
  end-page: 132
  article-title: The role of insulin‐like growth factor I components in the regulation of vitamin D
  publication-title: Curr Pharm Biotechnol
– volume: 221
  start-page: R13
  year: 2014
  end-page: R29
  article-title: Endocrine regulation of fetal skeletal muscle growth: impact on future metabolic health
  publication-title: J Endocrinol
– volume: 280
  start-page: 4294
  year: 2013
  end-page: 4314
  article-title: Mechanisms regulating skeletal muscle growth and atrophy
  publication-title: FEBS J
– volume: 21
  start-page: 319
  year: 2014
  end-page: 329
  article-title: Vitamin D metabolism, mechanism of action, and clinical applications
  publication-title: Chem Biol
– volume: 72
  start-page: 329
  year: 1997
  end-page: 348
  article-title: Role of fetal and infant growth in programming metabolism in later life
  publication-title: Biol Rev Camb Philos Soc
– volume: 132
  start-page: 133
  year: 1993
  end-page: 138
  article-title: Insulin‐like growth factor‐I regulation of renal 25‐hydroxyvitamin D‐1‐hydroxylase activity
  publication-title: Endocrinology
– volume: 1852
  start-page: 490
  year: 2015
  end-page: 506
  article-title: Muscle‐specific GSK‐3β ablation accelerates regeneration of disuse‐atrophied skeletal muscle
  publication-title: Biochim Biophys Acta
– volume: 25
  start-page: 1028
  year: 2011
  end-page: 1039
  article-title: Novel insights into the regulation of skeletal muscle protein synthesis as revealed by a new nonradioactive in vivo technique
  publication-title: FASEB J
– volume: 7
  year: 2012
  article-title: Muscle fiber type‐dependent differences in the regulation of protein synthesis
  publication-title: PLoS ONE
– volume: 19
  start-page: 478
  year: 2012
  end-page: 487
  article-title: PI3K/AKT signaling determines a dynamic switch between distinct KSRP functions favoring skeletal myogenesis
  publication-title: Cell Death Differ
– volume: 12
  start-page: 2259
  year: 2021
  end-page: 2261
  article-title: Ethical guidelines for publishing in the Journal of Cachexia, Sarcopenia and Muscle: update 2021
  publication-title: J Cachexia Sarcopenia Muscle
– volume: 32
  start-page: 1144
  year: 2016
  end-page: 1152
  article-title: Improving maternal vitamin D status promotes prenatal and postnatal skeletal muscle development of pig offspring
  publication-title: Nutrition
– volume: 9
  year: 2014
  article-title: Leucine supplementation improves skeletal muscle regeneration after cryolesion in rats
  publication-title: PLoS ONE
– volume: 71
  start-page: 1968
  year: 2004
  end-page: 1973
  article-title: Effect of maternal nutrient restriction in sheep on the development of fetal skeletal muscle
  publication-title: Biol Reprod
– volume: 57
  start-page: 2137
  year: 2013
  end-page: 2146
  article-title: 1,25(OH) 2 ‐vitamin D 3 enhances the stimulating effect of leucine and insulin on protein synthesis rate through Akt/PKB and mTOR mediated pathways in murine C2C12 skeletal myotubes
  publication-title: Mol Nutr Food Res
– volume: 173
  start-page: 180
  year: 2017
  end-page: 184
  article-title: Skeletal muscle vitamin D in patients with end stage osteoarthritis of the knee
  publication-title: J Steroid Biochem Mol Biol
– volume: 91
  start-page: 4116
  year: 2013
  end-page: 4122
  article-title: Improvement of maternal vitamin D status with 25‐hydroxycholecalciferol positively impacts porcine fetal skeletal muscle development and myoblast activity
  publication-title: J Anim Sci
– volume: 226
  year: 2019
  article-title: Opposing effects of 25‐hydroxy‐ and 1α,25‐dihydroxy‐vitamin D 3 on pro‐cachectic cytokine‐and cancer conditioned medium‐induced atrophy in C2C12 myotubes
  publication-title: Acta Physiol
– volume: 213
  start-page: 538
  year: 1982
  end-page: 544
  article-title: Human serum binding protein for vitamin D and its metabolites (DBP): evidence that actin is the DBP binding component in human skeletal muscle
  publication-title: Arch Biochem Biophys
– volume: 249
  start-page: 83
  year: 1974
  end-page: 84
  article-title: Calcium uptake by sarcoplasmic reticulum of muscle from vitamin D‐deficient rabbits
  publication-title: Nature
– volume: 157
  start-page: 98
  year: 2016
  end-page: 111
  article-title: Evidence for vitamin D receptor expression and direct effects of 1α,25(OH)2D3 in human skeletal muscle precursor cells
  publication-title: Endocrinology
– volume: 5
  year: 2010
  article-title: Estrogen regulates estrogen receptors and antioxidant gene expression in mouse skeletal muscle
  publication-title: PLoS ONE
– volume: 123
  start-page: 1939
  year: 1993
  end-page: 1951
  article-title: AIN‐93 purified diets for laboratory rodents: final report of the American Institute of Nutrition ad hoc writing committee on the reformulation of the AIN‐76A rodent diet
  publication-title: J Nutr
– volume: 13
  start-page: 4895
  year: 2021
  end-page: 4910
  article-title: Cholecalciferol (vitamin D3) has a direct protective activity against interleukin 6‐induced atrophy in C2C12 myotubes
  publication-title: Aging (Albany NY)
– volume: 357
  start-page: 266
  year: 2007
  end-page: 281
  article-title: Vitamin D deficiency
  publication-title: N Engl J Med
– volume: 303
  start-page: C396
  year: 2012
  end-page: C405
  article-title: VDR and CYP27B1 are expressed in C2C12 cells and regenerating skeletal muscle: potential role in suppression of myoblast proliferation
  publication-title: Am J Physiol Cell Physiol
– volume: 81
  start-page: 1768
  year: 1988
  end-page: 1773
  article-title: Vitamin D supply to the rat fetus and neonate
  publication-title: J Clin Invest
– volume: 97
  start-page: 602
  year: 2015
  end-page: 610
  article-title: Vitamin D receptor ablation and vitamin D deficiency result in reduced grip strength, altered muscle fibers, and increased myostatin in mice
  publication-title: Calcif Tissue Int
– volume: 155
  start-page: 2199
  year: 2014
  end-page: 2212
  article-title: Hyperplasia and cellularity changes in IGF‐1‐overexpressing skeletal muscle of crucian carp
  publication-title: Endocrinology
– volume: 144
  start-page: 5138
  year: 2003
  end-page: 5144
  article-title: Deletion of vitamin D receptor gene in mice results in abnormal skeletal muscle development with deregulated expression of myoregulatory transcription factors
  publication-title: Endocrinology
– volume: 154
  start-page: 3022
  year: 2013
  end-page: 3030
  article-title: Evidence for a specific uptake and retention mechanism for 25‐hydroxyvitamin D (25OHD) in skeletal muscle cells
  publication-title: Endocrinology
– volume: 10
  year: 2020
  article-title: Satellite cells in ageing: use it or lose it
  publication-title: Open Biol
– volume: 42
  year: 2020
  article-title: Overexpression of the vitamin D receptor (VDR) induces skeletal muscle hypertrophy
  publication-title: Mol Metab
– volume: 131
  start-page: 95
  year: 2021
  end-page: 106
  article-title: Muscle‐specific deletion of the vitamin D receptor in mice is associated with diaphragm muscle weakness
  publication-title: J Appl Physiol
– volume: 575
  start-page: 241
  year: 2006
  end-page: 250
  article-title: Maternal nutrient restriction affects properties of skeletal muscle in offspring
  publication-title: J Physiol
– ident: e_1_2_8_22_1
  doi: 10.1210/endo.132.1.8419119
– ident: e_1_2_8_25_1
  doi: 10.1113/jphysiol.2006.112110
– ident: e_1_2_8_32_1
  doi: 10.1210/en.2013-1938
– ident: e_1_2_8_37_1
  doi: 10.1371/journal.pone.0010164
– ident: e_1_2_8_5_1
  doi: 10.1056/NEJMra070553
– ident: e_1_2_8_3_1
  doi: 10.3389/fped.2019.00022
– ident: e_1_2_8_19_1
  doi: 10.1007/s00223-015-0054-x
– ident: e_1_2_8_13_1
  doi: 10.1096/fj.10-168799
– ident: e_1_2_8_29_1
  doi: 10.1016/j.molmet.2020.101059
– ident: e_1_2_8_31_1
  doi: 10.1098/rsob.200048
– ident: e_1_2_8_40_1
  doi: 10.1002/jcsm.12899
– ident: e_1_2_8_33_1
  doi: 10.1038/cdd.2011.117
– ident: e_1_2_8_15_1
  doi: 10.1371/journal.pone.0085283
– ident: e_1_2_8_30_1
  doi: 10.1210/en.2015-1685
– ident: e_1_2_8_10_1
  doi: 10.1210/en.2014-1016
– ident: e_1_2_8_18_1
  doi: 10.1210/en.2003-0502
– ident: e_1_2_8_7_1
  doi: 10.1210/en.2012-2245
– ident: e_1_2_8_36_1
  doi: 10.1038/249083a0
– ident: e_1_2_8_39_1
  doi: 10.1111/apha.13269
– ident: e_1_2_8_16_1
  doi: 10.1111/febs.12253
– ident: e_1_2_8_14_1
  doi: 10.1042/CS20060265
– ident: e_1_2_8_8_1
  doi: 10.1016/0003-9861(82)90581-1
– ident: e_1_2_8_27_1
  doi: 10.1016/j.nut.2016.03.004
– ident: e_1_2_8_12_1
  doi: 10.1093/jn/123.11.1939
– ident: e_1_2_8_35_1
  doi: 10.1016/j.bbadis.2014.12.006
– ident: e_1_2_8_21_1
  doi: 10.2174/138920106776597621
– ident: e_1_2_8_11_1
  doi: 10.1152/ajpcell.00014.2012
– ident: e_1_2_8_34_1
  doi: 10.1002/mnfr.201300074
– ident: e_1_2_8_26_1
  doi: 10.2527/jas.2013-6565
– ident: e_1_2_8_2_1
  doi: 10.1111/j.1469-185X.1997.tb00016.x
– ident: e_1_2_8_23_1
  doi: 10.1530/JOE-13-0567
– ident: e_1_2_8_4_1
  doi: 10.1016/j.chembiol.2013.12.016
– ident: e_1_2_8_9_1
  doi: 10.1016/j.jsbmb.2017.01.022
– ident: e_1_2_8_24_1
  doi: 10.1095/biolreprod.104.034561
– ident: e_1_2_8_28_1
  doi: 10.1371/journal.pone.0037890
– ident: e_1_2_8_6_1
  doi: 10.1172/JCI113518
– ident: e_1_2_8_38_1
  doi: 10.18632/aging.202669
– ident: e_1_2_8_20_1
  doi: 10.1152/japplphysiol.00194.2021
– ident: e_1_2_8_17_1
  doi: 10.1002/jcp.25388
SSID ssj0000461650
Score 2.3667514
Snippet Background Fetal stage is a critical developmental window for the skeletal muscle, but little information is available about the impact of maternal vitamin D...
Fetal stage is a critical developmental window for the skeletal muscle, but little information is available about the impact of maternal vitamin D (Vit. D)...
BackgroundFetal stage is a critical developmental window for the skeletal muscle, but little information is available about the impact of maternal vitamin D...
BACKGROUNDFetal stage is a critical developmental window for the skeletal muscle, but little information is available about the impact of maternal vitamin D...
Abstract Background Fetal stage is a critical developmental window for the skeletal muscle, but little information is available about the impact of maternal...
SourceID doaj
pubmedcentral
proquest
crossref
pubmed
wiley
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage 2175
SubjectTerms Animals
Diet
Fetal programming
Fetuses
Fluorides
Gene expression
Histology
Hormones
Hypertrophy
Metabolites
Muscle development
Musculoskeletal system
Original
Protein synthesis
Proteins
Rodents
Skeletal muscle
Sodium
Vitamin D
Vitamin deficiency
Weaning
SummonAdditionalLinks – databaseName: DOAJ Directory of Open Access Journals
  dbid: DOA
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Nb9QwEB2hHqpeUIFC0xZkBCek0MTxV460UFWVlgtU6s1yHLu06marbhep_54ZO13tCgQXbpHt2JOZsf0mtp8B3iuECRH7TakaH0oRRCidr0QZvJMyCN_3ydKTr-r0XJxdyIuVq75oT1imB86KO_S8w_p8r6voMJTQruOVE6FrVdQ6dnn0rfhKMJXGYKFqla5n5XRWWiIKWnKT8sNrP59-xImODlCvzEaJtP9PSPP3DZOrQDbNRCfb8HSEkOxTFv0ZPAnDc9icjIvkL2CYuMzszH5i4D-9Gthn1gdiiqBjlszlHRwMkR-bzlDN6cc6c0PPaJIjQ7FZZJc3D-gjD9gGmy7m2BDDihJbB-bGvJzL0H3mO3B-8uX78Wk5XqtQeqmMKmtPpO6uiaYLuo5aYIQRhG6NjxFTtTdeR5SljSEG5WLTNZwobbipa8eNb17CxjAbwi6wSnLjZK8RtTmBFZiqx1el963p6f6yAt49qtfeZvYMm3mSuSUj2GSEAo5I88sSxHidEtAP7OgH9l9-UMDBo93s2A3nlmscYxAAGsx-u8zGDkSrIm4IswWWwQAOwzQl6wJeZTMvJSHued6qtgC95gBroq7nDFc_Ekl32xAzoizgQ3KVv3y-PTv-NklPe_9DEfuwxemIRtqkeAAb93eL8BqB0333JvWRX6SDGCI
  priority: 102
  providerName: Directory of Open Access Journals
– databaseName: ProQuest Central
  dbid: BENPR
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1Lb9QwEB7BVkJcKt4ECjKCE1Jo4sSPnCpaWlWVtkJApd4ix7HLVt2kbXaR-u8742RDV6DeItvxa8aescfzDcAniWqCx3UTy8y6OHe5i41N8thZI4TLbV0HSk-P5eFJfnQqTocLt254VrnaE8NGXbeW7si3uUJ2QVmu-c7lVUxRo8i6OoTQeAgbPM20nsDG7v7x9x_jLQvBicsQppWTz7RAbWjEKOXb57abf0GBR47Ud6RSAO__n8b578PJuwptkEgHT2BzUCXZ1572T-GBa57Bo-lgLH8OzdT0CM_sz2xh5rOGfWO1I8QIcrdkpn_JwVADZPMWpztcsDPT1IyEHRGMtZ6dXdwgr9xgG2y-7LAhhhUF1A7M9b1ZlyEbdS_g5GD_195hPIRXiK2QWsapJXB3k3ldOZV6leNJw-Wq0NZ7TFVWW-WxL4V33knjsyrjBG3DdZoarm32EiZN27jXwBLBtRG1Qu3N5FiBTmr8VVhb6JrimEXwcTW95WWPolH2eMm8JCKUgQgR7NLMjyUI-ToktNdn5bCQSssr5C9bq8QbPFoqU_HE5K4qpFfKVzyCrRXdymE5duVf5ongw5iNC4msI6Zx7RLL4EEOj2tSpBG86sk89oQw6HkhiwjUGgOsdXU9p5n9DmDdRUYIiSKCz4FV7hl-ebT3cxq-3tw_hrfwmJMTRniGuAWTxfXSvUPVaFG9H_j_FmjxEFA
  priority: 102
  providerName: ProQuest
– databaseName: Scholars Portal Open Access Journals
  dbid: M48
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb9QwEB6VIlW9IN4ECjKCE1JK4viVA0JQqKpK4QIr9WY5jt0u6iawD8T-e8ZOstoVFQduUZzEjmcm8008_gbgtUCY4NFuUlFYlzLHXGpsxlJnDeeO2aaJkq6-iLMJO7_gF3sw1u8cJnBxY2gX6klN5tfHv3-u36PBvxsIRN9-t4vZMfotJW7BbYoeMaR2VQPMj19kJnIRi7XSsHOaIybaMJVu334IB4FtnJYh_XnLTUU2_5sg6N-ZlNsIN7qo07twZ8CW5EOvDPdgz7X34aAaVs8fQFuZnvKZ_JouzWzakk-kcYFCIuy_JKZP7SAICcmsw_mPf9yJaRsSvF-QIOk8ubxeo_KssQ8yWy2wI4IPijQe2Or7dV6CerV4CJPTz99OztKh3kJquVAizW1gezeFV7WTuZcMQw_HZKms93hWWmWlx7GU3nknjC_qggauG6ry3FBli0ew33atewIk41QZ3kiEc4bhA1TW4K3c2lI1obBZAq_G6dU_eloN3RMoUx3koaM8EvgYZn5zRaDCjie6-aUeLEtbWqPC2UZm3mCsKU1NM8NcXQovpa9pAkej3PSoXppK_PggMlTY_HLTjJYVlktM67oVXoORHcZvgucJPO7FvBnJqCYJyB0F2Bnqbks7vYrs3WURKBN5Am-iqvzj9fX5ydcqHj39726ewSENGzZiyuIR7C_nK_ccYdSyfhFt5A_A5x58
  priority: 102
  providerName: Scholars Portal
– databaseName: Wiley Online Library Open Access
  dbid: 24P
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV3da9UwFD_MCeKL-G3nlIg-CXVtmq-CLzodY3BF0MHeQpomc-JtZd0d7L_3nLS386IIvpV8N-ec5Hfy8QvAK4UwIaLd5KryIRdBhNz5QuTBOymD8G2bJL34pA6PxdGJPNmCt-u7MCM_xLzgRpaRxmsycNcMe9ekod_9sHyDs5VRN-Am4hpF7xdw8XleYSEqcZWeaOV0X1oiEpr5SfnedfaNGSkR9_8Nbf55aPJ3MJtmo4O7cGeCkezdKPd7sBW6-3BrMW2UP4Bu4UZ2Z3aJzv_yrGMfWBuILYKuWjI3nuJgiP7YsseuTovrzHUto4mOhMX6yE5_XKGeXGEdbLkasCKGBSXGDoyN45YuQxUaHsLxwcev-4f59LRC7qUyKi89Ebu7Kpom6DJqgV5GELo2PkYM1d54HbEtdQwxKBerpuJEa8NNWTpufPUItru-C0-AFZIbJ1uNyM0JLMAULWaV3tempTfMMni57l77c2TQsCNXMrckBJuEkMF76vk5BbFep4D-_NRORmQ9b1C3fKuL6NCt1K7hhROhqVXUOjY8g9213OxkioPlGscZBIEGo1_M0WhEtDPiutCvMA06ceiqKVlm8HgU89wS4p_ntaoz0BsKsNHUzZju7Fsi6q4rYkeUGbxOqvKP37dH-18W6WvnfxI_hducrmOkA4m7sH1xvgrPECRdNM-TLfwCB3AQLQ
  priority: 102
  providerName: Wiley-Blackwell
Title Maternal vitamin D deficiency affects the morphology and function of glycolytic muscle in adult offspring rats
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjcsm.12986
https://www.ncbi.nlm.nih.gov/pubmed/35582969
https://www.proquest.com/docview/2705392982
https://search.proquest.com/docview/2666550651
https://pubmed.ncbi.nlm.nih.gov/PMC9398225
https://doaj.org/article/c2b604cd70fa4487ab20a4eb96f77fb2
Volume 13
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3da9swED-aDsZexr7nrQsa29PASSzry49r1lIKLmFbIW9GlqUuo7ZL0wz63-8k2yFhYw97MUaSLVl38v1OOv0E8FEgTHA4bmKRGhszy2yszYzF1mjOLTNVFSSdX4izS3a-5MsD4MNemBC0b8rVpLmuJ83qR4itvKnNdIgTmy7yeZZ61jk-HcEIze-Oix5-v0wkIpzMSv02aY4AaEtLSqc_zbqeoI1T_uwiTy1OMx_rvGOTAnX_3_Dmn2GTu3A22KPTJ_C4B5Lkc9fgp3Bgm2fwMO-Xyp9Dk-uO35n8Qve_XjXkC6ms54vwmy2J7uI4COI_UrfY2WF6neimIt7UeXGR1pGr63vUlHusg9SbNVZE8EWBswNzXbeoS1CJ1i_g8vTk-_ws7g9XiA0XSsSJ8dTuOnWqtDJxkqGfYZnMlHEOU6VRRjpsS-ass0K7tEypJ7ahKkk0VSZ9CYdN29jXQGacKs0ridhNM3yBmlX4KDcmU5U_xSyCD0P3Fjcdh0bRsSXTwsujCPKI4Nj3_LaE570OCe3tVdFLvzC0RO0ylZw5jY6l1CWdaWbLTDgpXUkjOBrkVvSDcV1QiX8ahIEKs99vs3EY-bUR3dh2g2XQjUNnTfAkgledmLctGdQkArmnAHtN3c9BzQ1U3b2mRvApqMo_Pr84n3_Lw92b_67mLTyifndGiE88gsO72419h5jprhzDiLIFXuVSjuHB8cnF4us4zD_gNWdqHMbQb6j5HRg
link.rule.ids 230,314,727,780,784,864,885,2102,2221,11562,12056,21388,24318,27924,27925,31719,31720,33744,33745,43310,43805,46052,46476,50814,50923,53791,53793,73745,74302
linkProvider National Library of Medicine
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1Lb9QwEB7BVgIuiGcJFDCCE1Jo4sSxc0K0tFpKd4WglXqLHMcui7pJ2-wi9d8z42RDV6DeItvxa2Y8M358A_AuQzPBodyEWWJsmNrUhtpEaWiNFsKmpqo8pSfTbHycHpyIk37Dre2vVa7WRL9QV42hPfJtLpFdUJcr_vH8IqSoUXS62ofQuA0bhJwuRrCxszf99n3YZSE48cyHaeX0ZlqgNTRglPLtX6adf0CFRw-pr2klD97_P4vz34uT1w1ar5H2H8D93pRknzraP4Rbtn4Edyb9YfljqCe6Q3hmv2cLPZ_V7DOrLCFG0HNLprubHAwtQDZvcLr9BjvTdcVI2RHBWOPY6dkV8soVtsHmyxYbYliRR-3AXNcd6zJko_YJHO_vHe2Owz68QmhEprIwNgTurhOnSitjJ1P0NGwqc2Wcw1RplJEO-5I762ymXVImnKBtuIpjzZVJnsKobmr7DFgkuNKikmi96RQrUFGFvwpjclVRHLMA3q6mtzjvUDSKDi-ZF0SEwhMhgB2a-aEEIV_7hObytOgFqTC8RP4ylYycRtdS6pJHOrVlnjkpXckD2FrRrejFsS3-Mk8Ab4ZsFCQ6HdG1bZZYBh05dNcyEQew2ZF56Alh0PM8ywOQawyw1tX1nHr204N15wkhJIoA3ntWuWH4xcHuj4n_en7zGF7D3fHR5LA4_DL9-gLucXqQ4a8kbsFocbm0L9FMWpSveln4A0X8Ezg
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3db9MwED9BJ028IL4XGGAET0ihiRPbyRNiH9UYtJqASXuzHMceRTQZS4u0_56z44ZVoL1FtuOvu_Od7fPvAN5wNBMsyk3MM23i3OQmVjrJY6MVYybXde0pPZ3xo9P8-IydBf-nLrhVrtdEv1DXrXZn5GMqkF1Qlxd0bINbxMnB5P3Fr9hFkHI3rSGcxm3YQq2Y0BFs7R3OTr4MJy4OWpz7kK3UvZ9maBkNeKV0_EN3i3eo_Nyj6msaygP5_8_6_NeJ8rpx67XT5B7cDWYl-dDzwX24ZZoHsD0NF-cPoZmqHu2Z_J4v1WLekANSG4ce4Z5eEtV7dRC0Bsmixan3h-1ENTVxis8Rj7SWnP-8Qr65wjbIYtVhQwQr8ggemGv7K16CLNU9gtPJ4bf9oziEWog14wWPU-2A3lVmi8qI1Iocdx0mF2WhrcVUoQstLPaltMYarmxWZdTB3NAiTRUtdPYYRk3bmB0gCaOFYrVAS07lWEGR1Pgr07osahfTLILX6-mVFz2ihuyxk6l0RJCeCBHsuZkfSjgUbJ_QXp7LIFRS0wp5TdcisQq3mUJVNFG5qUpuhbAVjWB3TTcZRLOTfxkpgldDNgqVuylRjWlXWAY3dbh14yyN4ElP5qEnDo-elryMQGwwwEZXN3Oa-XcP3F1mDi2RRfDWs8oNw5fH-1-n_uvpzWN4CdsoBvLzx9mnZ3CHurcZ3jtxF0bLy5V5jhbTsnoRROEPDeAXZQ
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Maternal+vitamin+D+deficiency+affects+the+morphology+and+function+of+glycolytic+muscle+in+adult+offspring+rats&rft.jtitle=Journal+of+cachexia%2C+sarcopenia+and+muscle&rft.au=Reis%2C+Natany+G.&rft.au=Assis%2C+Ana+P.&rft.au=Lautherbach%2C+Nat%C3%A1lia&rft.au=Gon%C3%A7alves%2C+Dawit+A.&rft.date=2022-08-01&rft.pub=John+Wiley+and+Sons+Inc&rft.issn=2190-5991&rft.eissn=2190-6009&rft.volume=13&rft.issue=4&rft.spage=2175&rft.epage=2187&rft_id=info:doi/10.1002%2Fjcsm.12986&rft_id=info%3Apmid%2F35582969&rft.externalDBID=PMC9398225
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2190-5991&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2190-5991&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2190-5991&client=summon