240 Prolonged Maternofetal Inflammation in the Pregnant Ewe at Mid-Gestation Increases Subsequent Fetal Inflammatory Tone and Disrupts Skeletal Muscle Growth and Glucose Metabolism Near Term

Abstract Chronic maternofetal inflammation in late gestation (i.e., peak fetal growth) causes fetal intrauterine growth restriction (IUGR) in sheep, which was associated with deficits in growth, body composition, and metabolic function before and after birth. However, the impact of sustained materno...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of animal science 2023-11, Vol.101 (Supplement_3), p.166-167
Hauptverfasser: Hicks, Zena M, Gibbs, Rachel L, Beer, Haley N, White, Melanie R, Lacey, Taylor A, Grijalva, Pablo Cesar C, Most, Micah S, Schmidt, Ty B B, Peterson, Jessica L L, Yates, Dustin T
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 167
container_issue Supplement_3
container_start_page 166
container_title Journal of animal science
container_volume 101
creator Hicks, Zena M
Gibbs, Rachel L
Beer, Haley N
White, Melanie R
Lacey, Taylor A
Grijalva, Pablo Cesar C
Most, Micah S
Schmidt, Ty B B
Peterson, Jessica L L
Yates, Dustin T
description Abstract Chronic maternofetal inflammation in late gestation (i.e., peak fetal growth) causes fetal intrauterine growth restriction (IUGR) in sheep, which was associated with deficits in growth, body composition, and metabolic function before and after birth. However, the impact of sustained maternofetal inflammation during mid-gestation (i.e., peak placental growth and development) has not been explored. Therefore, our objective was to determine the effects of sustained maternofetal inflammation during this critical window on subsequent fetal inflammatory tone, metabolism, and myoblast (i.e., muscle stem cell) function. Pregnant ewes were injected every 3rd day from the 50th to 65th d of gestational age (dGA; term = 150 dGA) with saline (control; n = 12) or bacterial lipopolysaccharide endotoxin to induce maternofetal inflammation and IUGR (MI-IUGR; n = 12). Fetuses were surgically catheterized on dGA 118 to collect blood samples, and a hyperinsulinemic-euglycemic clamp (HEC) was performed on dGA 123. Fetuses were necropsied on dGA 125 to collect semitendinosus muscle samples. Fetal plasma TNFα concentrations tended to be greater (P = 0.07) for MI-IUGR fetuses (440 ± 45 pg/m l) than for controls (348 ± 24 pg/mL). Fetal blood O2 partial pressures were 12% less (P < 0.05) and maternofetal O2 gradients tended to be 11% greater (P = 0.08) for MI-IUGR fetuses than for controls. Hindlimb-specific glucose uptake rates did not differ between fetal groups, but hindlimb-specific glucose oxidation rates were reduced (P < 0.05) by 15% under basal conditions and by 27% under hyperinsulinemic conditions for MI-IUGR fetuses compared with controls. Semitendinosus glycogen content and β2 adrenoceptor content did not differ between fetal groups, but semitendinosus content of the TNFα receptor, TNFR1, was 41% greater (P < 0.05) for MI-IUGR fetuses than for controls. Immunohistochemistry revealed 18% fewer (P < 0.05) proliferating myoblasts (pax7+/Ki67+) and 38% fewer (P < 0.05) differentiated myoblasts (myogenin+) in semitendinosus from MI-IUGR fetuses compared with controls, which coincided with 13% smaller (P < 0.05) muscle fibers. From these findings, we conclude that sustained maternofetal inflammation during peak placental development at mid-gestation resulted in enhanced fetal inflammatory tone near term, which in turn impaired myoblast function, muscle fiber hypertrophy, and muscle glucose metabolism.
doi_str_mv 10.1093/jas/skad281.202
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10633054</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1093/jas/skad281.202</oup_id><sourcerecordid>3051767852</sourcerecordid><originalsourceid>FETCH-LOGICAL-c2002-f5077f125225247dde0de4fae33775b977ec4237196efddb1bbf7508ec0629b33</originalsourceid><addsrcrecordid>eNqFkV-LEzEUxYMoWFeffQ34Jsw2fyaTmSeRdbcWtipYn0NmctNON5PUJOOyX87PZtwWYZ-EQB7u75zck4PQW0ouKen48qDTMt1pw1p6yQh7hhZUMFFx2vDnaEEIo1XbUvYSvUrpQAhlohML9JvVBH-LwQW_A4M3OkP0wULWDq-9dXqadB6Dx6PHeQ8FhZ3XPuPre8A6481oqhWkfILWfoigEyT8fe4T_JyhkDdPzUJ8wNvgi9ob_GlMcT7mwt-Be-Q2cxoc4FUM93n_yKzcPIQEeFPmfXBjmvAX0BFvIU6v0QurXYI35_sC_bi53l59rm6_rtZXH2-rgZXklRVESlsis3JqaQwQA7XVwLmUou-khKFmXNKuAWtMT_veSkFaGEjDup7zC_Th5Huc-wnMUHJF7dQxjpOODyroUT2d-HGvduGXoqThnIi6OLw7O8RQ_iVldQhz9GVpVeZUNrIVrFDLEzXEkFIE--8JStTfmlWpWZ1rVqXmonh_UoT5-F_4Dwb0ru4</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3051767852</pqid></control><display><type>article</type><title>240 Prolonged Maternofetal Inflammation in the Pregnant Ewe at Mid-Gestation Increases Subsequent Fetal Inflammatory Tone and Disrupts Skeletal Muscle Growth and Glucose Metabolism Near Term</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Hicks, Zena M ; Gibbs, Rachel L ; Beer, Haley N ; White, Melanie R ; Lacey, Taylor A ; Grijalva, Pablo Cesar C ; Most, Micah S ; Schmidt, Ty B B ; Peterson, Jessica L L ; Yates, Dustin T</creator><creatorcontrib>Hicks, Zena M ; Gibbs, Rachel L ; Beer, Haley N ; White, Melanie R ; Lacey, Taylor A ; Grijalva, Pablo Cesar C ; Most, Micah S ; Schmidt, Ty B B ; Peterson, Jessica L L ; Yates, Dustin T</creatorcontrib><description><![CDATA[Abstract Chronic maternofetal inflammation in late gestation (i.e., peak fetal growth) causes fetal intrauterine growth restriction (IUGR) in sheep, which was associated with deficits in growth, body composition, and metabolic function before and after birth. However, the impact of sustained maternofetal inflammation during mid-gestation (i.e., peak placental growth and development) has not been explored. Therefore, our objective was to determine the effects of sustained maternofetal inflammation during this critical window on subsequent fetal inflammatory tone, metabolism, and myoblast (i.e., muscle stem cell) function. Pregnant ewes were injected every 3rd day from the 50th to 65th d of gestational age (dGA; term = 150 dGA) with saline (control; n = 12) or bacterial lipopolysaccharide endotoxin to induce maternofetal inflammation and IUGR (MI-IUGR; n = 12). Fetuses were surgically catheterized on dGA 118 to collect blood samples, and a hyperinsulinemic-euglycemic clamp (HEC) was performed on dGA 123. Fetuses were necropsied on dGA 125 to collect semitendinosus muscle samples. Fetal plasma TNFα concentrations tended to be greater (P = 0.07) for MI-IUGR fetuses (440 ± 45 pg/m l) than for controls (348 ± 24 pg/mL). Fetal blood O2 partial pressures were 12% less (P < 0.05) and maternofetal O2 gradients tended to be 11% greater (P = 0.08) for MI-IUGR fetuses than for controls. Hindlimb-specific glucose uptake rates did not differ between fetal groups, but hindlimb-specific glucose oxidation rates were reduced (P < 0.05) by 15% under basal conditions and by 27% under hyperinsulinemic conditions for MI-IUGR fetuses compared with controls. Semitendinosus glycogen content and β2 adrenoceptor content did not differ between fetal groups, but semitendinosus content of the TNFα receptor, TNFR1, was 41% greater (P < 0.05) for MI-IUGR fetuses than for controls. Immunohistochemistry revealed 18% fewer (P < 0.05) proliferating myoblasts (pax7+/Ki67+) and 38% fewer (P < 0.05) differentiated myoblasts (myogenin+) in semitendinosus from MI-IUGR fetuses compared with controls, which coincided with 13% smaller (P < 0.05) muscle fibers. From these findings, we conclude that sustained maternofetal inflammation during peak placental development at mid-gestation resulted in enhanced fetal inflammatory tone near term, which in turn impaired myoblast function, muscle fiber hypertrophy, and muscle glucose metabolism.]]></description><identifier>ISSN: 0021-8812</identifier><identifier>EISSN: 1525-3163</identifier><identifier>DOI: 10.1093/jas/skad281.202</identifier><language>eng</language><publisher>US: Oxford University Press</publisher><subject>Adrenergic receptors ; Blood ; Body composition ; Endotoxins ; Fetuses ; Gestation ; Gestational age ; Glucose ; Glucose metabolism ; Glycogen ; Glycogens ; Hypertrophy ; Immunohistochemistry ; Inflammation ; Limbs ; Lipopolysaccharides ; Metabolism ; Muscles ; Myoblasts ; Myogenin ; Oxidation ; Placenta ; Pregnancy ; Skeletal muscle ; Stem cells ; Tumor necrosis factor receptors ; Tumor necrosis factor-α</subject><ispartof>Journal of animal science, 2023-11, Vol.101 (Supplement_3), p.166-167</ispartof><rights>The Author(s) 2023. Published by Oxford University Press on behalf of the American Society of Animal Science. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. 2023</rights><rights>The Author(s) 2023. Published by Oxford University Press on behalf of the American Society of Animal Science. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10633054/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10633054/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,724,777,781,882,1579,27905,27906,53772,53774</link.rule.ids></links><search><creatorcontrib>Hicks, Zena M</creatorcontrib><creatorcontrib>Gibbs, Rachel L</creatorcontrib><creatorcontrib>Beer, Haley N</creatorcontrib><creatorcontrib>White, Melanie R</creatorcontrib><creatorcontrib>Lacey, Taylor A</creatorcontrib><creatorcontrib>Grijalva, Pablo Cesar C</creatorcontrib><creatorcontrib>Most, Micah S</creatorcontrib><creatorcontrib>Schmidt, Ty B B</creatorcontrib><creatorcontrib>Peterson, Jessica L L</creatorcontrib><creatorcontrib>Yates, Dustin T</creatorcontrib><title>240 Prolonged Maternofetal Inflammation in the Pregnant Ewe at Mid-Gestation Increases Subsequent Fetal Inflammatory Tone and Disrupts Skeletal Muscle Growth and Glucose Metabolism Near Term</title><title>Journal of animal science</title><description><![CDATA[Abstract Chronic maternofetal inflammation in late gestation (i.e., peak fetal growth) causes fetal intrauterine growth restriction (IUGR) in sheep, which was associated with deficits in growth, body composition, and metabolic function before and after birth. However, the impact of sustained maternofetal inflammation during mid-gestation (i.e., peak placental growth and development) has not been explored. Therefore, our objective was to determine the effects of sustained maternofetal inflammation during this critical window on subsequent fetal inflammatory tone, metabolism, and myoblast (i.e., muscle stem cell) function. Pregnant ewes were injected every 3rd day from the 50th to 65th d of gestational age (dGA; term = 150 dGA) with saline (control; n = 12) or bacterial lipopolysaccharide endotoxin to induce maternofetal inflammation and IUGR (MI-IUGR; n = 12). Fetuses were surgically catheterized on dGA 118 to collect blood samples, and a hyperinsulinemic-euglycemic clamp (HEC) was performed on dGA 123. Fetuses were necropsied on dGA 125 to collect semitendinosus muscle samples. Fetal plasma TNFα concentrations tended to be greater (P = 0.07) for MI-IUGR fetuses (440 ± 45 pg/m l) than for controls (348 ± 24 pg/mL). Fetal blood O2 partial pressures were 12% less (P < 0.05) and maternofetal O2 gradients tended to be 11% greater (P = 0.08) for MI-IUGR fetuses than for controls. Hindlimb-specific glucose uptake rates did not differ between fetal groups, but hindlimb-specific glucose oxidation rates were reduced (P < 0.05) by 15% under basal conditions and by 27% under hyperinsulinemic conditions for MI-IUGR fetuses compared with controls. Semitendinosus glycogen content and β2 adrenoceptor content did not differ between fetal groups, but semitendinosus content of the TNFα receptor, TNFR1, was 41% greater (P < 0.05) for MI-IUGR fetuses than for controls. Immunohistochemistry revealed 18% fewer (P < 0.05) proliferating myoblasts (pax7+/Ki67+) and 38% fewer (P < 0.05) differentiated myoblasts (myogenin+) in semitendinosus from MI-IUGR fetuses compared with controls, which coincided with 13% smaller (P < 0.05) muscle fibers. From these findings, we conclude that sustained maternofetal inflammation during peak placental development at mid-gestation resulted in enhanced fetal inflammatory tone near term, which in turn impaired myoblast function, muscle fiber hypertrophy, and muscle glucose metabolism.]]></description><subject>Adrenergic receptors</subject><subject>Blood</subject><subject>Body composition</subject><subject>Endotoxins</subject><subject>Fetuses</subject><subject>Gestation</subject><subject>Gestational age</subject><subject>Glucose</subject><subject>Glucose metabolism</subject><subject>Glycogen</subject><subject>Glycogens</subject><subject>Hypertrophy</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Limbs</subject><subject>Lipopolysaccharides</subject><subject>Metabolism</subject><subject>Muscles</subject><subject>Myoblasts</subject><subject>Myogenin</subject><subject>Oxidation</subject><subject>Placenta</subject><subject>Pregnancy</subject><subject>Skeletal muscle</subject><subject>Stem cells</subject><subject>Tumor necrosis factor receptors</subject><subject>Tumor necrosis factor-α</subject><issn>0021-8812</issn><issn>1525-3163</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNqFkV-LEzEUxYMoWFeffQ34Jsw2fyaTmSeRdbcWtipYn0NmctNON5PUJOOyX87PZtwWYZ-EQB7u75zck4PQW0ouKen48qDTMt1pw1p6yQh7hhZUMFFx2vDnaEEIo1XbUvYSvUrpQAhlohML9JvVBH-LwQW_A4M3OkP0wULWDq-9dXqadB6Dx6PHeQ8FhZ3XPuPre8A6481oqhWkfILWfoigEyT8fe4T_JyhkDdPzUJ8wNvgi9ob_GlMcT7mwt-Be-Q2cxoc4FUM93n_yKzcPIQEeFPmfXBjmvAX0BFvIU6v0QurXYI35_sC_bi53l59rm6_rtZXH2-rgZXklRVESlsis3JqaQwQA7XVwLmUou-khKFmXNKuAWtMT_veSkFaGEjDup7zC_Th5Huc-wnMUHJF7dQxjpOODyroUT2d-HGvduGXoqThnIi6OLw7O8RQ_iVldQhz9GVpVeZUNrIVrFDLEzXEkFIE--8JStTfmlWpWZ1rVqXmonh_UoT5-F_4Dwb0ru4</recordid><startdate>20231106</startdate><enddate>20231106</enddate><creator>Hicks, Zena M</creator><creator>Gibbs, Rachel L</creator><creator>Beer, Haley N</creator><creator>White, Melanie R</creator><creator>Lacey, Taylor A</creator><creator>Grijalva, Pablo Cesar C</creator><creator>Most, Micah S</creator><creator>Schmidt, Ty B B</creator><creator>Peterson, Jessica L L</creator><creator>Yates, Dustin T</creator><general>Oxford University Press</general><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>U9A</scope><scope>5PM</scope></search><sort><creationdate>20231106</creationdate><title>240 Prolonged Maternofetal Inflammation in the Pregnant Ewe at Mid-Gestation Increases Subsequent Fetal Inflammatory Tone and Disrupts Skeletal Muscle Growth and Glucose Metabolism Near Term</title><author>Hicks, Zena M ; Gibbs, Rachel L ; Beer, Haley N ; White, Melanie R ; Lacey, Taylor A ; Grijalva, Pablo Cesar C ; Most, Micah S ; Schmidt, Ty B B ; Peterson, Jessica L L ; Yates, Dustin T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2002-f5077f125225247dde0de4fae33775b977ec4237196efddb1bbf7508ec0629b33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Adrenergic receptors</topic><topic>Blood</topic><topic>Body composition</topic><topic>Endotoxins</topic><topic>Fetuses</topic><topic>Gestation</topic><topic>Gestational age</topic><topic>Glucose</topic><topic>Glucose metabolism</topic><topic>Glycogen</topic><topic>Glycogens</topic><topic>Hypertrophy</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Limbs</topic><topic>Lipopolysaccharides</topic><topic>Metabolism</topic><topic>Muscles</topic><topic>Myoblasts</topic><topic>Myogenin</topic><topic>Oxidation</topic><topic>Placenta</topic><topic>Pregnancy</topic><topic>Skeletal muscle</topic><topic>Stem cells</topic><topic>Tumor necrosis factor receptors</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hicks, Zena M</creatorcontrib><creatorcontrib>Gibbs, Rachel L</creatorcontrib><creatorcontrib>Beer, Haley N</creatorcontrib><creatorcontrib>White, Melanie R</creatorcontrib><creatorcontrib>Lacey, Taylor A</creatorcontrib><creatorcontrib>Grijalva, Pablo Cesar C</creatorcontrib><creatorcontrib>Most, Micah S</creatorcontrib><creatorcontrib>Schmidt, Ty B B</creatorcontrib><creatorcontrib>Peterson, Jessica L L</creatorcontrib><creatorcontrib>Yates, Dustin T</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of animal science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hicks, Zena M</au><au>Gibbs, Rachel L</au><au>Beer, Haley N</au><au>White, Melanie R</au><au>Lacey, Taylor A</au><au>Grijalva, Pablo Cesar C</au><au>Most, Micah S</au><au>Schmidt, Ty B B</au><au>Peterson, Jessica L L</au><au>Yates, Dustin T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>240 Prolonged Maternofetal Inflammation in the Pregnant Ewe at Mid-Gestation Increases Subsequent Fetal Inflammatory Tone and Disrupts Skeletal Muscle Growth and Glucose Metabolism Near Term</atitle><jtitle>Journal of animal science</jtitle><date>2023-11-06</date><risdate>2023</risdate><volume>101</volume><issue>Supplement_3</issue><spage>166</spage><epage>167</epage><pages>166-167</pages><issn>0021-8812</issn><eissn>1525-3163</eissn><abstract><![CDATA[Abstract Chronic maternofetal inflammation in late gestation (i.e., peak fetal growth) causes fetal intrauterine growth restriction (IUGR) in sheep, which was associated with deficits in growth, body composition, and metabolic function before and after birth. However, the impact of sustained maternofetal inflammation during mid-gestation (i.e., peak placental growth and development) has not been explored. Therefore, our objective was to determine the effects of sustained maternofetal inflammation during this critical window on subsequent fetal inflammatory tone, metabolism, and myoblast (i.e., muscle stem cell) function. Pregnant ewes were injected every 3rd day from the 50th to 65th d of gestational age (dGA; term = 150 dGA) with saline (control; n = 12) or bacterial lipopolysaccharide endotoxin to induce maternofetal inflammation and IUGR (MI-IUGR; n = 12). Fetuses were surgically catheterized on dGA 118 to collect blood samples, and a hyperinsulinemic-euglycemic clamp (HEC) was performed on dGA 123. Fetuses were necropsied on dGA 125 to collect semitendinosus muscle samples. Fetal plasma TNFα concentrations tended to be greater (P = 0.07) for MI-IUGR fetuses (440 ± 45 pg/m l) than for controls (348 ± 24 pg/mL). Fetal blood O2 partial pressures were 12% less (P < 0.05) and maternofetal O2 gradients tended to be 11% greater (P = 0.08) for MI-IUGR fetuses than for controls. Hindlimb-specific glucose uptake rates did not differ between fetal groups, but hindlimb-specific glucose oxidation rates were reduced (P < 0.05) by 15% under basal conditions and by 27% under hyperinsulinemic conditions for MI-IUGR fetuses compared with controls. Semitendinosus glycogen content and β2 adrenoceptor content did not differ between fetal groups, but semitendinosus content of the TNFα receptor, TNFR1, was 41% greater (P < 0.05) for MI-IUGR fetuses than for controls. Immunohistochemistry revealed 18% fewer (P < 0.05) proliferating myoblasts (pax7+/Ki67+) and 38% fewer (P < 0.05) differentiated myoblasts (myogenin+) in semitendinosus from MI-IUGR fetuses compared with controls, which coincided with 13% smaller (P < 0.05) muscle fibers. From these findings, we conclude that sustained maternofetal inflammation during peak placental development at mid-gestation resulted in enhanced fetal inflammatory tone near term, which in turn impaired myoblast function, muscle fiber hypertrophy, and muscle glucose metabolism.]]></abstract><cop>US</cop><pub>Oxford University Press</pub><doi>10.1093/jas/skad281.202</doi><tpages>2</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0021-8812
ispartof Journal of animal science, 2023-11, Vol.101 (Supplement_3), p.166-167
issn 0021-8812
1525-3163
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10633054
source Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; PubMed Central
subjects Adrenergic receptors
Blood
Body composition
Endotoxins
Fetuses
Gestation
Gestational age
Glucose
Glucose metabolism
Glycogen
Glycogens
Hypertrophy
Immunohistochemistry
Inflammation
Limbs
Lipopolysaccharides
Metabolism
Muscles
Myoblasts
Myogenin
Oxidation
Placenta
Pregnancy
Skeletal muscle
Stem cells
Tumor necrosis factor receptors
Tumor necrosis factor-α
title 240 Prolonged Maternofetal Inflammation in the Pregnant Ewe at Mid-Gestation Increases Subsequent Fetal Inflammatory Tone and Disrupts Skeletal Muscle Growth and Glucose Metabolism Near Term
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T15%3A37%3A28IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=240%20Prolonged%20Maternofetal%20Inflammation%20in%20the%20Pregnant%20Ewe%20at%20Mid-Gestation%20Increases%20Subsequent%20Fetal%20Inflammatory%20Tone%20and%20Disrupts%20Skeletal%20Muscle%20Growth%20and%20Glucose%20Metabolism%20Near%20Term&rft.jtitle=Journal%20of%20animal%20science&rft.au=Hicks,%20Zena%20M&rft.date=2023-11-06&rft.volume=101&rft.issue=Supplement_3&rft.spage=166&rft.epage=167&rft.pages=166-167&rft.issn=0021-8812&rft.eissn=1525-3163&rft_id=info:doi/10.1093/jas/skad281.202&rft_dat=%3Cproquest_pubme%3E3051767852%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=3051767852&rft_id=info:pmid/&rft_oup_id=10.1093/jas/skad281.202&rfr_iscdi=true