دورية أكاديمية
أعرض في EDS

Maternal obesity: sex-specific in utero changes in fetal brain autophagy and mTOR.

التفاصيل البيبلوغرافية
العنوان: Maternal obesity: sex-specific in utero changes in fetal brain autophagy and mTOR.
المؤلفون: Merabova N; Department of Family Medicine, Medical College of Wisconsin-Prevea, Green Bay, Wisconsin, USA., Ugartemendia L; Department of Obstetrics, Gynecology and Reproductive Sciences, McGovern Medical School at University of Texas Health Science Center at Houston, Houston, Texas, USA., Edlow AG; Department of Obstetrics and Gynecology, Massachusetts General Hospital, Vincent Center for Reproductive Biology, Boston, Massachusetts, USA., Ibarra C; Department of Obstetrics, Gynecology and Reproductive Sciences, McGovern Medical School at University of Texas Health Science Center at Houston, Houston, Texas, USA., Darbinian N; Shriners Pediatric Research Center, Center for Neural Repair and Rehabilitation, Temple University, Philadelphia, Pennsylvania, USA., Tatevosian G; Shriners Pediatric Research Center, Center for Neural Repair and Rehabilitation, Temple University, Philadelphia, Pennsylvania, USA., Goetzl L; Department of Obstetrics, Gynecology and Reproductive Sciences, McGovern Medical School at University of Texas Health Science Center at Houston, Houston, Texas, USA.
المصدر: Obesity (Silver Spring, Md.) [Obesity (Silver Spring)] 2024 Jun; Vol. 32 (6), pp. 1136-1143. Date of Electronic Publication: 2024 Apr 21.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: John Wiley & Sons Country of Publication: United States NLM ID: 101264860 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1930-739X (Electronic) Linking ISSN: 19307381 NLM ISO Abbreviation: Obesity (Silver Spring) Subsets: MEDLINE
أسماء مطبوعة: Publication: 2013- : Malden, MA : John Wiley & Sons
Original Publication: Silver Spring, MD : NAASO, the Obesity Society, c2006-
مواضيع طبية MeSH: Autophagy* , Obesity, Maternal*/metabolism , Brain*/metabolism , TOR Serine-Threonine Kinases*/metabolism , Adiponectin*/metabolism , Adiponectin*/blood , Beclin-1*/metabolism , Microtubule-Associated Proteins*/metabolism, Humans ; Female ; Pregnancy ; Male ; Case-Control Studies ; Adult ; Autophagy-Related Protein 5/metabolism ; Autophagy-Related Protein 5/genetics ; Autophagy-Related Protein 7/genetics ; Autophagy-Related Protein 7/metabolism ; Receptors, Adiponectin/metabolism ; Receptors, Adiponectin/genetics ; Fetus/metabolism ; RNA, Messenger/metabolism ; Sex Factors ; Gestational Age ; Down-Regulation ; Obesity/metabolism
مستخلص: Objective: Maternal obesity affects 39.7% of reproductive-age women in the United States. Emerging research has suggested that in utero exposure to maternal obesity is associated with adverse neurodevelopmental outcomes, but knowledge of underlying mechanisms in human samples is lacking.
Methods: A matched case-control study was performed in women with singleton fetuses who were undergoing elective pregnancy termination at gestational ages 15 to 21 weeks. Maternal adiponectin levels from plasma were measured using ELISA kits. RNA was extracted from fetal brain tissue using RNeasy Mini Kit (QIAGEN). mRNA expression from ADIPOR1, ADIPOR2, MTOR, ATG5, ATG7, BECN1, and MAP1LC3B was quantified through the ΔΔCt method and using GAPDH as a housekeeping gene.
Results: We have identified transcription patterns associated with inhibition of autophagy in male fetal brain tissue exposed to maternal obesity (↑MTOR, ↓ATG5, ↓ATG7, and ↓MAP1LC3B), with female fetuses demonstrating either no change in transcription or nonsignificant changes associated with increased autophagy. There was significant downregulation of the autophagy-associated gene BECN1 in both male and female individuals who were exposed to obesity in utero.
Conclusions: We present novel evidence suggesting that in utero exposure to maternal obesity in humans may significantly affect neurodevelopment, especially in male fetuses, through alterations in normal autophagy molecular mechanisms and with adiponectin as a potential mediator.
(© 2024 The Obesity Society.)
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معلومات مُعتمدة: R01HD069238 Eunice Kennedy Shriver National Institute of Child Health and Human Development; OPP1119489 Grand Challenges in Global Health
المشرفين على المادة: EC 2.7.11.1 (TOR Serine-Threonine Kinases)
0 (Adiponectin)
0 (Beclin-1)
EC 2.7.1.1 (MTOR protein, human)
0 (Microtubule-Associated Proteins)
0 (BECN1 protein, human)
0 (Autophagy-Related Protein 5)
EC 6.2.1.45 (Autophagy-Related Protein 7)
0 (MAP1LC3B protein, human)
EC 6.2.1.45 (ATG7 protein, human)
0 (ATG5 protein, human)
0 (Receptors, Adiponectin)
0 (RNA, Messenger)
تواريخ الأحداث: Date Created: 20240422 Date Completed: 20240528 Latest Revision: 20240806
رمز التحديث: 20240807
DOI: 10.1002/oby.24017
PMID: 38644654
قاعدة البيانات: MEDLINE
الوصف
تدمد:1930-739X
DOI:10.1002/oby.24017