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The Melatonin and Enriched Environment Ameliorated Low Protein-Induced Intrauterine Growth Retardation by IGF-1 And mtor Signaling Pathway and Autophagy Inhibition in Rats.
- Source :
-
Current molecular medicine [Curr Mol Med] 2021; Vol. 21 (3), pp. 246-256. - Publication Year :
- 2021
-
Abstract
- CDATA[Aim: The present study investigated whether melatonin (MEL) and enriched environment (EE) might protect against intrauterine growth retardation (IUGR) in rats.<br />Methods: Sprague-Dawley rats were randomly allocated to 3 groups: control (C), model (M) and EE+MEL group. Animals were housed in an enriched environment (EE+MEL group) or remained in a standard environment (C group, M group). IUGR rat model was built by feeding a low protein diet during pregnancy. MEL was administered by gavaging. At day 1 post-birth, the baseline characteristics and serum biochemical parameters, morphology of liver and small intestine, enzyme activities, and mRNA expression levels of fetal rats were determined. The autophagy marker LC3 and Beclin1 were determined by western blot analysis.<br />Results: EE+MEL markedly improved the baseline characteristics, hepatic and intestinal morphology of IUGR fetuses. In addition, the lactase activities in the fetal intestine were markedly increased by the EE+MEL. The levels of serum somatostatin (SST), Growth hormone (GH), GH releasing hormone (GHRH), Insulin-like Growth Factor 1 (IGF-1), triiodothyronine (T3), and tetraiodothyronine (T4) were found to be recovered by EE+MEL. In addition, the EE+MEL significantly ameliorated the mRNA expression of SST, GHRH, and GHRH receptor (GHRHR), GH, GHR, IGF-1, and IGF-1 receptor (IGF1R), IGF binding protein-1 (IGFBP1), mammalian target of rapamycin (mTOR), S6 kinase 1 (S6K1) and eukaryotic initiation factor 4E (eIF4E)-binding protein 1 (4EBP1) in fetuses. In IUGR fetal livers, LC3 and Beclin1 were found to be increased at birth, while LC3 and Beclin1 were observed to be significantly decreased in the EE+MEL group.<br />Conclusion: EE+MEL could improve fetal rats' baseline characteristics, serum biochemical parameters, birth weight, intestinal and hepatic morphology and enzyme activities. These effects could be explained by the activation of the IGF-1/IGFBP1 and IGF-1/mTOR/S6K1/4EBP1 signaling pathway and autophagy inhibition.<br /> (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)
- Subjects :
- Animals
Autophagy drug effects
Autophagy genetics
Diet, Protein-Restricted adverse effects
Disease Models, Animal
Female
Fetal Growth Retardation genetics
Fetal Growth Retardation metabolism
Fetal Growth Retardation pathology
Gene Expression Regulation drug effects
Growth Hormone genetics
Insulin-Like Growth Factor Binding Protein 1 genetics
Male
Pregnancy
Rats
Rats, Sprague-Dawley
Signal Transduction drug effects
Fetal Growth Retardation drug therapy
Insulin-Like Growth Factor I genetics
Melatonin pharmacology
TOR Serine-Threonine Kinases genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1875-5666
- Volume :
- 21
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- Current molecular medicine
- Publication Type :
- Academic Journal
- Accession number :
- 32713334
- Full Text :
- https://doi.org/10.2174/1566524020666200726221735