Leptin Supplementation During Lactation Restores Key Liver Metabolite Levels Malprogrammed by Gestational Calorie Restriction

Introduction Perinatal nutritional factors can program offspring metabolic phenotype and risk to obesity. This study investigates the potential role of leptin supplementation (during lactation) in ameliorating the malprogrammed effects caused by mild maternal calorie restriction during gestation, on...

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Detalles Bibliográficos
Autores: Yau-Qiu, Zhi Xin, Madrid-Gambin, Francisco, Brennan, Lorraine, Palou, Andreu, Rodriguez, Ana María
Tipo de recurso: artículo
Fecha de publicación:2021
País:España
Institución:Conselleria de Salut i Consum del Govern de les Illes Balears
Repositorio:Docusalut
Idioma:inglés
OAI Identifier:oai:docusalut.com:20.500.13003/19666
Acceso en línea:https://hdl.handle.net/20.500.13003/19666
Access Level:acceso abierto
Palabra clave:Maternal Nutritional Physiological Phenomena
Energy Intake
DNA Methylation
Fatty Acids
Lactation
Pregnancy
Liver
Male
Metabolome
Rats, Wistar
Leptin
Female
Rats
Animals
Caloric Restriction
Animales
Fenómenos Fisiologicos Nutricionales Maternos
Ratas Wistar
Femenino
Hígado
Masculino
Restricción Calórica
Lactancia
Ratas
Ingestión de Energía
Ácidos Grasos
Embarazo
Metilación de ADN
Leptina
Metaboloma
calorie restriction
leptin
liver
metabolic programming
perinatal nutrition
Descripción
Sumario:Introduction Perinatal nutritional factors can program offspring metabolic phenotype and risk to obesity. This study investigates the potential role of leptin supplementation (during lactation) in ameliorating the malprogrammed effects caused by mild maternal calorie restriction during gestation, on young rat offspring liver metabolic response. Methods and Results Untargeted and targeted metabolomics studies on liver samples are performed by NMR and GC-MS, respectively. Global DNA methylation and the expression by RT-PCR of key genes involved in different pathways are also determined. By NMR, 15 liver metabolites are observed to be altered in the offspring of gestational calorie-restricted dams (CR group), at days 25-27 of life. Physiological leptin supplementation during lactation partially reverted the effect of CR condition for most of these metabolites. Moreover, targeted fatty acid analysis by GC-MS shows a significant decrease in the hepatic concentration of certain very long-chain fatty acids (VLCFA) in CR offspring, partially or totally reverted by leptin supplementation. No remarkable changes are found in global DNA methylation or mRNA expression. Conclusion Physiological leptin supplementation during lactation contributes to the reversion of changes caused by maternal mild calorie restriction on the liver metabolome. This agrees with a putative role of leptin supplementation preventing or reversing metabolic disturbances caused by gestational metabolic malprogramming.