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Blocking Leptin Action One Week After Weaning Reverts most of the Programming Caused by Neonatal Hyperleptinemia in the Adult Rat

Authors :
Egberto Gaspar de Moura
Natália da Silva Lima
Leonardo Lemos de Souza
Annyelle Anastácio Cordeiro
E.C. de Oliveira
Patricia Cristina Lisboa
M. C. F. Passos
Juliana G. Franco
Karen Jesus Oliveira
C. C. Pazos Moura
P. A. Trotta
Source :
Hormone and Metabolic Research. 43:171-177
Publication Year :
2011
Publisher :
Georg Thieme Verlag KG, 2011.

Abstract

Hyperleptinemia during lactation programs for higher serum leptin in 30-day-old and adult rats, associated with metabolic changes. Here we evaluated the inhibition of serum leptin at 29 and 30 days on the metabolic phenotype of rats programmed with leptin during lactation. Pups from Wistar rats were saline-injected or leptin-injected from postnatal day 1 to day 10. At 29 and 30 days old, animals were injected with anti-leptin antibody (LA and CA) or saline (LS and CS). In adult animals, higher visceral (+53%) and total fat mass (+33%), hyperleptinemia (+67%), hypertriglyceridemia (+47%), and hypoadiponectinemia (-44%) observed in LS group compared to CS were prevented by immunoneutralization of leptin, since LA group had those parameters values similar to CS group. However, immunoblockade of leptin in normal animals led to the same metabolic changes seen in leptin-treated animals, in addition to lower serum adiponectin (-77% vs. CS) and higher insulin resistance index (+37%). Liver sirtuin1 (SIRT1) was higher (+41%) only in LA group, suggesting a role for SIRT1 in the prevention of leptin programming. Hypothalamic OBR was lower and SOCS3 higher in LS group and these changes were normalized in LA group. In conclusion, blocking leptin action one week after weaning seems to revert most of the alterations observed in rats programmed by neonatal hyperleptinemia. Higher liver SIRT1 expression may be one of the mechanisms involved, leading to a better glucose and lipid metabolism. Our data suggest that the lack or the excess of leptin programs an adverse metabolic phenotype in adulthood.

Details

ISSN :
14394286 and 00185043
Volume :
43
Database :
OpenAIRE
Journal :
Hormone and Metabolic Research
Accession number :
edsair.doi.dedup.....13d1b3f234ece3583f711680daa94542
Full Text :
https://doi.org/10.1055/s-0031-1271694