Horm Metab Res 2009; 41(12): 874-879
DOI: 10.1055/s-0029-1234070
Animals, Clinical

© Georg Thieme Verlag KG Stuttgart · New York

Early Maternal Hyperleptinemia Programs Adipogenic Phenotype in Rats

F. Pereira-Toste1 , F. P. Toste1 , E. Oliveira1 , P. A. Trotta1 , P. C. Lisboa1 , E. G. de Moura1 , M. C. F. Passos1 , 2
  • 1Department of Physiological Sciences, State University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil
  • 2Department of Applied Nutrition, Nutrition Institute, State University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil
Further Information

Publication History

received 05.02.2009

accepted after second revision 06.07.2009

Publication Date:
14 August 2009 (online)


We have previously reported on the treatment of maternal rats with leptin during the three last days of lactation program for overweight and leptin hypothalamic resistance in the offspring. Here we have investigated whether treatment of maternal rats with leptin in the first ten days of lactation can program metabolic dysfunctions on the adult offspring. Lactating rats were divided into 2 groups: rats (LEP) injected with recombinant mouse leptin (8 μg/100 g/body weight, daily during the first 10 days of lactation) and control group (C) that received the same volume of saline. After weaning, all pups had free access to normal diet, their body weight and food intake were monitored at 4 days interval until 180 days, when they were tested for food intake and response to either leptin (0.5 mg/kg body weight, ip) or saline. The offspring from leptin-treated mothers gained more weight from day 69 onward and had higher food intake from day 145 onward, higher amount of visceral adipose tissue (57%), higher serum glucose (10%), and higher serum leptin (135%) at 180 days compared to control group. The food intake was not reduced as expected after acute injection of leptin in these animals, suggesting resistance to the anorexigenic effect of leptin. We conclude that maternal hyperleptinemia in early lactation programed higher food intake, body weight gain due to higher total and visceral fat mass, and resistance to anorexigenic effect of leptin in the adult offspring even when this hyperleptinemia occurred at the beginning of lactation.



Prof. M. C.F. Passos, PhD 

Departamento de Ciências Fisiológicas – 5o andar

Instituto de Biologia

Universidade do Estado do Rio de Janeiro

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87- Rio de Janeiro

RJ 20550-030


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