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Horm Metab Res 2010; 42(7): 483-490
DOI: 10.1055/s-0030-1249103
Original Basic

© Georg Thieme Verlag KG Stuttgart · New York

Leptin Treatment During Lactation Programs Leptin Synthesis, Intermediate Metabolism, and Liver Microsteatosis in Adult Rats

I. H. Trevenzoli1 , A. L. Rodrigues1 , E. Oliveira1 , A. A. Thole2 , L. Carvalho2 , M. S. Figueiredo1 , F. P. Toste1 , J. F. N. Neto1 , M. C. F. Passos1 , 3 , P. C. Lisboa1 , E. G. Moura1
  • 1Departamento Ciências Fisiológicas, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil
  • 2Departamento Histologia, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil
  • 3Departamento Nutrição Aplicada, Instituto de Nutrição, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil
Weitere Informationen

Publikationsverlauf

received 26.11.2009

accepted 11.02.2010

Publikationsdatum:
25. März 2010 (online)

Auch verfügbar auf
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Abstract

Epidemiological and experimental studies have associated development of metabolic syndrome with stressful events (nutritional, hormonal, or environmental) in early life. This phenomenon is known as programing and changes in adipokines levels in early life, especially leptin, seem to be involved with its development. We have shown that neonatal hyperleptinemia on lactation programs for leptin resistance, hyperthyroidism, and higher corticosterone and catecholamines levels with cardiovascular consequences. In the present study, we evaluated the effect of hyperleptinemia during lactation on the glucose and lipid metabolism and liver morphology of adult rats, which were saline or leptin-treated (8 μg/100 g of body weight) daily, for the first 10 days of life. Leptin group had lower body mass during treatment, but higher body mass and hyperleptinemia at adulthood, without difference in fat mass. We showed that the probable source of hyperleptinemia is the higher leptin content in the subcutaneous adipose tissue. The programed rats showed hyperinsulinemia and hypoadiponectinemia with higher expression of the hypothalamic Suppressor of Cytokine Signaling 3 (SOCS3), suggesting insulin resistance. Besides, they presented higher liver glycogen and hypertriglyceridemia. We also observed liver microsteatosis in the leptin-programed adult rats. Our data show that neonatal hyperleptinemia alters glucose metabolism, which seems to be partially compensated by the hyperinsulinemia. However, changes in the lipid metabolism are not compensated. It is probable that these changes induced by neonatal hyperleptinemia result from a selective tissue specific resistance both to insulin and leptin at adulthood, and the increase of SOCS3 may play an important role in this process.

Key words

programming - insulin - adiponectin - glycogen - triglycerides - SOCS3

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Correspondence

Dr. E. G. Moura

Departamento de Ciências

Fisiológicas – 5° andar

Instituto de Biologia

Universidade do Estado do

Rio de Janeiro

Av. 28 de Setembro

87 Rio de Janeiro

RJ 20551-030

Brazil

Telefon: +55/21/2587 6434

Fax: +55/21/2587 6129

eMail: egberto@pq.cnpq.br

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