期刊
HORMONE AND METABOLIC RESEARCH
卷 42, 期 7, 页码 483-490出版社
GEORG THIEME VERLAG KG
DOI: 10.1055/s-0030-1249103
关键词
programming; insulin; adiponectin; glycogen; triglycerides; SOCS3
资金
- National Council for Scientific and Technological Development (Conselho Nacional de Desenvolvimento Cientfico e Tecnologico - CNPq)
- Coordination for the Enhancement of Higher Education Personnel (Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior - CAPES)
- State of Rio de Janeiro Carlos Chagas Filho Research Foundation (Fundacao Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro - FAPERJ)
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 mu g/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 hyper-triglyceridemia. We also observed liver micro-steatosis 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.
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