Literature DB >> 25948073

Detraining in pregnancy and/or lactation modulates neuropeptidergic hypothalamic systems in offspring mice.

Leandro Fernandes1, Bruno F A Calegare1, Vanessa Cavalcante-Silva1, Vânia D'Almeida2.   

Abstract

Manipulations in metabolic parameters during pregnancy/lactation can impact the development of short- and long-term energy control mechanisms, which are mainly modulated by neural and hormonal inputs to the hypothalamus. Thus, we tested how mice training and detraining during pregnancy and lactation affect hypothalamus gene expression and change biometric and metabolic profiles of the offspring. Three-month-old female Swiss mice were submitted to an 8-week exercise program (swimming 5 times/week, 1 h/day). Following this physical exercise protocol, these conditioned animals and the control group were submitted to matting. After pregnancy verification, the animals were distributed into four groups: training during pregnancy and lactation (T); detraining after pregnancy confirmation (DP); detraining during lactation (DL); and control (CT), without interventions. After weaning, the offspring of the four groups were derived into these as follows: TO, DPO, DLO, and CTO, respectively. The body weight was lower in conditioned females compared to control at weeks 4-8 of the exercise regimen. No statistical difference in dam's body weight was observed during pregnancy. Related to offspring, at post-natal day 90, the animals were euthanized and DPO and DLO showed decrease in Npy and Cart expression in hypothalamus, and DLO also had increased Lep gene expression in white adipose tissue. Additionally, DPO showed increase in plasma triglycerides levels, total liver weight, and decrease in brown adipose tissue compared to CTO. Together, these results support that detraining during critical periods of development leads to altered gene expression in hypothalamic neuropeptidergic systems.

Entities:  

Keywords:  Detraining; Hypothalamus; Pregnancy; Programming; Swimming

Mesh:

Substances:

Year:  2015        PMID: 25948073     DOI: 10.1007/s12020-015-0612-z

Source DB:  PubMed          Journal:  Endocrine        ISSN: 1355-008X            Impact factor:   3.633


  44 in total

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