Loading…

Perinatal nicotine exposure increases obesity susceptibility by peripheral leptin resistance in adult female rat offspring

[Display omitted] •Perinatal nicotine exposure promotes obesity and metabolic disorders.•Perinatal nicotine exposure induces peripheral leptin resistance in female rats.•The expression of lipolysis genes were affected dominantly in adipose tissue.•The expression of lipogenesis genes were affected do...

Full description

Saved in:
Bibliographic Details
Published in:Toxicology letters 2018-02, Vol.283, p.91-99
Main Authors: Zhang, Wan-xia, Li, Yin-ping, Fan, Jie, Chen, Hui-jian, Li, Gai-ling, Ouyang, Yan-Qiong, Yan, You-e
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:[Display omitted] •Perinatal nicotine exposure promotes obesity and metabolic disorders.•Perinatal nicotine exposure induces peripheral leptin resistance in female rats.•The expression of lipolysis genes were affected dominantly in adipose tissue.•The expression of lipogenesis genes were affected dominantly in liver. Maternal nicotine (NIC) exposure causes overweight, hyperleptinemia and metabolic disorders in adult offspring. Our study aims to explore the underlying mechanism of perinatal NIC exposure increases obesity susceptibility in adult female rat offspring. In our model, we found that adult NIC-exposed females presented higher body weight and subcutaneous and visceral fat mass, as well as larger adipocytes, while no change was found in food intake. Serum profile showed a higher serum glucose, insulin and leptin levels in NIC-exposed females. In adipose tissue and liver, the leptin signaling pathway was blocked at 26 weeks, presented lower Janus tyrosine kinase 2 and signal transducer and activator of transcription 3 gene expression, higher suppressor of cytokine signaling 3 gene expression (in adipose tissue) and lower leptin receptors gene expression (in liver), indicating that peripheral leptin resistance occurred in NIC-exposed adult females. In female rats, the expression of lipolysis genes was affected dominantly in adipose tissue, but lipogenesis genes was affected in liver. Furthermore, the glucose and insulin tolerance tests showed a delayed glucose clearance and a higher area under the curve in NIC-exposed females. Therefore, perinatal NIC exposure programed female rats for adipocyte hypertrophy and obesity in adult life, through the leptin resistance in peripheral tissue.
ISSN:0378-4274
1879-3169
DOI:10.1016/j.toxlet.2017.11.015