1. Maternal nicotine exposure impairs brown adipose tissue via AMPK-SIRT1-PGC-1α signals in male offspring.
- Author
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Li GL, Ping J, Chen HJ, Zhang WX, Fan J, Peng DS, Zhang L, and Yan YE
- Subjects
- Adipose Tissue, Brown pathology, Adipose Tissue, Brown ultrastructure, Animals, Female, Gene Expression Regulation drug effects, Genes, Mitochondrial, Male, Pregnancy, Rats, Wistar, Uncoupling Protein 1 metabolism, Rats, AMP-Activated Protein Kinases metabolism, Adipose Tissue, Brown metabolism, Nicotine adverse effects, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha metabolism, Prenatal Exposure Delayed Effects metabolism, Prenatal Exposure Delayed Effects pathology, Signal Transduction drug effects, Sirtuin 1 metabolism
- Abstract
Aims: Maternal nicotine exposure during pregnancy and lactation is associated with obesity in offspring. Brown adipose tissue (BAT) is correlated with energy metabolism and obesity. In this study, we explored the mechanism of maternal nicotine exposure on BAT changes in male offspring., Main Methods: Pregnant rats were randomly assigned to nicotine (1.0 mg/kg twice per day, subcutaneous administration) or control groups. In vitro, C3H10T1/2 cells were induced to differentiate into mature brown adipocytes, and 0-50 μM nicotine was given to C3H10T1/2 cells during the differentiation process., Key Findings: Nicotine-exposed males had white-like adipocytes and abnormal mitochondria structure in iBAT at 26 weeks. The expression of mitochondrial genes, UCP1 and AMPK-SIRT1-PGC-1α pathway were downregulated in the nicotine group at 26 weeks rather than 4 weeks. In vitro, 50 μM nicotine decreased the expression of mitochondrial genes, UCP1 and AMPK-SIRT1-PGC-1α pathway in brown adipocytes., Significance: Maternal nicotine exposure showed the "programming" effect on the decreased brown-like phenotype in BAT of adult male offspring via downregulating AMPK-SIRT1-PGC-1α pathway. This impairment of BAT may be a potential mechanism of nicotine-induced obesity in male offspring., (Copyright © 2020 Elsevier Inc. All rights reserved.)
- Published
- 2021
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