Key result
Prenatal and lactation nicotine exposure in male rat offspring led to higher body and iBAT weight, a whitening phenotype with impaired mitochondria, and decreased expression of iBAT-related genes.
Why the study?
Does prenatal and lactation nicotine exposure affect the morphology and function of brown adipose tissue in male rat offspring?
Does prenatal and lactation nicotine exposure affect the morphology and function of brown adipose tissue in male rat offspring?
Prenatal and lactation nicotine exposure induces a 'whitening' phenotype and impairs mitochondrial function in the brown adipose tissue of male rat offspring.
Prenatal nicotine exposure was associated with higher offspring weight and iBAT alterations in rats; hypothesis-generating for developmental cardiometabolic programming.
The aim of this study was to investigate the effects of prenatal and lactation nicotine exposure on the morphology and function of brown adipose tissue (BAT) in male rat offspring. We conducted a morphological assay and gene expression study of interscapular BAT (iBAT) in male rat offspring. The male offspring from nicotine-exposed dams exhibited higher body weight and iBAT weight. Hematoxylin and eosin staining and transmission electron microscopy showed that iBAT from nicotine-exposed male offspring presented a "whitening" phenotype characterized by lipid droplet accumulation and impaired mitochondria with a randomly oriented and fractured cristae. The expression of the iBAT structure and function-related genes all decreased in nicotine-exposed male offspring. These data indicate that prenatal and lactation nicotine exposure affects morphology and function of iBAT in male rat offspring.
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Fan et al. (2016) studied Prenatal and lactation nicotine exposure. Prenatal and lactation nicotine exposure vs. Unexposed dams/offspring was evaluated on Morphology and function of interscapular brown adipose tissue (iBAT). Prenatal and lactation nicotine exposure in male rat offspring led to higher body and iBAT weight, a whitening phenotype with impaired mitochondria, and decreased expression of iBAT-related genes.
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