Abstract
Maternal smoking is a risk factor for progeny obesity. We have previously shown, in a rat model of neonatal tobacco smoke exposure, a mild increase in food intake and a considerable increase in visceral adiposity in the adult offspring. Males also had secondary hyperthyroidism, while females had only higher T4. Since brown adipose tissue (BAT) hypofunction is related to obesity, here we tested the hypothesis that higher levels of thyroid hormones are not functional in BAT, suggesting a lower metabolic rate. We evaluated autonomic nerve activity in BAT and its function in adult rats that were exposed to tobacco smoke during lactation. At birth, litters were adjusted to 3 male and 3 female pups/litter. From postnatal day (PND) 3 to 21, Wistar lactating rats and their pups were divided into SE group, smoke-exposed in a cigarette smoking machine (4 times/day) and C group, exposed to filtered air. Offspring were sacrificed at PND180. Adult SE rats of both genders had lower interscapular BAT autonomic nervous system activity, with higher BAT mass but no change in morphology. BAT UCP1 and CPT1a protein levels were decreased in the SE groups of both genders. Male SE rats had lower β3-AR, TRα1, and TRβ1 expression while females showed lower PGC1α expression. BAT Dio2 mRNA and hypothalamic POMC and MC4R levels were similar between groups. Hypothalamic pAMPK level was higher in SE males and lower in SE females. Thus, neonatal cigarette smoke exposure induces lower BAT thermogenic capacity, which can be obesogenic at adulthood.
Highlights
The ‘‘developmental origins of health and disease’’ (DOHaD) concept relates the influence of disturbances during a critical window of development on the induction of permanent changes that determine a pattern of health or disease later in life [1]
Our research group has been studying the effect of tobacco smoke exposure exclusively during lactation and we have demonstrated that this insult can cause obesity development and endocrine disorders in the adult offspring [7,8]
We have demonstrated that exposure to cigarette smoke exclusively during lactation was capable of causing brown adipose tissue (BAT) hypofunction in the adult offspring of both genders, reducing autonomic nerve activity and important markers related to thermogenesis
Summary
The ‘‘developmental origins of health and disease’’ (DOHaD) concept relates the influence of disturbances during a critical window of development on the induction of permanent changes that determine a pattern of health or disease later in life [1]. Evidence indicates that environmental and nutritional changes during periods of great plasticity (intrauterine life and/or lactation) induce metabolic disorders, for instance obesity, in the offspring. Our research group has been studying the effect of tobacco smoke exposure exclusively during lactation and we have demonstrated that this insult can cause obesity development and endocrine disorders in the adult offspring [7,8]. In this model, adult offspring have higher total body fat and visceral fat despite a mild hyperphagia, suggesting that they are hypometabolic. All these changes are capable of altering the brown adipose tissue (BAT) thermogenesis [10]
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