Nicotine exposure during breastfeeding reduces sympathetic activity in brown adipose tissue and increases in white adipose tissue in adult rats: Sex-related differences.

Abstract Nicotine transfer via breast milk induces obesity in the adult offspring. We hypothesize that sympathetic nervous system (SNS) activity, brown adipose tissue (BAT) thermogenesis and white adipose tissue (WAT) lipogenesis/adipogenesis are altered in adult rats that were exposed to nicotine exclusively during the breastfeeding period. Lactating Wistar rats were separated into two groups: nicotine (NIC), dams implanted with osmotic minipumps containing 6 mg/kg of nicotine at postnatal day (PN) 2; control, dams were implanted with saline-containing minipumps. Euthanasia occurred at PN120 or PN180. NIC offspring had lower BAT SNS activity and higher BAT lipid content. NIC males showed lower UCP1, β3-AR and CPT1a, while NIC females showed lower UCP1, TRα1, CPT1a, suggesting lower thermogenesis. NIC males showed higher WAT SNS activity, WAT β3-AR, adrenal catecholamine, FAS, PPARγ and adipocytes area, while NIC females showed higher ACC, FAS, CEBPβ and PPARγ. These findings indicate increased lipogenesis/adipogenesis in both sexes, with a possible compensatory sympathetic activated-lipolysis in males. NIC males had higher hypothalamic pAMPK/AMPK, explaining the lower BAT sympathetic activity. Neonatal nicotine exposure reduces BAT SNS activity and thermogenesis, and, only in males, increases WAT adipogenesis/lipogenesis, despite higher WAT SNS activity. These alterations can be associated with obesogenesis in this programming model.