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Nicotine exposure during breastfeeding alters the expression of endocannabinoid system biomarkers in female but not in male offspring at adulthood

Published online by Cambridge University Press:  23 February 2023

Rosiane Aparecida Miranda
Affiliation:
Laboratory of Endocrine Physiology, Biology Institute, Rio de Janeiro State University, RJ, Brazil
Vanessa Silva Tavares Rodrigues
Affiliation:
Laboratory of Endocrine Physiology, Biology Institute, Rio de Janeiro State University, RJ, Brazil
Thamara Cherem Peixoto
Affiliation:
Laboratory of Endocrine Physiology, Biology Institute, Rio de Janeiro State University, RJ, Brazil
Alex C. Manhães
Affiliation:
Laboratory of Neurophysiology, Biology Institute, Rio de Janeiro State University, RJ, Brazil
Egberto Gaspar de Moura
Affiliation:
Laboratory of Endocrine Physiology, Biology Institute, Rio de Janeiro State University, RJ, Brazil
Patricia Cristina Lisboa*
Affiliation:
Laboratory of Endocrine Physiology, Biology Institute, Rio de Janeiro State University, RJ, Brazil
*
Address for correspondence: Dr. Patrícia Cristina Lisboa, Physiological Sciences Department; Biology Institute, Rio de Janeiro State University, 28 DE Setembro Avenue, 87, Rio de Janeiro, RJ, 20551-031, Brazil. Email: pclisboa@uerj.br

Abstract

Early nicotine exposure compromises offspring’s phenotype at long-term in both sexes. We hypothesize that offspring exposed to nicotine during breastfeeding show deregulated central and peripheral endocannabinoid system (ECS), compromising several aspects of their metabolism. Lactating rats received nicotine (NIC, 6 mg/Kg/day) or saline from postnatal day (PND) 2 to 16 through implanted osmotic minipumps. Offspring were analyzed at PND180. We evaluated protein expression of N-acylphosphatidylethanolamide-phospholipase D (NAPE-PLD), fatty acid amide hydrolase (FAAH), diacylglycerol lipase (DAGL), monoacylglycerol lipase (MAGL) and cannabinoid receptors (CB1 and/or CB2) in lateral hypothalamus, paraventricular nucleus of the hypothalamus, liver, visceral adipose tissue (VAT), adrenal and thyroid. NIC offspring from both sexes did not show differences in hypothalamic ECS markers. Peripheral ECS markers showed no alterations in NIC males. In contrast, NIC females had lower liver DAGL and CB1, higher VAT DAGL, higher adrenal NAPE-PLD and higher thyroid FAAH. Endocannabinoids biosynthesis was affected by nicotine exposure during breastfeeding only in females; alterations in peripheral tissues suggest lower action in liver and higher action in VAT, adrenal and thyroid. Effects of nicotine exposure during lactation on ECS markers are sex- and tissue-dependent. This characterization helps understanding the phenotype of the adult offspring in this model and may contribute to the development of new pharmacological targets for the treatment of several metabolic diseases that originate during development.

Type
Original Article
Copyright
© The Author(s), 2023. Published by Cambridge University Press in association with International Society for Developmental Origins of Health and Disease

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