Fetal and neonatal nicotine exposure and postnatal glucose homeostasis: identifying critical windows of exposure

Abstract

Fetal and lactational exposure to nicotine at concentrations comparable with those in women who smoke causes impaired glucose tolerance in male offspring in postnatal life. It remains unknown whether there are critical windows of susceptibility to nicotine exposure. Female nulliparous Wistar rats were given saline vehicle or nicotine bitartrate (1 mg/kg per day) prior to pregnancy, which was then: A) discontinued during pregnancy and lactation; B) continued until parturition; C) continued until weaning; and D) discontinued during pregnancy and restarted from lactation until weaning. At 26 weeks of age, offspring in each group were challenged with an oral glucose load. b-Cell mass, apoptosis, and proliferation were measured at birth, and at 4 and 26 weeks of age. The animals in group C (exposed to nicotine throughout pregnancy and lactation) had reduced b-cell mass from birth through 26 weeks of age and impaired glucose homeostasis at 26 weeks of age. b-Cell mass was also reduced at birth and at 4 weeks of age in animals exposed to nicotine during pregnancy alone (group B). However, enhanced proliferation following weaning led to recovery of this defect to 98% of control levels by week 26. The response to the glucose load in groups A, B, and D did not differ from controls. Continued exposure to nicotine from conception through lactation results in permanent b-cell loss and subsequent impaired glucose tolerance. This model of type 2 diabetes requires that nicotine exposure occurs both in utero and during lactation.

Neonatal nicotine exposure causes insulin and leptin resistance and inhibits hypothalamic leptin signaling in adult rat offspring

“…Some studies have shown that fetal and postnatal NIC exposure causes impaired glucose tolerance in neonatal offspring (Somm et al 2008). According to Bruin et al (2007), NIC exposure from conception until lactation results in permanent b-cell depletion and subsequent impaired glucose tolerance. Therefore, the development of diabetes requires that NIC exposure occurs in both gestation and lactation periods.…”

Endocrine effects of tobacco smoke exposure during lactation in weaned and adult male offspring

“…In rodents, it has been demonstrated that adult offspring from mothers who were exposed to nicotine during gestation and/or lactation become obese and have other metabolic disorders such as cardiovascular disorders, permanent b-cell loss, and insulin resistance (Bruin et al 2007, Somm et al 2009). Therefore, it seems that nicotine has the potential to act as an obesogenic factor in the offspring.…”

Effects of tobacco smoke exposure during lactation on nutritional and hormonal profiles in mothers and offspring

“…This was associated with some alterations in lipid profile of mothers and pups, such as higher high-density lipoprotein cholesterol (HDL-C). At weaning, offspring whose mothers were exposed to nicotine had type 2 diabetes (Bruin et al 2007) and increased adipose tissue weight (Soom et al 2008). When maternal nicotine exposure occurred only during lactation, the 15-day-old pups showed higher adiposity, hyperleptinemia, hypothyroidism, hypercorticosteronemia, and higher adrenal catecholamine content (Oliveira et al 2009.…”