Cigarette Smoke During Breastfeeding in Rats Changes Glucocorticoid and Vitamin D Status in Obese Adult Offspring

Maternal smoking increases obesogenesis in the progeny. Obesity is associated with several hormonal dysfunctions. In a rat model of postnatal tobacco smoke exposure, we previously reported increased central fat depot and disruption of some hormonal systems in the adult offspring. As both glucocorticoids and vitamin D alter lipogenesis and adipogenesis, here we evaluated the metabolism of these two hormones in visceral adipose tissue (VAT) and liver by Western blotting, and possible associations with lipogenesis biomarkers in adult rats that were exposed to tobacco smoke during their suckling period. At postnatal day (PN) 3, dams and offspring of both sexes were exposed (S group) or not (C group) to tobacco smoke, 4 × 1 h/day. At PN180, corticosteronemia was lower in S male and higher in S female offspring, without alterations in peripheral glucocorticoid metabolism and receptor. Adrenal ACTH receptor (MC2R) was higher in both sexes of S group. Despite unchanged serum vitamin D, liver 25-hydroxylase was higher in both sexes of S group. Male S offspring had higher 1α-hydroxylase, acetyl-CoA carboxylase (ACC), and fatty acid synthase (FAS) in VAT. Both sexes showed increased ACC protein content and reduced sirtuin mRNA in liver. Male S offspring had lower liver peroxisome proliferator-activated receptor-α. Tobacco exposure during lactation induced abdominal obesity in both sexes via distinct mechanisms. Males and females seem to develop HPA-axis dysfunction instead of changes in glucocorticoid metabolism and action. Lipogenesis in VAT and liver, as well as vitamin D status, are more influenced by postnatal smoke exposure in male than in female adult rat offspring

Alterations of the expression levels of CPT-1, SCD1, TR beta-1 and related microRNAs are involved in lipid metabolism impairment in adult rats caused by maternal coconut oil intake during breastfeeding

We studied the molecular and epigenetic mechanisms associated with dysfunctions caused by postnatal coconut oil exposure. Lactating dams were divided into soybean oil (SO) and coconut oil (CO) groups (0.5 g/kg/gavage). Half of the CO offspring received CO in their chow throughout their lifetime (CO + C). Adult CO offspring had higher liver TR beta-1 mRNA, which is consistent with lower miR-181a and lower DIO2 mRNA in brown adipose tissue (BAT) and higher CPT-1 mRNA in white adipose tissue (WAT). CO + C offspring exhibited higher BAT miR-382*, but DIO2 was unaltered. This group also had higher liver SCD1, miR-122 expression, and WAT SCD1 mRNA. CO and CO + C offspring had lower hepatic CPT-1 mRNA. The disturbances in CO offspring may be partially attributed to alterations in the enzymes involved in lipid metabolism, which may be mediated via mechanisms associated with miR-122. Continuous exposure to CO prohibits some of these changes63CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQCOORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL DE NÍVEL SUPERIOR - CAPESFUNDAÇÃO CARLOS CHAGAS FILHO DE AMPARO À PESQUISA DO ESTADO DO RIO DE JANEIRO - FAPERJsem informaçãosem informaçãosem informaçã