Prenatal smoke (Nicotine) exposure and offspring's metabolic disease susceptibility in adulthood

He, Bo; Zhang, Qi; Guo, Yu; Ao, Ying; Tie, Kai; Xiao, Hao; Chen, Liaobin; Xu, Dan; Wang, Hui

doi:10.1016/j.fct.2022.113384

Cited by 12 publications

(14 citation statements)

References 139 publications

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“…In addition, gestational nicotine exposure was associated with the intrauterine growth retardation of rat fetuses and aberrant HPA development and metabolic disorder affecting many systems such as adrenal gland, testis, hippocampus, etc. [80][81][82]. Nicotine affected the intrauterine neuroendocrine metabolic programming in fetuses by overexposure to maternal glucocorticoids which further affected the regulatory physiology of HPA, glucocorticoid-insulin-like growth factor (IGF)-1 axis, renin-angiotensin system, and other endocrine systems.…”

Section: Hormone Relationships Relevance and Conclusionmentioning

confidence: 99%

“…In this regard, nicotine exposure in fetuses increased blood corticosteroids, decreased placental 11β-hydroxysteroid dehydrogenase-2 expression, increased the expression of glucocorticoid receptor, decreased fetal hypothalamic CRH, decreased the expression of adrenal StAR and cholesterol side-chain cleavage enzyme, and dysregulated fetal liver IGF-1, its receptor and insulin receptor [85]. Prenatally exposed rats showed a propensity for metabolic disorder during adult age which was suggested to be due to the in utero dysregulation of hippocampal developmental physiology [80,82,86]. These fetal-originated neuro-metabolic modulations leading to an adulthood onset of disorders also exhibited epigenetic heritability in subsequent generations probably through the effects of glucocorticoids on the epigenome (DNA methylation, histone acetylation, and microRNA) [83,84].…”

Section: Hormone Relationships Relevance and Conclusionmentioning

confidence: 99%

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Potential Disruption of Systemic Hormone Transport by Tobacco Alkaloids Using Computational Approaches

Rehan

Zargar

Sheikh

et al. 2022

Toxics

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Tobacco/nicotine is one of the most toxic and addictive substances and continues to pose a significant threat to global public health. The harmful effects of smoking/nicotine affect every system in the human body. Nicotine has been associated with effects on endocrine homeostasis in humans such as the imbalance of gonadal steroid hormones, adrenal corticosteroid hormones, and thyroid hormones. The present study was conducted to characterize the structural binding interactions of nicotine and its three important metabolites, cotinine, trans-3′-hydroxycotinine, and 5′-hydroxycotinine, against circulatory hormone carrier proteins, i.e., sex-hormone-binding globulin (SHBG), corticosteroid-binding globulin (CBG), and thyroxine-binding globulin (TBG). Nicotine and its metabolites formed nonbonded contacts and/or hydrogen bonds with amino acid residues of the carrier proteins. For SHBG, Phe-67 and Met-139 were the most important amino acid residues for nicotine ligand binding showing the maximum number of interactions and maximum loss in ASA. For CBG, Trp-371 and Asn-264 were the most important amino acid residues, and for TBG, Ser-23, Leu-269, Lys-270, Asn-273, and Arg-381 were the most important amino acid residues. Most of the amino acid residues of carrier proteins interacting with nicotine ligands showed a commonality with the interacting residues for the native ligands of the proteins. Taken together, the results suggested that nicotine and its three metabolites competed with native ligands for binding to their carrier proteins. Thus, nicotine and its three metabolites may potentially interfere with the binding of testosterone, estradiol, cortisol, progesterone, thyroxine, and triiodothyronine to their carrier proteins and result in the disbalance of their transport and homeostasis in the blood circulation.

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Section: Hormone Relationships Relevance and Conclusionmentioning

confidence: 99%

Section: Hormone Relationships Relevance and Conclusionmentioning

confidence: 99%

Potential Disruption of Systemic Hormone Transport by Tobacco Alkaloids Using Computational Approaches

Rehan

Zargar

Sheikh

et al. 2022

Toxics

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“…It is thought that the placental damage caused by nicotine is either the direct cause of or greatly contributes to these outcomes. [5][6][7][8] Nicotine acts directly on the placenta altering placental development by disrupting trophoblastic invasion and differentiation, increasing collagen content in villous stroma, decreasing angiogenesis, inducing placental hypoxia and oxidative stress, and downregulating labyrinth vascularisation. [1][2][3]5,9,10 Holloway et al proposed that changes to trophoblastic invasion and differentiation are likely mediated by placental nACHR (nicotinic acetylcholine receptors).…”

Section: Introductionmentioning

confidence: 99%

“…[5][6][7][8] Nicotine acts directly on the placenta altering placental development by disrupting trophoblastic invasion and differentiation, increasing collagen content in villous stroma, decreasing angiogenesis, inducing placental hypoxia and oxidative stress, and downregulating labyrinth vascularisation. [1][2][3]5,9,10 Holloway et al proposed that changes to trophoblastic invasion and differentiation are likely mediated by placental nACHR (nicotinic acetylcholine receptors). 9 This disruption contributes to an increase in vascular resistance which alters the maternal-fetal circulation.…”

Section: Introductionmentioning

confidence: 99%

“…The organs studied, and which seem to be most affected are the lungs, kidneys, and brain. [4][5][6]8 In the lungs, nicotine induces formation of oxygen radicals and reduces the antioxidant capacity of the lungs. These alterations form mutations within the lung DNA resulting in disruption of lung growth and maintenance, which is thought to age the lungs of the offspring much faster than normal.…”

Section: Introductionmentioning

confidence: 99%

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The impact of smoking and nicotine exposure during pregnancy on fetal nephrogenesis: a systematic review

Popham,

Kandasamy

2023

J Dev Orig Health Dis

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The effect of smoking and nicotine exposure during pregnancy on fetal nephrogenesis is a growing area of research. The objective of this systematic review is to summarise the current evidence in this research field. Our literature search identified a total of 415 articles from PubMed, Embase, Scopus, and Cochrane. After electronic sorting and manual screening, 18 eligible articles were found, 6 being human studies and 12 being animal studies. Articles that did not study nicotine or smoking, did not focus on fetal kidney development, or did not include nicotine or smoking exposure during pregnancy were excluded from the systematic review. The main outcomes of the studies were kidney weight, volume and size, kidney histopathology and morphology, and kidney function. Evidence from human studies identified a reduction in fetal kidney size, volume, and weight in offspring exposed to smoking during pregnancy; and the greatest impact was seen in offspring exposed to >5–10 cigarettes per day. Animal studies investigated kidney histopathology and highlighted kidney injury and microscopic changes in response to nicotine exposure during pregnancy. Further research is required to determine the impact on kidney function. Recreational nicotine use is evolving, and with the increasing use of urine cotinine in the evaluation of nicotine exposure, further research is needed.

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The Increased Apoptosis of Mesenchymal Stem Cells Mediated Osteopenia Due to Prenatal Nicotine Exposure in Female Offspring Rats via IGF1 Pathway

Li,

Xiao,

et al. 2024

Environmental Toxicology

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Nicotine exposure is a common adverse environment during pregnancy and causes developmental toxicity of long bones in offspring. However, the effect of prenatal nicotine exposure (PNE) on bone mass accumulation in female offspring and its mechanism remained to be further investigated. In this study, we constructed a PNE rat model and collected the long bone and the bone marrow mesenchymal stem cells (BMSCs) from female offspring rats for the detection of bone mass, cell apoptosis, and the expressions of osteogenesis‐ and apoptosis‐related genes. The results revealed that PNE induced low bone mass in female offspring rats and was associated with the suppression of osteogenic function. Moreover, the apoptosis of BMSCs derived from the PNE female offspring rats was raised, and the expression ratio of apoptosis marker genes BAX/BCL‐2 was significantly increased. Further, PNE inhibited the expression and function of insulin‐like growth factor l (IGF1) signaling pathway in BMSCs. However, the exogenous IGF1 treatment partially ameliorated the increased apoptosis of BMSCs derived from the PNE female offspring rats. In conclusion, PNE induced low bone mass in female offspring rats, which was attributed to the increased apoptosis of BMSCs due to functional inhibition of IGF1 signaling pathway.

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Prenatal smoke (Nicotine) exposure and offspring's metabolic disease susceptibility in adulthood

Cited by 12 publications

References 139 publications

Potential Disruption of Systemic Hormone Transport by Tobacco Alkaloids Using Computational Approaches

Potential Disruption of Systemic Hormone Transport by Tobacco Alkaloids Using Computational Approaches

The impact of smoking and nicotine exposure during pregnancy on fetal nephrogenesis: a systematic review

The Increased Apoptosis of Mesenchymal Stem Cells Mediated Osteopenia Due to Prenatal Nicotine Exposure in Female Offspring Rats via IGF1 Pathway

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