Effects of Nicotine on Bone and Calciotropic Hormones in Growing Female Rats

Iwaniec, Urszula T.; Fung, Yiu K.; Cullen, D. M.; Akhter, Mohammed P.; Haven, Mary C.; Schmid, Marian J.

doi:10.1007/s00223001099

Cited by 38 publications

(44 citation statements)

References 25 publications

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“…However, vertebral and femoral mass and strength were little affected by nicotine treatment in either the intact or the OVX rats. The results [7,8,14,26] suggest that tobacco agents other than nicotine are responsible for the decreased bone density and increased fracture risk observed in smokers [6,12,17,18,23,24]. This study's limitation was that it investigated nicotine effects after bone loss had been established.…”

Section: Discussionmentioning

confidence: 97%

“…Such high doses were used because treatment of rats with nicotine at serum concentrations within the range observed in smokers had no effect on the biomechanical properties of bone [7,8,14,26]. However, treatment of rats with nicotine at serum nicotine concentrations 2.5-fold greater than that found in smokers resulted in lower femoral size and ultimate load (fracture load), suggesting that nicotine, at high intakes, may compromise bone mass and strength [13].…”

Section: Discussionmentioning

confidence: 99%

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Effects of nicotine on bone mass and strength in aged female rats

Akhter

Iwaniec

Haynatzki

et al. 2003

Journal Orthopaedic Research

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This study investigated the effects of nicotine on bone mass and biomechanical properties in aged, estrogen-replete (shamoperated) and estrogen-deplete (ovariectomized) female rats. Eight month old, retired breeder, sham-operated and ovariectomized Sprague-Dawley rats were left untreated for 12 weeks to establish cancellous osteopenia in the ovariectomized group. The animals were then administered saline, low dose nicotine (6.0 mg/kg/day) or high dose nicotine (9.0 mg/kg/day) via osmotic minipumps for 12 weeks. Vertebrae and femora were collected at necropsy for determination of bone mass and strength. As expected, ovariectomy had a negative effect on most endpoints evaluated. Vertebral body bone mineral content (BMC) and density (BMD) and the structural (ultimate load and yield load) and material (ultimate stress, yield stress, and flexural modulus of elasticity) strength properties were lower in the OVX rats than in the sham-operated rats. Femoral diaphysis BMC, BMD, ultimate load, and flexural modulus were also lower in the OVX rats than in the sham-operated rats. The nicotine doses administered resulted in serum nicotine levels that averaged 1.54.5-fold greater than those observed in heavy smokers. Despite the high doses used, nicotine had no effect on vertebral BMC, BMD, or any of the structural and material strength properties in either the OVX or the Sham rats. In addition, nicotine had no effect on femoral diaphysis BMC, BMD, ultimate load, stiffness, ultimate stress, or flexural modulus. Femoral yield load and stress were lower in low dose nicotine-treated rats than in vehicle-treated rats. However, differences were not detected between the high dose nicotine-and vehicle-treated rats for either femoral yield load or stress. The results suggest that tobacco agents other than nicotine are responsible for the decreased bone density and increased fracture risk as observed in smokers.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Effects of nicotine on bone mass and strength in aged female rats

Akhter

Iwaniec

Haynatzki

et al. 2003

Journal Orthopaedic Research

Self Cite

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“…It is important to consider that nicotine may have a priming effect in calcium metabolism and regulation during lactation with possible programming consequences in calcium hormonal regulation in adulthood, because nicotine administration in female rats results in lower serum calcitriol with no differences in serum Ca C or PTH (Iwaniec et al 2002) and because serum cotinine (a nicotine metabolite) has a significant inverse relationship with bone mineral content in a clinical study (Benson & Shulman 2005).…”

Section: Discussionmentioning

confidence: 99%

Calcium supplementation reverts central adiposity, leptin, and insulin resistance in adult offspring programed by neonatal nicotine exposure

Nobre¹,

Lisboa²,

Santos-Silva³

et al. 2011

Journal of Endocrinology

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Obesity is a worldwide epidemic. Calcium influences energy metabolism regulation, causing body weight loss. Because maternal nicotine exposure during lactation programs for obesity, hyperleptinemia, insulin resistance (IR), and hypothyroidism, we decided to evaluate the possible effect of dietary calcium supplementation on these endocrine dysfunctions in this experimental model. Osmotic minipumps containing nicotine solution (N: 6 mg/kg per day for 14 days) or saline (C) were s.c. implanted in lactating rats 2 days after giving birth (P2). At P120, N and C offspring were subdivided into four groups: 1) C -standard diet; 2) C with calcium supplementation (CCa, 10 g calcium carbonate/kg rat chow); 3) N -standard diet; and 4) N with calcium supplementation (NCa). Rats were killed at P180. As expected, N offspring showed higher visceral and total body fat, hyperleptinemia, lower hypothalamus leptin receptor (OB-R) content, hyperinsulinemia, and higher IR index. Also, higher tyrosine hydroxylase (TH) expression (C51%), catecholamine content (C37%), and serum 25-hydroxyvitamin D 3 (C76%) were observed in N offspring. Dietary calcium supplementation reversed adiposity, hyperleptinemia, OB-R underexpression, IR, TH overexpression, and vitamin D. However, this supplementation did not reverse hypothyroidism. In NCa offspring, Sirt1 mRNA was lower in visceral fat (K37%) and higher in liver (C42%). In conclusion, dietary calcium supplementation seems to revert most of the metabolic syndrome parameters observed in adult offspring programed by maternal nicotine exposure during lactation. It is conceivable that the reduction in fat mass per se, induced by calcium therapy, is the main mechanism that leads to the increment of insulin action.

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“…Probably, the best experimental evidence for the negative effect of nicotine on bone derives from studies of bone metabolism following injury. In the rabbit fracture healing model, several investigators have found that bone graft vascularization and subsequent bone formation is reduced with nicotine treatment 8 . In the present study, the lack of significant differences regarding the other parameters investigated (BA, BW, BH) may in part be due to the random sampling variability.…”

Section: Discussionmentioning

confidence: 99%

Histologic evaluation of the effect of nicotine administration on bone regeneration: a study in dogs

Saldanha¹,

Pimentel²,

Casati³

et al. 2004

Braz. oral res.

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ABSTRACT:The objective of this study was to investigate the histometric impact of nicotine on bone regeneration of surgically created alveolar ridge defects in dogs. Sixteen mongrel dogs were used. One defect was surgically created unilaterally in the mandible, and left to heal spontaneously. The animals were randomly assigned to one of the following groups: Group 1 -control (n = 8) and Group 2 -subcutaneous nicotine administration (2 mg/kg) twice a day (n = 8). After 4 months, the animals were sacrificed and the specimens routinely processed for semi-serial decalcified sections. Bone height (BH), bone width (BW), bone density (BD), and bone area (BA) of the newly-formed bone were evaluated. Intergroup analysis (Mann-Whitney rank sum test) showed that regardless of the presence of nicotine, no significant differences were observed regarding bone width (BW), bone area (BA) and bone height (BH) (p > 0.05). On the other hand, it was demonstrated that nicotine administration significantly influenced the proportion of mineralized tissue within the limits of the newly-formed bone (BD) (p < 0.001). Within the limits of the present study, it can be concluded that nicotine might affect but not prevent bone healing in defects left to heal spontaneously. DESCRIPTORS: Smoking; Nicotine; Tobacco; Bone regeneration. RESUMO:O objetivo do presente estudo foi avaliar histometricamente a influência da nicotina sobre a regeneração óssea de defeitos criados cirurgicamente em rebordos alveolares edêntulos de cães. Defeitos ósseos foram criados cirurgicamente em um dos lados da mandíbula de dezesseis cães e foram deixados para que curassem espontaneamente. Os animais foram aleatoriamente designados para um dos seguintes grupos: Grupo 1 -controle (n = 8) e Grupo 2 -administração subcutânea de nicotina (2 mg/kg) duas vezes ao dia durante 4 meses (n = 8). Os animais foram sacrificados, e secções semi-seriadas descalcificadas, obtidas. Os parâmetros histométricos avaliados foram altura, largura, área e densidade do tecido ósseo neoformado. A análise intergrupos (Mann-Whitney "rank sum test") demonstrou que a administração de nicotina não influenciou altura, largura e área de tecido ósseo neoformado (p > 0,05). Entretanto, a administração de nicotina influenciou significativamente a densidade do tecido ósseo neoformado (p < 0,001). Dentro dos limites do presente estudo, pode-se concluir que a nicotina pode afetar, mas não impedir a regeneração de defeitos ósseos criados cirurgicamente em mandíbulas edêntulas de cães.

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Effects of Nicotine on Bone and Calciotropic Hormones in Growing Female Rats

Cited by 38 publications

References 25 publications

Effects of nicotine on bone mass and strength in aged female rats

Effects of nicotine on bone mass and strength in aged female rats

Calcium supplementation reverts central adiposity, leptin, and insulin resistance in adult offspring programed by neonatal nicotine exposure

Histologic evaluation of the effect of nicotine administration on bone regeneration: a study in dogs

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