Nicotine, its metabolism and an overview of its biological effects

Background: The global health transition is linked with an increased burden of non-communicable diseases with cardiovascular diseases leading the epidemic. In sub-Saharan Africa (SSA), the prevalence of obesity has increased during the past decades and there is a need to investigate the associated driving factors. In Burkina Faso obesity remains low, especially in rural areas. In this study we recruited middle-aged adults, as part of a larger study on genetic and environmental contributions to cardiometabolic disease among Africans. Objectives: To investigate the distribution of BMI and prevalence of obesity in a cross-sectional population-based study and to determine the sociodemographic and behavioural correlates with BMI. Methods: Participants (N = 2,076) were recruited from the Nanoro Health and Demographic Surveillance System area and were aged 40–60 years. We applied hierarchical modelling to identify factors associated with BMI and structural equation modelling to identify mediated effects of sociodemographic and behavioural variables on BMI. Results: Data are presented on 2,076 participants (49.9% female). Men had significantly higher BMI than women with medians of 21.1 (19.2 – 23.4) vs 19.8 (18.1 – 21.6) (p < 0.001), and there were significantly more underweight women compared to men (31.0% vs 17.4%) (p < 0.001). More men were overweight and obese than women (11.9% vs 5.2% and 2.2% vs 1.4%). Socioeconomic status was the major contributor to increased BMI for men, and education was the main contributor in women. Tobacco smoking and chewing, and problematic alcohol consumption were associated with a decrease in BMI in men and women. Conclusion: Overweight and obesity are relatively low among adults in rural Burkina Faso, and men had a higher median BMI than women. Behavioural factors, including tobacco use and alcohol consumption, contributed to a decrease in BMI, whereas socioeconomic status and education (which were both generally low in this community) contributed to an increase in BMI.

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“…The lower weight decrease among women compared to men may be due to differences in nicotine absorption through the digestive tract [40]. …”

Section: Discussionmentioning

confidence: 99%

Gender differences in sociodemographic and behavioural factors associated with BMI in an adult population in rural Burkina Faso – an AWI-Gen sub-study

Boua

Sorgho

Rouamba

et al. 2018

Global Health Action

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“…In adult rats, nicotine exposure has been shown to produce oxidative tissue injuries in vivo [23,24] and can induce oxidative stress in pancreatic tissue in vitro [25]. Oxidative stress has been shown to decrease insulin secretion and to increase apoptosis in beta cells [reviewed in Ref.…”

Section: Discussionmentioning

confidence: 99%

Fetal and neonatal exposure to nicotine in Wistar rats results in increased beta cell apoptosis at birth and postnatal endocrine and metabolic changes associated with type 2 diabetes

et al. 2005

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Fetal and neonatal exposure to nicotine in Wistar rats results in increased beta cell apoptosis at birth and postnatal endocrine and metabolic changes associated with type 2 diabetes Abstract Aims/hypothesis: Epidemiological studies report an increased risk of obesity and type 2 diabetes in children born to women who smoked during pregnancy. This study examines the effect of fetal and neonatal exposure to nicotine, the major addictive component of cigarettes, on postnatal growth, adiposity and glucose homeostasis. Methods: Female Wistar rats were given either saline (vehicle) or nicotine (1 mg kg −1 day −1 ) during pregnancy and lactation. Serum and pancreas tissue were collected from the infant rats at birth. Postnatal growth was assessed weekly until the rats reached 26 weeks of age and glucose homeostasis was examined by OGTTs performed at 7 and 26 weeks of age. Results: Exposure to nicotine resulted in increased postnatal growth and adiposity. Nicotine exposure also resulted in dysglycaemia at 7 and 26 weeks of age. Serum insulin concentrations were decreased in the pups exposed to nicotine at birth. This was associated with increased beta cell apoptosis (pups of saline-treated mothers 8.8±1.21% apoptotic beta cells; pups of nicotine-treated mothers 27.8±3.1% apoptotic beta cells). Conclusions/interpretation: Fetal and neonatal exposure to nicotine results in metabolic changes in the offspring that are consistent with obesity and type 2 diabetes. We propose that these metabolic changes may be a consequence of the initial insult to the beta cell during fetal life and that this animal model has many characteristics of diabetes in humans.

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“…Nicotine inhibits proliferation of a variety of cells essential for normal fracture repair, such as fibroblasts, red blood cells, and macrophages. 25,26 Nicotine also increases platelet adhesiveness, which increases the risk of thrombotic microvascular occlusion and tissue ischemia at the site of injury. 25 Carbon monoxide greatly diminishes the oxygen carrying capacity of red blood cells and shifts the oxygen dissociation curve to the left, so that oxygen is less likely to dissociate from red blood cells at the site of injury.…”

Section: Discussionmentioning

confidence: 99%

Smoking delays chondrogenesis in a mouse model of closed tibial fracture healing

et al. 2006

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Smoking delays the healing process and increases morbidity associated with many common musculoskeletal disorders, including long bone fracture. In the current study, a murine model of tibial fracture healing was used to test the hypothesis that smoking delays chondrogenesis after fracture. Mice were divided into two groups, a nonsmoking control group and a group exposed to cigarette smoke for 1 month prior to surgical tibial fracture. Mice were euthanized at 7, 14, and 28 days after surgery. The outcomes measured were immunohistochemical staining for type II collagen protein expression as a marker of cartilage matrix and proliferating cell nuclear antigen (PCNA) staining to measure proliferation at the site of injury. Toluidine blue staining and histomorphometry were used to quantify areas of cartilaginous and noncartilaginous fracture callus. Radiographs were analyzed for evidence of remodeling after injury. At day 7 after injury, mice exposed to cigarette smoke had a smaller fracture callus with less cartilage matrix compared to controls. Proliferation was present at high levels in both groups at this time point, but proliferating cells had a more immature morphology in the smoking group. At day 14, chondrogenesis was more active in smokers compared to controls, while a higher percentage of bone was present in the control animals. At day 28, X-ray analysis revealed a larger fracture callus remaining in the smoking animals. Together, these findings show that the chondrogenic phase of tibial fracture healing is delayed by smoking. This study represents, to our knowledge, the first analysis of molecular and cellular mechanisms of healing in a smoking mouse fracture model. ß

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Nicotine, its metabolism and an overview of its biological effects

Cited by 323 publications

References 101 publications

Gender differences in sociodemographic and behavioural factors associated with BMI in an adult population in rural Burkina Faso – an AWI-Gen sub-study

Gender differences in sociodemographic and behavioural factors associated with BMI in an adult population in rural Burkina Faso – an AWI-Gen sub-study

Fetal and neonatal exposure to nicotine in Wistar rats results in increased beta cell apoptosis at birth and postnatal endocrine and metabolic changes associated with type 2 diabetes

Smoking delays chondrogenesis in a mouse model of closed tibial fracture healing

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