Smokeless nicotine administration is associated with hypertension but not with a deterioration in glucose tolerance in rats

Swislocki, Arthur L; Tsuzuki, Akiko; Tait, M.; Khuu, D. T.; Fann, K. Y.

doi:10.1016/s0026-0495(97)90270-5

Cited by 16 publications

(6 citation statements)

References 34 publications

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“…Previously, Swislocki et al showed that subcutaneous implanted nicotine pellets had no effect on insulin sensitivity in adult and juvenile rats [45], [46]. These discrepancies may be explained by a variety of factors, especially dosage, treatment duration, and route of nicotine administration [47].…”

Section: Discussionmentioning

confidence: 99%

Chronic Exposure to Nicotine Enhances Insulin Sensitivity through α7 Nicotinic Acetylcholine Receptor-STAT3 Pathway

Guo

Wang

et al. 2012

PLoS ONE

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This study was to investigate the effect of nicotine on insulin sensitivity and explore the underlying mechanisms. Treatment of Sprague-Dawley rats with nicotine (3 mg/kg/day) for 6 weeks reduced 43% body weight gain and 65% blood insulin level, but had no effect on blood glucose level. Both insulin tolerance test and glucose tolerance test demonstrated that nicotine treatment enhanced insulin sensitivity. Pretreatment of rats with hexamethonium (20 mg/kg/day) to antagonize peripheral nicotinic receptors except for α7 nicotinic acetylcholine receptor (α7-nAChR) had no effect on the insulin sensitizing effect of nicotine. However, the insulin sensitizing effect but not the bodyweight reducing effect of nicotine was abrogated in α7-nAChR knockout mice. Further, chronic treatment with PNU-282987 (0.53 mg/kg/day), a selective α7-nAChR agonist, significantly enhanced insulin sensitivity without apparently modifying bodyweight not only in normal mice but also in AMP-activated kinase-α2 knockout mice, an animal model of insulin resistance with no sign of inflammation. Moreover, PNU-282987 treatment enhanced phosphorylation of signal transducer and activator of transcription 3 (STAT3) in skeletal muscle, adipose tissue and liver in normal mice. PNU-282987 treatment also increased glucose uptake by 25% in C2C12 myotubes and this effect was total abrogated by STAT3 inhibitor, S3I-201. All together, these findings demonstrated that nicotine enhanced insulin sensitivity in animals with or without insulin resistance, at least in part via stimulating α7-nAChR-STAT3 pathway independent of inflammation. Our results contribute not only to the understanding of the pharmacological effects of nicotine, but also to the identifying of new therapeutic targets against insulin resistance.

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Section: Discussionmentioning

confidence: 99%

Chronic Exposure to Nicotine Enhances Insulin Sensitivity through α7 Nicotinic Acetylcholine Receptor-STAT3 Pathway

Guo

Wang

et al. 2012

PLoS ONE

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“…At low dose levels (1 mg/kg-day) permanent changes in glucose homeostasis were observed only when exposure occurred during both fetal and neonatal life (i.e., pregnancy and lactation); however, when dams were exposed to 3 mg/kg-day (Somm et al 2008) or 6 mg/kg-day (Oliveira et al 2010), then either fetal or lactational exposure was sufficient to affect glycemic control. Importantly, no effects on glucose homeostasis were observed in Wistar rats (Jose et al 2009) or in a series of studies (Jose et al 2009; Swislocki 2003; Swislocki and Fakiri 2008; Swislocki et al 1997) in Sprague-Dawley rats treated with nicotine after weaning. Taken together, these data suggest that cigarette smoke or nicotine exposure during gestation and lactation is the critical window of exposure.…”

Section: Animal Studies On Developmental Exposure To Nicotinementioning

confidence: 98%

Evaluation of the Association between Maternal Smoking, Childhood Obesity, and Metabolic Disorders: A National Toxicology Program Workshop Review

Behl

Rao

Aagaard

et al. 2013

Environ Health Perspect

146

115

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Background: An emerging literature suggests that environmental chemicals may play a role in the development of childhood obesity and metabolic disorders, especially when exposure occurs early in life.Objective: Here we assess the association between these health outcomes and exposure to maternal smoking during pregnancy as part of a broader effort to develop a research agenda to better understand the role of environmental chemicals as potential risk factors for obesity and metabolic disorders.Methods: PubMed was searched up to 8 March 2012 for epidemiological and experimental animal studies related to maternal smoking or nicotine exposure during pregnancy and childhood obesity or metabolic disorders at any age. A total of 101 studies—83 in humans and 18 in animals—were identified as the primary literature.Discussion: Current epidemiological data support a positive association between maternal smoking and increased risk of obesity or overweight in offspring. The data strongly suggest a causal relation, although the possibility that the association is attributable to unmeasured residual confounding cannot be completely ruled out. This conclusion is supported by findings from laboratory animals exposed to nicotine during development. The existing literature on human exposures does not support an association between maternal smoking during pregnancy and type 1 diabetes in offspring. Too few human studies have assessed outcomes related to type 2 diabetes or metabolic syndrome to reach conclusions based on patterns of findings. There may be a number of mechanistic pathways important for the development of aberrant metabolic outcomes following perinatal exposure to cigarette smoke, which remain largely unexplored.Conclusions: From a toxicological perspective, the linkages between maternal smoking during pregnancy and childhood overweight/obesity provide proof-of-concept of how early-life exposure to an environmental toxicant can be a risk factor for childhood obesity.

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“…Chronic intake of high-fat diets or alcohol adversely affects the tissue free radical defense system [4,5]. Recent studies also have shown that nicotine treatment increased the coronary disease risk profile by increasing the blood pressure [6].…”

Section: Introductionmentioning

confidence: 99%

A Comparative Study of Antioxidants S-Allyl Cysteine Sulfoxide and Vitamin E on the Damages Induced by Nicotine in Rats

et al. 2003

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The dietary consumption of antioxidant-rich fruits and vegetables is inversely correlated with the incidence of various diseases like cardiovascular diseases and lung cancer. We have tried to find out how far the S-allyl cysteine sulfoxide (SACS) isolated from garlic (Allium sativum L.) can combat the nicotine-induced peroxidative damage in rats. The effects have been compared with the standard antioxidant vitamin E. Administration of SACS or vitamin E (100 mg/kg) to nicotine (0.6 mg/kg) treated rats for 21 days showed decreased concentrations of thiobarbituric acid reactive substances, hydroperoxides, and conjugated dienes in liver, lungs, and heart as compared with the values found in rats treated with nicotine alone. The activities of catalase and superoxide dismutase increased. The levels of the antioxidants like vitamins A, C, and E in the liver and glutathione in all tissues increased significantly in SACS-treated or vitamin E fed rats. However, the antioxidant status was higher when vitamin E was administered as compared with SACS administered to nicotine-treated rats.

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Smokeless nicotine administration is associated with hypertension but not with a deterioration in glucose tolerance in rats

Cited by 16 publications

References 34 publications

Chronic Exposure to Nicotine Enhances Insulin Sensitivity through α7 Nicotinic Acetylcholine Receptor-STAT3 Pathway

Chronic Exposure to Nicotine Enhances Insulin Sensitivity through α7 Nicotinic Acetylcholine Receptor-STAT3 Pathway

Evaluation of the Association between Maternal Smoking, Childhood Obesity, and Metabolic Disorders: A National Toxicology Program Workshop Review

A Comparative Study of Antioxidants S-Allyl Cysteine Sulfoxide and Vitamin E on the Damages Induced by Nicotine in Rats

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