Effects of chronic nicotine administration of insulin, glucose, epinephrine, and norepinephrine

doi:10.1016/0024-3205(88)90679-0

Life Sciences

Volume 42, Issue 2, 1988, Pages 161-170

https://doi.org/10.1016/0024-3205(88)90679-0 Get rights and content

Abstract

There is an inverse relationship between nicotine administration and body weight. Previous research indicates that this relationship results partially from effects of nicotine on energy intake. The present research includes two animal studies designed to investigate the effects of chronic nicotine administration on biochemical responses that affect energy utilization. The results indicate that chronic nicotine administration is accompanied by significant decreases in circulating insulin levels. Nicotine increases levels of catecholamines, but this effect is short-lived. The effects of nicotine on insulin are consistent with the conclusion that nicotine administration increases energy utilization.

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Cited by (63)

Nicotine’ actions on energy balance: Friend or foe?
2021, Pharmacology and Therapeutics
Citation Excerpt :
A considerable amount of literature exists regarding nicotine's action on energy expenditure. These studies have reported increased energy expenditure in humans and rodents after exposure to cigarette smoke or nicotine (Grunberg et al., 1988; Hofstetter et al., 1986; Martinez de Morentin et al., 2012; Perkins, 1992; Seoane-Collazo et al., 2019). Energy expenditure encompasses obligatory (basal metabolic rate) and facultative (physical activity and thermogenesis) aspects (Cannon & Nedergaard, 2004; Cannon & Nedergaard, 2017; Contreras et al., 2015; Silva, 2006).
Obesity has reached pandemic proportions and is associated with severe comorbidities, such as type 2 diabetes mellitus, hepatic and cardiovascular diseases, and certain cancer types. However, the therapeutic options to treat obesity are limited. Extensive epidemiological studies have shown a strong relationship between smoking and body weight, with non-smokers weighing more than smokers at any age. Increased body weight after smoking cessation is a major factor that interferes with their attempts to quit smoking. Numerous controlled studies in both humans and rodents have reported that nicotine, the main bioactive component of tobacco, exerts a marked anorectic action. Furthermore, nicotine is also known to modulate energy expenditure, by regulating the thermogenic activity of brown adipose tissue (BAT) and the browning of white adipose tissue (WAT), as well as glucose homeostasis. Many of these actions occur at central level, by controlling the activity of hypothalamic neuropeptide systems such as proopiomelanocortin (POMC), or energy sensors such as AMP-activated protein kinase (AMPK). However, direct impact of nicotine on metabolic tissues, such as BAT, WAT, liver and pancreas has also been described. Here, we review the actions of nicotine on energy balance. The relevance of this interaction is interesting, because considering the restricted efficiency of obesity treatments, a possible complementary approach may focus on compounds with known pharmacokinetic profile and pharmacological actions, such as nicotine or nicotinic acetylcholine receptors signaling.
Drug-induced stress responses and addiction risk and relapse
2019, Neurobiology of Stress
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Regarding the ANS, naïve or light smokers’ catecholamine response has been mostly documented in animal models, but several human studies have studied the cardiovascular effects of nicotine in nonsmokers. Epinephrine has been reliably shown to increase in a dose-dependent fashion in response to nicotine (Grunberg et al., 1988; Mello, 2010; Morse, 1989; Watts, 1960), particularly under conditions of nicotine self-administration (Donny et al., 2000). Nicotine also increases cardiovascular output in animals (Watts, 1960), a finding that has been replicated in non-smoking humans (Foulds et al., 1997; Perkins et al., 2009).
A number of studies have assessed the effects of psychoactive drugs on stress biology, the neuroadaptations resulting from chronic drug use on stress biology, and their effects on addiction risk and relapse. This review mainly covers human research on the acute effects of different drugs of abuse (i.e., nicotine, cannabis, psychostimulants, alcohol, and opioids) on the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system (ANS) responses. We review the literature on acute peripheral stress responses in naïve or light recreational users and binge/heavy or chronic drug users. We also discuss evidence of alterations in tonic levels, or tolerance, in the latter relative to the former and associated changes in the phasic stress responses. We discuss the impact of the stress system tolerance in heavy users on their response to drug- and stress-related cue responses and craving as compared to control subjects. A summary is provided of the effects of glucocorticoid responses and their adaptations on brain striatal and prefrontal cortices involved in the regulation of drug seeking and relapse risk. Finally, we summarize important considerations, including individual difference factors such as gender, co-occurring drug use, early trauma and adversity and drug use history and variation in methodologies, that may further influence the effects of these drugs on stress biology.
Impact of chronic nicotine administration on bone mineral content in young and adult rats: A comparative study
2013, European Journal of Pharmacology
Citation Excerpt :
Nicotine-induced decreases in bone wet weights may, at least in part, contribute to the decreases in body weight in nicotine-treated rats and these results are in agreement with those of previous studies (Hermizi et al., 2007; Ypsilantis et al., 2013). Independent of its bone weight-lowering effect, experimental studies have shown that nicotine reduces body weight by raising the resting metabolic rate and increasing energy expenditure while blunting the expected increase in food intake in response to the increase in metabolic rate (Blaha et al., 1998; Grunberg et al., 1988; Bishop et al., 2004). In this study, the femur, the longest bone in the body which consists mostly of compact (cortical) bone, and the lumbar vertebrae, the largest segments of the movable part of the vertebral column which consist mostly of spongy (cancellous) bone (Iwamoto et al., 2000; Jiang et al. 2007), were chosen to evaluate the effects of nicotine on these two types of bone.
The aim of this study was to evaluate the effects of chronic nicotine administration on bone mineral homeostasis in rapidly growing young rats in comparison to effects in adult male rats. Two doses of nicotine (3 and 4.5 mg/kg/day, as nicotine hydrogen tartrate) were used and rat treatment was continued for 6 months. In this study, all nicotine-treated rats weighed less than control rats and the effect was dose-dependent. Also, rats treated with nicotine had lower femoral wet weight and showed a significant reduction in femoral mid-shaft cortical width and femoral and lumbar vertebral ash weights. These effects were associated with a significant reduction of ash calcium and phosphorus contents of the femora and lumbar vertebrae. The bone mineral-lowering effects of nicotine were more severe in the lumbar vertebral spongy bone than in the femoral compact bone and these changes were more marked in adult rats than in young rats. An additional interesting observation was that the femora of young rats treated with nicotine were significantly shorter than those of control young rats. Also, the values of the femoral ash weight per unit length were significantly decreased in nicotine-treated adult rats but not in nicotine-treated young rats. Thus, these results show that nicotine-induced changes in bone vary with age. The clinical relevance of this study is that it may provide justification to insist that all people in general and the risky young group in particular should be warned against the hazards of the negative effects of nicotine on bone.
The effects of chronic nicotine on meal patterns, food intake, metabolism and body weight of male rats
2010, Pharmacology Biochemistry and Behavior
It is unclear what contribution food intake and metabolism have in causing weight loss after administering a dose of nicotine equivalent to smoking one to three packs of cigarettes per day because previous studies have been of a very short duration. To address this question, male Sprague Dawley rats were housed in computerized food intake modules and fed 45 mg pellets: Group 1 [nicotine injected with 1.4 mg/kg/day (free base), fed ad libitum]; and Group 2 [saline injected and pair-fed by computer with Group 2]; and Group 3 [saline injected (i.p.), fed ad libitum]. The rats received 4 equally spaced injections over the dark phase. Treatment consisted of: Phase 1 (nicotine or saline for 14 days), Phase 2 (all rats saline for 8 days and Phase 3 (pair-fed group “unyoked” for 6 days)). Nicotine inhibited food intake over the first 6 days. On termination of nicotine, there was no compensatory hyperphagia in either Groups 1 or 2; and their body weight was reduced starting on day 5 until day 28. In another study, rats were housed in an indirect calorimetry system. Saline or nicotine was injected for 14 days, as noted above; then all rats were injected with saline for 4 days and then no injections for 10 days to follow changes in body weight. Energy expenditure (Kcal/Kg^0.75) was measured for 18 days. Nicotine significantly reduced food intake on 7 of 14 days of nicotine injections. The body weight of the nicotine injected rats was significantly reduced starting on day 3 until day 25. There were no differences in energy expenditures of the groups, which suggested that a decrease in food intake and not an increase in metabolism was the reason the rats lost weight after administering nicotine.
Sensitivity of young rats to nicotine exposure: Physiological and biochemical parameters
2009, Ecotoxicology and Environmental Safety
Citation Excerpt :
In fact, we verified that the decrease of glycogen in rats exposed to 56 days to nicotine was accompanied by liver and body weight reduction. These effects can be related, at least in part, to classical effect of nicotine on adrenergic mechanism, by increase of plasma levels of catecholamine (β-adrenergic effect) (Andersson and Arner, 1993; Grunberg et al., 1988), inducing lypolisis (Andersson and Arner, 2001) and decreasing glycogen synthesis (Liu et al., 2003). Still, it is speculate that the effect of nicotine can be mediated directly through nicotine receptors in the liver reducing glycogen synthesis (Dewar et al., 2002).
This work has investigated the effects of prolonged exposure of young rats to nicotine on some physiological and biochemical parameters. Wistar male rats (30 days old) were treated (s.c.) with saline or nicotine 5 mg/kg/day for 28 or 56 days. They received five injections (1 mg/kg) per day (8, 10, 12:00 a.m., 2 and 4:00 p.m.) on the dark period of the cycle. Nicotine exposure for 56 days reduced body and liver weights. Moreover, nicotine exposure for 28 or 56 days decreased the hepatic glycogen but not blood glucose levels. The activities of blood and hepatic PBG-synthase, and blood and cerebral acetylcholinesterase were not affected by in vivo exposure. However, these activities were inhibited by nicotine in vitro. Results show that although high levels of plasma cotinine were found in both intervals of exposures, the parameters here analyzed were not affected by prolonged nicotine exposure except the storage of glucose, and body and liver weights.
A longitudinal study of the influence of smoking on the onset of obesity at a telecommunications company in Japan
2006, Preventive Medicine
To clarify the influence of smoking on the onset of obesity.
A 5-year follow-up study was carried out on 25,312 workers at the time of their annual health check-up from 1992 to 1997. Pooled logistic regression analyses by sex were performed with age, working conditions and lifestyle as independent variables and the onset of obesity (BMI ≥ 26.4) as a dependent variable adjusted for the time period.
In males, the following factors increased the risk of the onset of obesity: smoking equal to or more than 20 cigarettes per day (versus nonsmokers), monthly holidays fewer than 5 days (versus > 7 days), one-way commute more than 90 min (versus ≤ 60 min), sleeping less than 5 h, moderate and high preference for fatty meals (versus little preference). In females, 30–39 years, 40–49 years and 50–59 years (versus 20–29 years), being an ex-smoker, smoking fewer than 20 cigarettes per day, smoking equal to or more than 20 cigarettes per day (versus nonsmokers, respectively) and high preference for fatty meals (versus little preference) increased the risk of the onset of obesity.
This study revealed that smoking independently increases the risk of the onset of obesity regardless of sex.

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^☆: This work was supported by the USUHS Protocol No. 007223. The opinions or assertions contained herein are the private ones of the authors and are not to be construed as official or reflecting the views of the DoD, the USUHS, or Fred Hutchinson Cancer Research Center.

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Effects of chronic nicotine administration of insulin, glucose, epinephrine, and norepinephrine☆

Abstract

Addict. Behav.

Eur. J. of Pharmacol.

Am. J. Clin. Nutrition

Pharm. Biochem. & Behav.

Am. J. Clin. Nutrition

European J. of Pharmacology

Metabolism

Pharmacol. Biochem. & Behav.

Brit. J. Addict.

British Empire Cancer Campaign, Ann. Rep.

Psychopharm.

J. Appl. Soc. Psychol.

Psychopharm.

Pharm. Biochem. & Behav.

Policlinico

Intl. J. of Obesity

Arch. Environ. Health

J. Med.

Science