Enhanced vulnerability to tobacco use in persons with diabetes: A behavioral and neurobiological framework

O’Dell, Laura E.; Nazarian, Arbi

doi:10.1016/j.pnpbp.2015.06.005

Cited by 20 publications

(13 citation statements)

References 134 publications

(135 reference statements)

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“…STZ treatment also modifies cell signaling molecules downstream from dopamine receptors that are known to play a role in the neuroadaptations in drug abuse. For instance, STZ treated rats exhibit an increase in the phosphorylation of the serine/threonine kinase AKT and the dopamine- and cyclic AMP regulated-neuronal phosphoprotein DARPP-32 in the nucleus accumbens [59]. It is presently unclear whether the changes in receptor levels and signal transductions following STZ administration is a result of enhanced BGLs and/or hypoinsulinemia.…”

Section: Discussionmentioning

confidence: 99%

Insulin dependent and independent normalization of blood glucose levels reduces the enhanced rewarding effects of nicotine in a rodent model of diabetes

Íbias

O’Dell

Nazarian

2018

Behavioural Brain Research

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The rewarding effects of nicotine have been previously shown to be enhanced in rodent models of diabetes. It is presently unclear whether the enhanced nicotine reward observed in the diabetes models are mediated via an insulin or glucose mechanism. This study examined whether the enhanced rewarding effects of nicotine observed in streptozotocin (STZ)-treated rats are insulin-mediated. Male and female rats were treated with STZ and the rewarding effects of nicotine (0.2 mg/kg) were measured using the conditioned place preference (CPP) procedure. Some STZ-treated animals received insulin supplementation via subcutaneous immediately after STZ administration, while other rats received daily injections of dapagliflozin (10 mg/kg), a sodium-glucose cotransporter-2 inhibitor. Both male and female STZ-treated rats displayed hyperglycemia, and their blood glucose levels (BGLs) were normalized to control levels following insulin supplementation or dapagliflozin administration. STZ-treated male rats displayed higher nicotine CPP relative to vehicle-treated controls. This effect was abolished in rats that received insulin supplementation or dapagliflozin administration. STZ-treated female rats displayed reduced levels of nicotine CPP as compared to male rats, regardless of treatment condition. These results suggest that glucose plays a major role in modulating the rewarding effects of nicotine in male rats treated with STZ.

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Section: Discussionmentioning

confidence: 99%

Insulin dependent and independent normalization of blood glucose levels reduces the enhanced rewarding effects of nicotine in a rodent model of diabetes

Íbias

O’Dell

Nazarian

2018

Behavioural Brain Research

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“…With regard to a potential mechanism, we recently suggested that enhanced tobacco use vulnerability in persons with diabetes is likely mediated via a suppression of dopamine signaling in the mesolimbic pathway (O’Dell and Nazarian, 2016). Although our physiology is motivationally programmed to experience pleasurable stimuli, recent theories suggest that deficits in dopamine systems may weaken inhibitory control of excessive pleasure seeking (George et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

“…The results revealed that the rewarding effects of nicotine were uniquely exacerbated in rats that received the HFD regimen and also displayed insulin resistance (Richardson et al, 2014). Based on these studies, we recently hypothesized that strong rewarding effects of nicotine help promote tobacco use in persons with diabetes (for a review see O’Dell and Nazarian, 2016). …”

Section: Introductionmentioning

confidence: 99%

Both nicotine reward and withdrawal are enhanced in a rodent model of diabetes

et al. 2017

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Rationale It is presently unclear whether diabetic rats experience greater rewarding effects of nicotine and/or negative affective states produced by nicotine withdrawal. Objective The present study utilized a rodent model of diabetes to examine the rewarding effects of nicotine and negative affective states and physical signs produced by withdrawal. Methods Separate groups of rats received systemic administration of either vehicle or streptozotocin (STZ), which destroys insulin-producing beta cells in the pancreas and elevates glucose levels. Place conditioning procedures were utilized to compare the rewarding effects of nicotine (conditioned place preference; CPP) and negative affective states produced by withdrawal (conditioned place aversion; CPA) in vehicle- and STZ-treated rats. CPA and physical signs of withdrawal were compared after administration of the nicotinic receptor antagonist mecamylamine to precipitate withdrawal in nicotine-dependent rats. A subsequent study utilized elevated plus maze (EPM) procedures to compare anxiety-like behavior produced by nicotine withdrawal in vehicle- and STZ-treated rats. Results STZ-treated rats displayed greater rewarding effects produced nicotine and a larger magnitude of aversive effects and physical signs produced by withdrawal as compared to vehicle-treated controls. STZ-treated rats also displayed higher levels of anxiety-like behavior on the EPM during nicotine withdrawal as compared to controls. Conclusion The finding that both nicotine reward and withdrawal are enhanced in a rodent model of diabetes implies that the strong behavioral effects of nicotine promote tobacco use in persons with metabolic disorders, such as diabetes.

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“…However, many persons with T2D continue to smoke, despite these contraindications. Increasing rodent and human evidence indicates that T2D may increase the rewarding effects of dopamine, as disrupted insulin signaling during T2D suppresses dopamine signaling in the mesolimbic reward pathway [63]. …”

Section: Smoking Cessation and Glucose Homeostasismentioning

confidence: 99%

Smoking and the risk of type 2 diabetes

Maddatu

Anderson-Baucum

Evans‐Molina

2017

Translational Research

232

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Despite accumulating evidence demonstrating strong epidemiological and mechanistic associations between cigarette smoking, hyperglycemia, and the development of type 2 diabetes, tobacco abuse has not been uniformly recognized as a modifiable risk factor in diabetes prevention or screening strategies. In this review, we highlight population-based studies that have linked cigarette smoking with an increased risk of type 2 diabetes and summarize clinical and preclinical studies offering insight into mechanisms through which cigarette smoking and nicotine exposure impact body composition, insulin sensitivity, and pancreatic β cell function. Key questions for future studies are identified and strategies for smoking cessation as a means to decrease diabetes risk are discussed.

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Enhanced vulnerability to tobacco use in persons with diabetes: A behavioral and neurobiological framework

Cited by 20 publications

References 134 publications

Insulin dependent and independent normalization of blood glucose levels reduces the enhanced rewarding effects of nicotine in a rodent model of diabetes

Insulin dependent and independent normalization of blood glucose levels reduces the enhanced rewarding effects of nicotine in a rodent model of diabetes

Both nicotine reward and withdrawal are enhanced in a rodent model of diabetes

Smoking and the risk of type 2 diabetes

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