Meal patterns and body weight after nicotine in male rats as a function of chow or high-fat diet

Wellman, Paul J.; Bellinger, Larry L.; Cepeda-Benito, Antonio; Susabda, Agnes; Ho, Dao H.; Davis, Kristina W.

doi:10.1016/j.pbb.2005.11.002

Cited by 25 publications

(40 citation statements)

References 41 publications

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“…The results differ from those previously observed following intermittent bolus nocturnal administration of nicotine (five daily i.p. injections at a 1.4 -4 mg/kg/day dose for 1 week), which resulted in anorexia only during the dark phase and reportedly due only to decreases in meal size in rats maintained on low-fat diets (Bellinger et al, 2003;Wellman et al, 2005). Contrary to the present results, rats receiving noncontingent bolus nicotine doses exhibited increased meal frequency and shorter intermeal intervals (Bellinger et al, 2003).…”

Section: Discussioncontrasting

confidence: 89%

“…For example, nicotine decreases feeding and body weight, and withdrawal from nicotine produces rebound overeating and an increase in weight gain, an effect that is mirrored in human subjects (Jo et al, 2002). However, studies examining the effects of nicotine on food intake have used noncontingent administration of nicotine via minipumps (Blaha et al, 1998;Miyata et al, 2001) or bolus administration of high-nicotine doses (Bellinger et al, 2003;Wellman et al, 2005) that might produce different effects than self-regulated intake of small unit doses of nicotine. Therefore, the present study also examined overall food intake, and microstructural changes in food intake, in rats receiving continuous access to voluntary nicotine IVSA.…”

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confidence: 99%

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Extended Access to Nicotine Self-Administration Leads to Dependence: Circadian Measures, Withdrawal Measures, and Extinction Behavior in Rats

O’Dell¹,

Chen²,

Smith³

et al. 2006

J Pharmacol Exp Ther

120

112

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The present study characterized nicotine intake, circadian patterns of food and water intake, precipitated somatic signs of withdrawal, and extinction of nicotine-seeking behavior in rats with 23-h access to intravenous self-administration (IVSA). Separate groups of animals were allowed access to nicotine IVSA (0.015, n ϭ 9; 0.03, n ϭ 14; 0.06, n ϭ 16; mg/kg/0.1 ml infusion/s; fixed ratio 1) and trained to nosepoke for food and water 23 h/day for 40 consecutive days. Somatic signs of nicotine withdrawal were examined following saline or mecamylamine administration (1.5 mg/kg i.p.), and extinction of nicotine-seeking behavior was assessed. A dose-dependent decrease in lever responding and an increase in nicotine intake were observed, with the highest nicotine dose producing the lowest amount of lever responding and the highest amount of nicotine intake. Nicotine acutely reduced diurnal and nocturnal food intake, producing smaller and fewer meals, and an increased rate of eating. Differences in rate of nicotine intake between the light and dark phase decreased significantly, especially in rats receiving higher unit nicotine doses (0.03 and 0.06 mg/kg), along with long-term decreases in the circadian profile and amplitude of feeding. Mecamylamine precipitated robust withdrawal signs, the magnitude of which was positively correlated with the total amount of self-administered nicotine. Extinction of nicotine-seeking behavior was observed and was facilitated by removal of nicotine-associated cues. The results demonstrate that rats will self-administer nicotine to the point of producing dependence, as measured by somatic signs, resistance to extinction, and measures of food intake.To more closely model tobacco use in humans, recent studies have examined extended access to nicotine intravenous self-administration (IVSA) in rats. For example, female rats display increased nicotine IVSA during the active phase of the light cycle during 3 weeks of continuous nicotine access (Cox et al., 1984). These rats also display a compensatory increase in nicotine IVSA when the dose is lowered (0.03 to 0.003 mg/kg) and a decrease in nicotine-seeking behavior when nicotine is replaced with saline. Moreover, male rats display nicotine IVSA in extended access models (6 -23 h) using low nicotine doses (0.00375 mg/kg/injection), and the level of nicotine intake approximates that of human smokers (Valentine et al., 1997;Paterson and Markou, 2004;Kenny and Markou, 2006). The 23-h access model of nicotine IVSA seems to be sensitive to genetic differences, since nicotine intake is more quickly acquired and persistently maintained in Lewis versus Holtzman and Fisher strains of male rats (Brower et al., 2002). Furthermore, the 23-h model of nicotine IVSA is sensitive to passive nicotine administration. Nicotine intake decreased following implantation of a minipump that delivers doses of nicotine that are equal to, or higher than, peak levels associated with simulated nicotine intake (LeSage et al., 2002). In addition, nicotine intake in ...

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Section: Discussioncontrasting

confidence: 89%

mentioning

confidence: 99%

Extended Access to Nicotine Self-Administration Leads to Dependence: Circadian Measures, Withdrawal Measures, and Extinction Behavior in Rats

O’Dell¹,

Chen²,

Smith³

et al. 2006

J Pharmacol Exp Ther

120

112

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“…In rodents freely fed on a high-fat diet, chronic nicotine, administered continuously or intermittently, maintains, and even increases, its effects on body weight and food intake compared with animals fed on a low-fat diet (Mangubat et al, 2012;Wellman et al, 2005), suggesting an increased prevalence of nicotine's effects on the homeostatic system under these conditions. Contrasting data were obtained in mice with oral nicotine self-administration (Fornari et al, 2007).…”

Section: Relationship Between Nicotine Effects On the Homeostatic Andmentioning

confidence: 99%

Nicotinic Regulation of Energy Homeostasis

Zoli

Picciotto

2012

Nicotine & Tobacco Research

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Introduction: The ability of nicotine, the primary psychoactive substance in tobacco smoke, to regulate appetite and body weight is one of the factors cited by smokers that prevents them from quitting and is the primary reason for smoking initiation in teenage girls. The regulation of feeding and metabolism by nicotine is complex, and recent studies have begun to identify nicotinic acetylcholine receptor (nAChR) subtypes and circuits or cell types involved in this regulation.

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“…On the other hand, numerous animal studies showed that nicotine reduces food intake (eg, Bellinger et al, 2010;Grunberg et al, 1988;Wellman et al, 2005;Yang et al, 1999). Specifically, nicotine's interactions with signaling pathways routed in the hypothalamus were implied in these anorexic effects (Li et al, 2000;Mineur et al, 2011).…”

Section: Nicotine Effects On Body Weightmentioning

confidence: 99%

Nicotine Alters Food–Cue Reactivity via Networks Extending From the Hypothalamus

Kroemer

Guevara

Vollstädt‐Klein

et al. 2013

Neuropsychopharmacol

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Obesity and smoking constitute two of the main causes of preventable deaths in the developed countries today. Many smokers motivate consumption as a means to control their body weight because smoking cessation increases the risk to gain weight. Although it is well established that nicotine reduces feeding in animals and that smoking is associated with reduced body weight in quasi-experimental studies of humans, acute nicotine effects are mixed and little is known about the brain networks supporting these effects. Thus, we investigated 26 normal-weighted never-smokers who received either nicotine (2 mg) or placebo gums following a double-blinded randomized cross-over design. We used functional magnetic resonance imaging (fMRI) to investigate reactivity to palatable food cues after both overnight fasting and following a standardized caloric intake (75 g oral glucose tolerance test (OGTT)). Participants viewed food or low-level control pictures in a block design and rated their current appetite after each block. Nicotine had a small-to mediumsized effect on subjective appetite and significantly altered food-cue reactivity in a region sensitive to caloric intake that extended from the right hypothalamus to the basal ganglia. During placebo sessions, the OGTT reduced functional coupling of this region with a 'salience network' (ie, amygdala, ventromedial prefrontal cortex) in processing of food pictures. Furthermore, nicotine reduced coupling with the nucleus accumbens and the OGTT reduced coupling with an 'interoceptive network' (ie, insula, operculum) instead. We conclude that locally restricted acute effects of nicotine in the hypothalamic area have profound effects on food-processing networks.

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Meal patterns and body weight after nicotine in male rats as a function of chow or high-fat diet

Cited by 25 publications

References 41 publications

Extended Access to Nicotine Self-Administration Leads to Dependence: Circadian Measures, Withdrawal Measures, and Extinction Behavior in Rats

Extended Access to Nicotine Self-Administration Leads to Dependence: Circadian Measures, Withdrawal Measures, and Extinction Behavior in Rats

Nicotinic Regulation of Energy Homeostasis

Nicotine Alters Food–Cue Reactivity via Networks Extending From the Hypothalamus

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