Short-term weight gain in abstaining women smokers

Pomerleau, Cynthia S.; Pomerleau, Ovide F.; Namenek, Rebecca J.; Mehringer, Ann M.

doi:10.1016/s0740-5472(99)00085-9

Cited by 33 publications

(22 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Particularly striking is the hyperphagia and resultant weight gain that typically accompanies smoking cessation Klesges et al, 1989;Pomerleau et al, 2000). Direct application of nicotine in the region of the LH (this paper) or in synaptic preparations of LH neurons in vitro enhances GABAergic transmission .…”

Section: Introductionmentioning

confidence: 86%

Cholinergic Modulation of Appetite-Related Synapses in Mouse Lateral Hypothalamic Slice

Jo¹,

Wiedl²,

Role³

2005

J. Neurosci.

View full text Add to dashboard Cite

Nicotine administration reduces appetite and alters feeding patterns; a major deterrent to smoking cessation is hyperphagia and resultant weight gain. We demonstrate here that lateral hypothalamic (LH) circuits involving melanin-concentrating hormone (MCH) neurons are subject to cholinergic modulation that may be related to the effects of nicotine on appetite control. Cholinergic input to the perifornical LH area of the mouse is confirmed by examination of immunostaining for vesicular acetylcholine (

show abstract

Section: Introductionmentioning

confidence: 86%

Cholinergic Modulation of Appetite-Related Synapses in Mouse Lateral Hypothalamic Slice

Jo¹,

Wiedl²,

Role³

2005

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…Likewise, nicotine regulates the levels of expression of NPY, orexin and an orexin receptor. The complexity arises in assessing which of the many changes that are elicited by nicotine in the lateral hypothalamus underlie the nicotine-induced hypophagia and, perhaps even more importantly, the persistent hyperphagia accompanying nicotine cessation Levin et al, 1987;Nordstrom et al, 1999;Pomerleau et al, 2000).…”

Section: Are the Anorectic Effects Of Nicotine Due To Modulation Of Cmentioning

confidence: 99%

“…Combined epidemiologic studies of more than a quarter of a million subjects converge on a strong inverse relationship between cigarette smoking and body weight, with smokers weighing significantly less than nonsmokers of the same age and sex (Albanes et al, 1987;Levin et al, 1987). Particularly striking is the hyperphagia and resultant weight gain that accompanies smoking cessation of 70 -80% of people who quit smoking, with women being most affected Klesges et al, 1989;Pomerleau, 1999;Pomerleau et al, 2000). Withdrawal of nicotine leads to increases in body weight of sufficient magnitude to confound maintained abstinence, significantly altering the outcomes of smoking cessation programs as manifest in weight-gain associated relapse (Nordstrom et al, 1999;Pomerleau, 1999).…”

Section: Introductionmentioning

confidence: 99%

Nicotinic receptor‐mediated effects on appetite and food intake

Jo¹,

Talmage

Role³

2002

J. Neurobiol.

276

197

View full text Add to dashboard Cite

ABSTRACT:It is well known, although not well understood, that smoking and eating just do not go together. Smoking is associated with decreased food intake and lower body weight. Nicotine, administered either by smoking or by smokeless routes, is considered the major appetite-suppressing component of tobacco. Perhaps the most renowned example of nicotine's influence on appetite and feeding behavior is the significant weight gain associated with smoking cessation. This article presents an overview of the literature at, or near, the interface of nicotinic receptors and appetite regulation. We first consider some of the possible sites of nicotine's action along the complex network of neural and non-neural regulators of feeding. We then present the hypothesis that the lateral hypothalamus is a particularly important locus of the anorectic effects of nicotine. Finally, we discuss the potential role of endogenous cholinergic systems in motivational feeding, focusing on cholinergic pathways in the lateral hypothalamus.

show abstract

“…Effects of excess, exogenous nicotine might also alter normal brain-gut interactions, impairing autonomic homeostasis and ultimately contributing to symptoms of nicotine toxicity: emesis, dysphagia, gastric stasis, and irritable bowel syndrome (Aggarwal et al 1994;Camilleri 1990;Camilleri and Bharucha 1996;van Orshoven et al 2006). In humans, smoking cessation leads to significant gains in body weight, affecting the efficacy of smoking cessation programs (Nordstrom et al 1999;Pomerleau et al 2000). Our findings are also consistent with a potential brain stem component of anorexigenic effects of nicotine, since nicotine decreases food intake per meal size without significant changes in meal frequency (Blaha et al 1998;Grunberg et al 1986;Jo et al 2002;Miyata et al 2001).…”

Section: Discussionmentioning

confidence: 99%

Nicotine enhances inhibition of mouse vagal motor neurons by modulating excitability of premotor GABAergic neurons in the nucleus tractus solitarii

Boychuk

et al. 2015

Journal of Neurophysiology

View full text Add to dashboard Cite

The caudal nucleus of the solitary tract (NTS) serves as the site of the first synapse for visceral sensory inputs to the central nervous system. The NTS sends functional projections to multiple brain nuclei, with gastric-related projections primarily targeting the dorsal motor nucleus of the vagus (DMV). Previous studies have demonstrated that the majority of caudal NTS neurons that project to the DMV respond robustly to nicotine and express nicotinic acetylcholine receptors (nAChRs). However, the cytochemical identity and relationship with specific viscera of DMV-projecting, nicotine-responsive caudal NTS neurons have not been determined. The present study used transgenic mice that express enhanced green fluorescent protein (EGFP) under a GAD67 promoter in a subset of GABAergic neurons, in vivo retrograde pseudorabies viral labeling to identify gastric-related vagal complex neurons, and patch-clamp electrophysiology in acute brain stem slices to test the hypothesis that gastric-related and GABAergic inhibitory synaptic input to the DMV from the caudal NTS is under a robust modulatory control by nAChRs. Our results suggest that activation of nAChRs in the caudal NTS, but not DMV, potentiates GABAergic, but not glutamatergic, input to the DMV. Gastric-related caudal NTS and DMV neurons are directly involved in this nicotinesensitive circuitry. Understanding the central patterns of nicotinic modulation of visceral sensory-motor circuitry may help develop therapeutic interventions to restore autonomic homeostasis in patients with autonomic impairments.GABA; nicotine receptor; nucleus tractus solitarii; parasympathetic reflex; vagal reflex THE DORSAL VAGAL COMPLEX (DVC) of the caudal brain stem consists of the nucleus tractus solitarii (NTS), the dorsal motor nucleus of the vagus (DMV), and the area postrema. A functional DVC is critical for maintenance of autonomic homeostasis, including gastrointestinal, cardiovascular, and respiratory reflexes. The caudal NTS is the site of the first synapse and a key integration center for autonomic visceral sensory input to the central nervous system (CNS) from the thoracic and most subdiaphragmatic viscera (Saper 2002). The caudal NTS sends excitatory (e.g., glutamatergic) and inhibitory (e.g., GABAergic) projections to preganglionic brain stem sites that modulate both parasympathetic and sympathetic reflexes (Bailey et al. 2006a;

show abstract

Short-term weight gain in abstaining women smokers

Cited by 33 publications

References 23 publications

Cholinergic Modulation of Appetite-Related Synapses in Mouse Lateral Hypothalamic Slice

Cholinergic Modulation of Appetite-Related Synapses in Mouse Lateral Hypothalamic Slice

Nicotinic receptor‐mediated effects on appetite and food intake

Nicotine enhances inhibition of mouse vagal motor neurons by modulating excitability of premotor GABAergic neurons in the nucleus tractus solitarii

Contact Info

Product

Resources

About