Nicotine and its withdrawal alter feeding induced by paraventricular hypothalamic injections of neuropeptide Y in Sprague-Dawley rats

Bishop, Christopher; Parker, Graham C.; Coscina, Donald V.

doi:10.1007/s00213-002-1101-7

Cited by 35 publications

(18 citation statements)

References 37 publications

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“…However, in another study, hypothalamic NPY peptide was found to be increased after 14 days of low-dose (4 mg/kg/day) nicotine treatment, which reduced food intake by 19.5% in rats (Li et al, 2000), suggesting that the present treatment may have been too short to cause significant changes in NPY peptide. Furthermore, previously it was found that nicotine can directly inhibit the hyperphagia produced by exogenous administration of NPY into the PVN (Bishop et al, 2002), suggesting it is possible that the effects of brain NPY can be offset by nicotine or other elements in cigarette smoke. The effects of nicotine administration on NPY peptide in mice have not been documented previously.…”

Section: Discussionmentioning

confidence: 99%

Effect of Short-Term Cigarette Smoke Exposure on Body Weight, Appetite and Brain Neuropeptide Y in Mice

Chen

Vlahos

Bozinovski

et al. 2004

Neuropsychopharmacol

143

107

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Although nicotinic receptors have been demonstrated in hypothalamic appetite-regulating areas and nicotine administration alters food intake and body weight in both animals and humans, the mechanisms underlying the effects of smoking on appetite circuits remain unclear. Conflicting effects of nicotine on the major orexigenic peptide, neuropeptide Y (NPY), have been observed in the brain, but the effects of smoking are unknown. Thus, we aimed to investigate how cigarette smoking affects body weight, food intake, plasma leptin concentration, hypothalamic NPY peptide, adipose mass and mRNA expression of uncoupling proteins (UCP), and tumor necrosis factor (TNF) a. Balb/C mice (8 weeks) were exposed to cigarette smoke (three cigarettes, three times a day for 4 consecutive days) or sham exposed. Body weight and food intake were recorded. Plasma leptin and brain NPY were measured by radioimmunoassay. UCPs and TNF a mRNA were measured by real-time PCR. Food intake dropped significantly from the first day of smoking, and weight loss became evident within 2 days. Brown fat and retroperitoneal white fat masses were significantly reduced, and plasma leptin concentration was decreased by 34%, in line with the decreased fat mass. NPY concentrations in hypothalamic subregions were similar between two groups. UCP1 mRNA was decreased in white fat and UCP3 mRNA increased in brown fat in smoking group. Short-term cigarette smoke exposure led to reduced body weight, food intake, and fat mass. The reduction in plasma leptin concentration may have been too modest to increase NPY production; alternatively, change in NPY or its function might have been offset by nicotine or other elements in cigarette smoke.

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Section: Discussionmentioning

confidence: 99%

Effect of Short-Term Cigarette Smoke Exposure on Body Weight, Appetite and Brain Neuropeptide Y in Mice

Chen

Vlahos

Bozinovski

et al. 2004

Neuropsychopharmacol

143

107

View full text Add to dashboard Cite

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“…An antagonist against corticotropin releasing factor (CRF) prevented increased ICSS thresholds in mecamylamine-precipitated, but not in spontaneous nicotine withdrawal (Bruijnzeel et al 2007). Altered responsiveness to neuropeptide Y in the paraventricular area may be relevant to withdrawal-induced changes in appetite and weight gain (Bishop et al 2002). Finally, there is preliminary evidence of hormonal correlates of withdrawal, including altered corticosteroid stress response (Semba et al 2004) and changes in brain and plasma concentrations of various steroids, such as progesterone (Concas et al 2006).…”

Section: Serotonin and Other Transmittersmentioning

confidence: 97%

Rodent Models of Nicotine Withdrawal Syndrome

Malin

Goyarzu

2009

Handbook of Experimental Pharmacology

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Simple, rapid and inexpensive rodent models of nicotine physical dependence and withdrawal syndrome have proved useful for preliminary screening of smoking cessation treatments. They have led to an exponential increase of knowledge regarding the underlying neurobiological mechanisms of dependence and withdrawal syndrome. The human nicotine withdrawal syndrome in smoking cessation is variable and multidimensional, involving irritability, anxiety, depression, cognitive and attentional impairments, weight gain, sleep disturbances, and craving for nicotine. Aside from sleep disturbances, analogous phenomena have been seen in rodent models using different measures of withdrawal intensity. It appears likely that different withdrawal phenomena may involve some partially divergent mechanisms. For example, depression-like phenomena may involve alterations in mechanisms such as the mesolimbic dopamine pathway from the ventral tegmental area to the nucleus accumbens. Irritability and anxiety may involve alterations in endogenous opioid systems and other regions, such as the amygdala. This chapter reviews many additional anatomical, neurochemical, and developmental elements that impact nicotine physical dependence.

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“…These factors should be taken into consideration in the design of future studies. (52) Conflicting findings have been reported, not only regarding the relationship between smoking and serum levels of leptin but also regarding the levels of other peptides that regulate food intake, such as NPY, (53) orexins (54) and ghrelin. (47) The parenteral administration of nicotine, as well as the administration of inhaled nicotine, has been shown to markedly reduce food intake in rats by inhibiting the synthesis of NPY, one of the hormones that increase appetite.…”

Section: Final Considerationsmentioning

confidence: 99%

Tabagismo e variação ponderal: a fisiopatologia e genética podem explicar esta associação?

Chatkin

2007

J. bras. pneumol.

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Tobacco use is the leading preventable cause of death in most countries, including Brazil. Smoking cessation is an important strategy for reducing the morbidity and mortality associated with tobacco-related diseases. An inverse relationship between nicotine use and body weight has been reported, in which body weight tends to be lower among smokers than among nonsmokers. Smoking abstinence results in an increase in body weight for both males and females. On average, sustained quitters gain from 5 to 6 kg, although approximately 10% gain more than 10 kg. Pharmacological treatment for smoking cessation attenuates weight gain. The importance of smoking cessation as a contributing cause of the current obesity epidemic has been little studied. In the USA, the rate of obesity attributable to smoking cessation has been estimated at approximately 6.0 and 3.2% for males and females, respectively. Although the mechanisms are unclear, there is evidence that dopamine and serotonin are appetite suppressants. The administration of nicotine, regardless of the delivery system, acutely raises the levels of these neurotransmitters in the brain, reducing the need for energy intake and consequently suppressing appetite. In addition, nicotine has a direct effect on adipose tissue metabolism, influencing the rate of weight gain following smoking cessation. Leptin, ghrelin and neuropeptide Y are substances that might constitute factors involved in the inverse relationship between nicotine and body mass index, although their roles as determinants or consequences of this relationship have yet to be determined. Smoking and body weightThe inter-relationship between smoking and body weight has been well established in various well-designed studies, most of which were published in the 1990s. (10,11) The body mass index (BMI) of smokers is frequently present lower than that of age-and gender-matched nonsmokers. In addition, comprehensive cross-sectional epidemiological studies, some of which considered to be classical on this subject, showed a significant inverse relationship between the regular tobacco use and body weight, which tends to be lower among smokers than among nonsmokers. (12,13) Smoking cessation results in weight gain both in males and females, and over 75% of smokers gain weight when they become abstinent. (14,15) Mean weight gain attributable to smoking cessation is 2.8 and 3.8 kg in males and females, respectively. In a systematic review of the literature, it was estimated that the mean body weight gain in individuals who quit smoking can reach 5-6 kg, and 13% of ex-smokers can gain more than 10 kg. (10) Although most reports on smoking cessation have indicated mid-and long-term weight gain, other studies have shown that the most critical period is immediately after smoking cessation. (10) In one study, (16) the increase in body weight was 5.2 and 4.9 kg in females and males, respectively, during the first year after cessation, with an increase of 3.4 and 2.6 kg, respectively, in the following years. In the same stud...

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Nicotine and its withdrawal alter feeding induced by paraventricular hypothalamic injections of neuropeptide Y in Sprague-Dawley rats

Abstract: These findings provide behavioral support that changes in PVN-NPY neurotransmission may play a functional role in the food intake and weight-modulating effects of NIC.

Cited by 35 publications

References 37 publications

Effect of Short-Term Cigarette Smoke Exposure on Body Weight, Appetite and Brain Neuropeptide Y in Mice

Effect of Short-Term Cigarette Smoke Exposure on Body Weight, Appetite and Brain Neuropeptide Y in Mice

Rodent Models of Nicotine Withdrawal Syndrome

Tabagismo e variação ponderal: a fisiopatologia e genética podem explicar esta associação?

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