The Effect of Smoking Cessation on Body Weight: Comparison
View Latest Version
Please note this is a comparison between Version 2 by Beatrix Zheng and Version 1 by Stamatina Driva.

Smokers with diabetes mellitus substantially lower their risks of microvascular and macrovascular diabetic complications, in particular cardiovascular disease, by quitting smoking. However, subsequent post-smoking-cessation weight gain may attenuate some of the beneficial effects of smoking cessation and discourage attempts to quit. Weight gain can temporarily exacerbate diabetes and deteriorate glycemic control and metabolic profile. The molecular mechanisms by which quitting smoking leads to weight gain are largely associated with the removal of nicotine’s effects on the central nervous system. 

  • smoking cessation
  • weight gain
  • nicotine
  • appetite-related peptides
  • diabetes

1. Introduction

Post-smoking-cessation weight gain (PSCWG) remains a cause of concern and an independent predictor of failure of a cessation attempt, mainly among teenage girls and women [1,2,3,4,5][1][2][3][4][5]. Moreover, the belief that smoking can be a weight-control strategy and fear of PSCWG have been reported as reasons to initiate or continue smoking or relapse after initiating smoking cessation [6,7][6][7]. Among smokers with type 2 diabetes mellitus (T2DM), PSCWG has been associated with cessation difficulties. Two-thirds of patients with diabetes claim that they would return to smoking if they gained substantial weight [8]. Given the magnitude of risks associated with smoking, particularly in persons with T2DM, a better understanding of how to approach the problem is needed.

2. Effects of Nicotine and Smoking Cessation on Appetite-Regulating Peptides

The suppression of appetite by nicotine has been attributed to various and complex effects of nicotine on peptides that regulate food intake and body weight, such as hypothalamic neuropeptides (neuropeptide Y, orexins), adipokines (leptin, adiponectin) and other metabolic hormones (ghrelin, GLP-1) [38,52][9][10]. WThe researchers focus on studies conducted in humans and mention only a few animal studies. The latter involve peptides, which have not received much attention in regard to smoking or smoking cessation in humans. We The researchers also present associations between smoking status, levels of peptides, appetite and body weight. A summary of the literature we the researchers identified is presented in Table 1.
Table 1. Summary of the literature on the effect of nicotine and smoking cessation on NPY, orexins, leptin, adiponectin, ghrelin, PYY, GLP-1 and CCK.
Appetite-Regulating Peptides Smoking Smoking Cessation
NPY ↓ levels of NPY ↑ levels of NPY correlated with body weight
Orexins dose-dependent ↑ prepro-orexin mRNA production upon chronic nicotine administration ↓ orexin levels during the initial withdrawal period (24 h of abstinence)
Leptin ↓ or ↑ plasma leptin concentration ↑ serum leptin levels positively correlated with ↑ body weight, BMI and body fat mass
Adiponectin ↓ plasma concentrations of adiponectin ↑ serum adiponectin levels in individuals with less abdominal obesity
Ghrelin ↑ or ↓ plasma levels of ghrelin, non-effect result in smokers No data
PYY, GLP-1 and CCK Not affected Not affected
NPY: neuropeptide-Y; PYY: peptide YY; GLP-1: glucagon-like peptide-1; CCK: cholecystokinin; ↑: increased; ↓: decreased.

2.1. NPY

Neuropeptide Y (NPY), a peptide that increases food intake, is classified as part of the pancreatic polypeptide family. This peptide shares 70% of its sequence homology with peptide YY (PYY) and it is located in the arcuate nucleus of the hypothalamus [33][11]. Some studies carried out in animals support a suppression of NPY expression, induced by nicotine administration [53,54,55][12][13][14]. Other laboratories reported an increase in NPY mRNA and its peptide after chronic nicotine treatment [56][15]. It was also suggested that chronic exposure to nicotine upregulates the NPY expression in forebrain areas involved in the regulation of feeding [56][15] with a simultaneous down-regulation of the NPY receptors [57][16]. This reduced hypothalamic NPY receptor density in response to nicotine could explain the decrease in food intake in smokers [58][17]. Studies that have measured plasma NPY levels in humans found these levels to be either elevated [59][18] in previously non-smoking adults after smoking or unchanged [60][19] in habitual smokers after acute smoking. Hussain at al. conducted the first study to show a relationship between cigarette smoking, NPY and body weight in humans. Smokers had decreased body weight and lower levels of NPY and leptin compared to never-smokers, whereas quitters had significantly increased body weight and higher levels of NPY and leptin compared to smokers. NPY levels were significantly correlated with body weight, BMI and waist circumference. NPY levels remained, in contrast to leptin, significantly lower in smokers and higher in quitters, even after adjusting for anthropometric parameters [61][20]. These results imply that the weight modulating effects of cigarette smoke directly involve effects on NPY expression independently of leptin [61][20]. Later, Stadler et al. reported that fasting NPY levels increased 3 months after smoking cessation [49][21].

2.2. Orexins

Orexin-A and Orexin-B are neuropeptides derived from prepro-orexin/hypocretin, the production of which and subsequent cleavage into orexins A and B are almost exclusively located in the area of lateral hypothalamus [57][16]. Similar to NPY, orexins are positive regulators of food intake. Therefore, it could be expected that orexin levels would decrease upon nicotine administration. Paradoxically, a dose-dependent increase in prepro-orexin mRNA production upon chronic nicotine administration was reported [62][22]. In a prospective cohort study where 200 quitters and 85 non-smokers were compared over the course of 4 weeks, a decline in orexin levels was reported during the initial withdrawal period (defined as 24 h of abstinence) among smokers who relapsed in the first 4 weeks [63][23].

2.3. Leptin

Leptin is an adipose-tissue-derived hormone that regulates both satiety and thermogenesis. Leptin suppresses food intake by decreasing appetite after eating and increasing metabolic rate [64][24]. It is released from adipocytes in direct proportion to fat mass [65][25]. There are conflicting results among different studies that examined the relation between smoking or smoking cessation and plasma leptin levels. It has been suggested that smoking, via nicotine mechanisms, might modify the sensitivity of hypothalamic leptin receptors, modulate leptin biosynthesis and consequently reduce body weight by augmenting the effects of leptin in the brain and by enhancing leptin binding or increasing the sensitivity of downstream transduction cascades [38,66][9][26]. Epidemiological studies [61,66][20][26] in different ethnic groups showed that plasma leptin, sOb-R leptin receptor and free leptin were significantly lower in smokers (moderate or heavy, cigarettes or sheesha) than non-smokers [65,67,68][25][27][28]. Other studies showed elevated plasma leptin concentrations in smokers [69,70][29][30] and suggested that this may be due to an increase in adipose tissue secretion of leptin or a decrease in leptin clearance [71][31]. In a recent study, female smokers not only showed significantly higher serum levels of leptin compared to female non-smokers, but also compared to male smokers [72][32]. However, most of the studies noted a significant increase in serum leptin levels after smoking cessation [69,73,74,75][29][33][34][35]. This increase was positively correlated with an increase in body weight, BMI and body fat mass [61,64,71,73,74][20][24][31][33][34]. Gonseth et al. reported a significant increase in serum leptin levels one year after smoking cessation, parallel with substantial weight in the same time period. This finding is in discordance with the theoretical effects of leptin. One explanation may be the development of leptin resistance in smokers [76][36]. More recently, Komiyama et al. found no significant changes in leptin levels in individuals with no increase in waist circumference after smoking cessation, but a significant increase in leptin levels in individuals with abdominal obesity. These observations may indicate that abdominal obesity caused leptin resistance despite smoking cessation [77][37]. However, another publication did not find an increase in leptin levels following smoking cessation, despite the weight gain [49][21]. One of the reasons for such a discrepancy might be the interaction between smoking and other factors such as diet, exercise, hormones and host inflammatory responses, which may also impair regulation of the actions of leptin [68][28].

2.4. Adiponectin

Adiponectin is a hormonal active adipocytokine secreted by adipose tissue, with insulin-sensitizing, anti-inflammatory and anti-atherogenic properties [65][25]. Oxidative stress and inflammatory cytokines produced by smoking, lipolysis induced by nicotine and increased consumption of circulating adiponectin, which accumulates in the injured vascular walls of smokers, are some of the mechanisms proposed to contribute to lower levels of adiponectin in smokers compared to non-smokers [46,71,78,79][31][38][39][40]. Smoking cessation improves the adiponectin profile in different time periods following cessation [80][41]. It has been reported in many studies that plasma concentrations of adiponectin were significantly lower in active smokers compared to non-smokers [81,82][42][43] and quitters [71,80,83,84][31][41][44][45] among both healthy persons and patients with coronary heart disease (CHD) [85][46]. In addition, a dose-dependent association between smoking intensity and adiponectin levels in current smokers has been observed [82][43]. Bergmann and Siekmeier found that in non-obese middle-aged women even moderate cigarette smoking adversely influenced the serum concentration of adiponectin, whereas among obese women there were no significant differences in adiponectin and leptin concentrations between smokers and non-smokers [65][25]. Efstathiou et al. reported that post-cessation adiponectin levels were significantly increased after two months in a healthy Greek population [86][47]. Otsuka et al. reported that plasma adiponectin levels in Japanese patients were elevated 6 months after smoking cessation [87][48]. In a study where early effects of smoking cessation were followed, serum adiponectin levels tended to increase 1 week after the end of treatment, but after 9 weeks, they were significantly decreased in weight gainers. In weight maintainers, adiponectin levels increased slightly after smoking cessation, but changes were not significant [88][49]. More recently, Komiyama et al. reported that serum adiponectin levels did not decrease 1 year after smoking cessation, despite weight gain, and increased abdominal obesity. However, in individuals with less abdominal obesity and a smaller increase in waist circumference, total adiponectin levels increased 1 year after cessation, showing the apparent beneficial effect of smoking cessation on adiponectin levels [77][37].

2.5. Ghrelin

Ghrelin is a known appetite-stimulating hormone synthesized and secreted in the stomach and hypothalamus [33][11]. Studies have showed that smoking acutely increased plasma levels of ghrelin, an unexpected finding in terms of explaining the known anorectic effect of smoking [89][50], as well as the observation that plasma ghrelin levels decreased after smoking cessation [74][34]. In another study, plasma concentrations of acetylated ghrelin, but not total ghrelin, were significantly higher in smokers than non-smokers [90][51]. More recently, in a study with a large sample size, total ghrelin serum levels were positively associated with active smoking [91][52]. Earlier, Kokkinos et al. found that fasting plasma ghrelin concentrations were not different between male smokers and non-smokers. Furthermore, smoking did not provoke any short-term change in ghrelin levels in smokers, but it induced a decline in non-smokers. Thus, it was suggested that if the anorectic effect of smoking is ghrelin-induced, this effect may be present only in people not habituated to smoke exposure. In habitual smokers, desensitization of receptors due to prolonged nicotine exposure could blunt ghrelin suppression by short-term smoking [92][53]. The lack of effect of acute smoking on serum ghrelin levels in smokers in a recent study was in line with this observation and, similarly, smoking interventions do not appear to affect levels of obestatin, which is a hormone encoded from the same gene as ghrelin [7]. These observations were not in line with previous ones, in which an acute increase in obestatin levels in smokers taking a smoke had been reported [93][54]. Pilhatsch et al. measured both appetite and ghrelin and found no effect of nicotine administration on ghrelin levels in healthy non-smokers, despite the decreased subjective appetite induced by nicotine. Taken together, these findings suggest that ghrelin may not play a major role in nicotine-related energy homeostasis [94][55]. In 26 healthy normal-weight never-smokers, Kroemer et al. found that nicotine administration decreased correlations with ghrelin levels in the mesocorticolimbic system, while subjects fasted. However, caloric load increased the modulatory effects of ghrelin on food-cue reactivity, particularly in the ventromedial prefrontal cortex and the amygdala. This effect was stronger during nicotine sessions [95][56]. There are also studies that showed alterations in ghrelin levels after nicotine restriction, but focused primarily on the predictive value of ghrelin measurements on smoking relapse and are outside the scope of this revisewarch [52][10].

2.6. PYY, GLP-1 and CCK

Enteroendocrine-cell (EEC) secretory hormones include PYY, glucagon-like peptide-1 (GLP-1) and cholecystokinin (CCK). A few studies have demonstrated the effect of smoking cessation on these hormones in humans [33][11]. PYY is an anorexigenic 36 amino-acid peptide, which is secreted by the enteroendocrine cells of the distal gastrointestinal tract. GLP-1 is a peptide produced and released postprandially by the intestinal enteroendocrine cells that acts on the hypothalamus to decrease food intake. CCK is a peptide released by enteroendocrine cells within the small intestine in response to mixed meals, acting as a satiety signal [96][57]. Fasting GLP-1, visfatin and PYY levels were unchanged 3 months after smoking cessation in a study conducted by Stadler et al. [49][21], and levels of gastric inhibitory polypeptide (GIP), GLP-1, amylin, insulin, PYY and pancreatic polypeptide (PP), measured after a meal challenge, were also not affected after 3 months of abstinence, according to Pancova et al. However, changes in incretin levels earlier after smoking cessation may have occurred [73][33]. PYY suppresses food intake, and although no significant change was observed on its levels after smoking abstinence, according to the above-mentioned studies, body weight showed a significant increase. More recently, Yanakkoulia et al. tried to explain the observed acute decrease in energy intake associated with acute smoking by investigating a series of hormonal factors; however, they failed to observe any significant difference in the changes in blood concentrations of CCK, GLP-1, ghrelin and obestatin over time between smoking and control condition [7].

References

  1. Bush, T.; Hsu, C.; Levine, M.D.; Magnusson, B.; Miles, L. Weight gain and smoking: Perceptions and experiences of obese quitline participants. BMC Public Health 2014, 14, 1229.
  2. Beebe, L.A.; Bush, T. Post-cessation weight concerns among women calling a state tobacco quitline. Am. J. Prev. Med. 2015, 48, S61–S64.
  3. Landrau-Cribbs, E.; Cabriales, J.A.; Cooper, T.V. General and smoking cessation weight concern in a Hispanic sample of light and intermittent smokers. Addict. Behav. 2015, 41, 29–33.
  4. Siahpush, M.; Singh, G.K.; Tibbits, M.; Pinard, C.A.; Shaikh, R.A.; Yaroch, A. It is better to be a fat ex-smoker than a thin smoker: Findings from the 1997–2004 National Health Interview Survey—National Death Index linkage study. Tob. Control 2014, 23, 395–402.
  5. Walker, J.F.; Loprinzi, P.D. Association of BMI changes between adolescence and young adulthood with smoking cessation. Am. J. Health Promot. 2019, 33, 358–362.
  6. Karfopoulou, E.; Mouliou, K.; Koutras, Y.; Yannakoulia, M. Behaviours associated with weight loss maintenance and regaining in a M editerranean population sample. A qualitative study. Clin. Obes. 2013, 3, 141–149.
  7. Yannakoulia, M.; Anastasiou, C.; Zachari, K.; Sidiropoulou, M.; Katsaounou, P.; Tenta, R. Acute effect of smoking and smoking abstinence on energy intake and appetite-related hormones blood concentrations. Physiol. Behav. 2018, 184, 78–82.
  8. Schauer, G.L.; Bush, T.; Cerutti, B.; Mahoney, L.; Thompson, J.R.; Zbikowski, S.M. Peer Reviewed: Use and Effectiveness of Quitlines for Smokers With Diabetes: Cessation and Weight Outcomes, Washington State Tobacco Quit Line, 2008. Prev. Chronic Dis. 2013, 10, E105.
  9. Jo, Y.H.; Talmage, D.A.; Role, L.W. Nicotinic receptor-mediated effects on appetite and food intake. J. Neurobiol. 2002, 53, 618–632.
  10. Schwartz, A.; Bellissimo, N. Nicotine and energy balance: A review examining the effect of nicotine on hormonal appetite regulation and energy expenditure. Appetite 2021, 164, 105260.
  11. Hu, T.; Yang, Z.; Li, M.D. Pharmacological effects and regulatory mechanisms of tobacco smoking effects on food intake and weight control. J. Neuroimmune Pharmacol. 2018, 13, 453–466.
  12. Frankish, H.M.; Dryden, S.; Wang, Q.; Bing, C.; MacFarlane, I.A.; Williams, G. Nicotine administration reduces neuropeptide Y and neuropeptide Y mRNA concentrations in the rat hypothalamus: NPY may mediate nicotine’s effects on energy balance. Brain Res. 1995, 694, 139–146.
  13. Bishop, C.; Parker, G.C.; Coscina, D.V. Nicotine and its withdrawal alter feeding induced by paraventricular hypothalamic injections of neuropeptide Y in Sprague-Dawley rats. Psychopharmacology 2002, 162, 265–272.
  14. Chen, H.; Hansen, M.J.; Jones, J.E.; Vlahos, R.; Bozinovski, S.; Anderson, G.P.; Morris, M.J. Cigarette smoke exposure reprograms the hypothalamic neuropeptide Y axis to promote weight loss. Am. J. Respir. Crit. Care Med. 2006, 173, 1248–1254.
  15. Li, M.D.; Kane, J.K.; Parker, S.L.; McAllen, K.; Matta, S.G.; Sharp, B.M. Nicotine administration enhances NPY expression in the rat hypothalamus. Brain Res. 2000, 867, 157–164.
  16. Li, M.D.; Parker, S.L.; Kane, J.K. Regulation of feeding-associated peptides and receptors by nicotine. Mol. Neurobiol. 2000, 22, 143–165.
  17. Kane, J.; Parker, S.; Li, M. Hypothalamic orexin-A binding sites are downregulated by chronic nicotine treatment in the rat. Neurosci. Lett. 2001, 298, 1–4.
  18. Rudehill, A.; Franco-Cereceda, A.; Hemsén, A.; Stensdotter, M.; Pernow, J.; Lundberg, J. Cigarette smoke-induced elevation of plasma neuropeptide Y levels in man. Clin. Physiol. 1989, 9, 243–248.
  19. Niedermaier, O.N.; Smith, M.L.; Beightol, L.A.; Zukowska-Grojec, Z.; Goldstein, D.S.; Eckberg, D.L. Influence of cigarette smoking on human autonomic function. Circulation 1993, 88, 562–571.
  20. Hussain, T.; Al-Daghri, N.M.; Al-Attas, O.S.; Draz, H.M.; Al-Rahman, S.H.A.; Yakout, S.M. Plasma neuropeptide Y levels relate cigarette smoking and smoking cessation to body weight regulation. Regul. Pept. 2012, 176, 22–27.
  21. Stadler, M.; Tomann, L.; Storka, A.; Wolzt, M.; Peric, S.; Bieglmayer, C.; Pacini, G.; Dickson, S.L.; Brath, H.; Bech, P. Effects of smoking cessation on b-cell function, insulin sensitivity, body weight, and appetite. Eur. J. Endocrinol. 2014, 170, 219–227.
  22. Kane, J.; Parker, S.; Matta, S.; Fu, Y.; Sharp, B.; Li, M. Nicotine up-regulates expression of orexin and its receptors in rat brain. Endocrinology 2000, 141, 3623–3629.
  23. al’Absi, M.; Lemieux, A.; Hodges, J.S.; Allen, S. Circulating orexin changes during withdrawal are associated with nicotine craving and risk for smoking relapse. Addict. Biol. 2019, 24, 743–753.
  24. Perkins, K.A.; Fonte, C. Effects of smoking status and smoking cessation on leptin levels. Nicotine Tob. Res. 2002, 4, 459–466.
  25. Bergmann, S.; Siekmeier, R. Influence of smoking and body weight on adipokines in middle aged women. Eur. J. Med. Res. 2009, 14, 21.
  26. Hodge, A.; Westerman, R.; De Courten, M.; Collier, G.R.; Zimmet, P.; Alberti, K. Is leptin sensitivity the link between smoking cessation and weight gain? Int. J. Obes. 1997, 21, 50–53.
  27. Al Mutairi, S.S.; Mojiminiyi, O.A.; Shihab-Eldeen, A.A.; Al Sharafi, A.; Abdella, N. Effect of smoking habit on circulating adipokines in diabetic and non-diabetic subjects. Ann. Nutr. Metab. 2008, 52, 329–334.
  28. Hilawe, E.H.; Yatsuya, H.; Li, Y.; Uemura, M.; Wang, C.; Chiang, C.; Toyoshima, H.; Tamakoshi, K.; Zhang, Y.; Kawazoe, N. Smoking and diabetes: Is the association mediated by adiponectin, leptin, or C-reactive protein? J. Epidemiol. 2015, 25, 99–109.
  29. Eliasson, B.; Smith, U. Leptin levels in smokers and long-term users of nicotine gum. Eur. J. Clin. Investig. 1999, 29, 145–152.
  30. Nicklas, B.J.; Tomoyasu, N.; Muir, J.; Goldberg, A.P. Effects of cigarette smoking and its cessation on body weight and plasma leptin levels. Metabolism 1999, 48, 804–808.
  31. Kryfti, M.; Dimakou, K.; Toumbis, M.; Daniil, Z.; Hatzoglou, C.; Gourgoulianis, K.I. Effects of smoking cessation on serum leptin and adiponectin levels. Tob. Induc. Dis. 2015, 13, 30.
  32. Glahn, A.; Rhein, M.; Frieling, H.; Dette, F.; Bleich, S.; Hillemacher, T.; Muschler, M. Smoking-induced changes in leptin serum levels and c/EBPalpha-related methylation status of the leptin core promotor during smoking cessation. Psychoneuroendocrinology 2019, 100, 106–112.
  33. Pankova, A.; Kralikova, E.; Kavalkova, P.; Stepankova, L.; Zvolska, K.; Haluzik, M. No change in serum incretins levels but rise of leptin levels after smoking cessation: A pilot study. Physiol. Res. 2016, 65.
  34. Lee, H.; Joe, K.-H.; Kim, W.; Park, J.; Lee, D.-H.; Sung, K.-W.; Kim, D.-J. Increased leptin and decreased ghrelin level after smoking cessation. Neurosci. Lett. 2006, 409, 47–51.
  35. Lemieux, A.; Nakajima, M.; Hatsukami, D.K.; Allen, S.; al’Absi, M. Changes in circulating leptin levels during the initial stage of cessation are associated with smoking relapse. Psychopharmacology 2015, 232, 3355–3361.
  36. Gonseth, S.; Locatelli, I.; Bize, R.; Nusslé, S.; Clair, C.; Pralong, F.; Cornuz, J. Leptin and smoking cessation: Secondary analyses of a randomized controlled trial assessing physical activity as an aid for smoking cessation. BMC Public Health 2014, 14, 911.
  37. Komiyama, M.; Wada, H.; Yamakage, H.; Satoh-Asahara, N.; Sunagawa, Y.; Morimoto, T.; Ozaki, Y.; Shimatsu, A.; Takahashi, Y.; Hasegawa, K. Analysis of changes on adiponectin levels and abdominal obesity after smoking cessation. PLoS ONE 2018, 13, e0201244.
  38. Andersson, K.; Arner, P. Systemic nicotine stimulates human adipose tissue lipolysis through local cholinergic and catecholaminergic receptors. Int. J. Obes. 2001, 25, 1225–1232.
  39. Iwashima, Y.; Katsuya, T.; Ishikawa, K.; Kida, I.; Ohishi, M.; Horio, T.; Ouchi, N.; Ohashi, K.; Kihara, S.; Funahashi, T. Association of hypoadiponectinemia with smoking habit in men. Hypertension 2005, 45, 1094–1100.
  40. Okamoto, Y.; Arita, Y.; Nishida, M.; Muraguchi, M.; Ouchi, N.; Takahashi, M.; Igura, T.; Inui, Y.; Kihara, S.; Nakamura, T. An adipocyte-derived plasma protein, adiponectin, adheres to injured vascular walls. Horm. Metab. Res. 2000, 32, 47–50.
  41. Toffolo, M.C.F.; da Silva Gomes, A.; van Keulen, H.V.; Louro, M.B.; Castro, F.M.; Luquetti, S.C.P.D.; Ferreira, A.P.; de Aguiar, A.S. Alteration of inflammatory adipokines after four months of smoking abstinence in multidisciplinary intervention program. Nutr. Hosp. 2018, 35, 434–441.
  42. Miyazaki, T.; Shimada, K.; Mokuno, H.; Daida, H. Adipocyte derived plasma protein, adiponectin, is associated with smoking status in patients with coronary artery disease. Heart 2003, 89, 663.
  43. Takefuji, S.; Yatsuya, H.; Tamakoshi, K.; Otsuka, R.; Wada, K.; Matsushita, K.; Sugiura, K.; Hotta, Y.; Mitsuhashi, H.; Oiso, Y. Smoking status and adiponectin in healthy Japanese men and women. Prev. Med. 2007, 45, 471–475.
  44. Won, W.-Y.; Lee, C.-U.; Chae, J.-H.; Kim, J.-J.; Lee, C.; Kim, D.-J. Changes of plasma adiponectin levels after smoking cessation. Psychiatr. Investig. 2014, 11, 173.
  45. Kotani, K.; Hazama, A.; Hagimoto, A.; Saika, K.; Shigeta, M.; Katanoda, K.; Nakamura, M. Adiponectin and smoking status: A systematic review. J. Atheroscler. Thromb. 2012, 19, 11833.
  46. Thamer, C.; Stefan, N.; Stumvoll, M.; Häring, H.; Fritsche, A. Reduced adiponectin serum levels in smokers. Atherosclerosis 2005, 179, 421–422.
  47. Efstathiou, S.P.; Skeva, I.I.; Dimas, C.; Panagiotou, A.; Parisi, K.; Tzanoumis, L.; Kafouri, A.; Bakratsas, K.; Mountokalakis, T.D. Smoking cessation increases serum adiponectin levels in an apparently healthy Greek population. Atherosclerosis 2009, 205, 632–636.
  48. Otsuka, F.; Kojima, S.; Maruyoshi, H.; Kojima, S.; Matsuzawa, Y.; Funahashi, T.; Kaikita, K.; Sugiyama, S.; Kimura, K.; Umemura, S. Smoking cessation is associated with increased plasma adiponectin levels in men. J. Cardiol. 2009, 53, 219–225.
  49. Inoue, K.; Takeshima, F.; Kadota, K.; Yoda, A.; Tatsuta, Y.; Nagaura, Y.; Yoshioka, S.; Nakamichi, S.; Nakao, K.; Ozono, Y. Early effects of smoking cessation and weight gain on plasma adiponectin levels and insulin resistance. Intern. Med. 2011, 50, 707–712.
  50. Bouros, D.; Tzouvelekis, A.; Anevlavis, S.; Doris, M.; Tryfon, S.; Froudarakis, M.; Zournatzi, V.; Kukuvitis, A. Smoking acutely increases plasma ghrelin concentrations. Clin. Chem. 2006, 52, 777–778.
  51. Koopmann, A.; Bez, J.; Lemenager, T.; Hermann, D.; Dinter, C.; Reinhard, I.; Hoffmann, H.; Wiedemann, K.; Winterer, G.; Kiefer, F. Effects of cigarette smoking on plasma concentration of the appetite-regulating peptide ghrelin. Ann. Nutr. Metab. 2015, 66, 155–161.
  52. Wittekind, D.A.; Kratzsch, J.; Mergl, R.; Enzenbach, C.; Witte, V.; Villringer, A.; Kluge, M. Higher fasting ghrelin serum levels in active smokers than in former and never-smokers. World J. Biol. Psychiatr. 2020, 21, 748–756.
  53. Kokkinos, A.; Tentolouris, N.; Kyriakaki, E.; Argyrakopoulou, G.; Doupis, J.; Psallas, M.; Kyriaki, D.; Katsilambros, N. Differentiation in the short-and long-term effects of smoking on plasma total ghrelin concentrations between male nonsmokers and habitual smokers. Metabolism 2007, 56, 523–527.
  54. Kukuvitis, A.; Froudarakis, M.; Tryfon, S.; Tzouvelekis, A.; Saroglou, M.; Karkavitsas, N.; Bouros, D. Acute effect of smoking on plasma Obestatin levels. Tob. Induc. Dis. 2010, 8, 2.
  55. Pilhatsch, M.; Scheuing, H.; Kroemer, N.; Kobiella, A.; Bidlingmaier, M.; Farger, G.; Smolka, M.N.; Zimmermann, U.S. Nicotine administration in healthy non-smokers reduces appetite but does not alter plasma ghrelin. Hum. Psychopharmacol. Clin. Exp. 2014, 29, 384–387.
  56. Kroemer, N.B.; Wuttig, F.; Bidlingmaier, M.; Zimmermann, U.S.; Smolka, M.N. Nicotine enhances modulation of food-cue reactivity by leptin and ghrelin in the ventromedial prefrontal cortex. Addict. Biol. 2015, 20, 832–844.
  57. Steinert, R.E.; Feinle-Bisset, C.; Asarian, L.; Horowitz, M.; Beglinger, C.; Geary, N. Ghrelin, CCK, GLP-1, and PYY (3–36): Secretory controls and physiological roles in eating and glycemia in health, obesity, and after RYGB. Physiol. Rev. 2017, 97, 411–463.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/)
Video Production Service
Feedback