Research Journal of Pharmacy and Technology

Open Access Open Access  Restricted Access Subscription Access
Open Access Open Access Open Access  Restricted Access Restricted Access Subscription Access

Unraveling the Association of Tobacco Smoking (Nicotine) with Gut and Adipocyte Appetite Regulator Hormones–A Systematic Review


Affiliations
1 Universiti Sultan Zainal Abidin, 20400 Terengganu, Malaysia
     

   Subscribe/Renew Journal


Lifestyle behaviour is the cause of about 70%–80% deaths in developing countries. Risk factors, such as smoking, alcohol consumption, physical inactivity, obesity, and poor nutrition are the major causes of mortality that are crucial for researchers and policymakers to improve health and reduce preventable deaths in the developing countries. In specific, cigarette smoking has an inverse implication with body weight or body mass index (BMI). Smoking cessation has been linked to weight gain indirectly mediated through gut and adipocyte appetite regulating hormones. This systematic review is achieved through MEDLINE search to collect the data which support this idea using PubMed, Google and MEDLINE databases.

Keywords

Association, Tobacco Smoking, Nicotine.
Subscription Login to verify subscription
User
Notifications
Font Size


  • Yilmaz Işikhan S, Güleç D. The Clustering of World Countries Regarding Causes of Death and Health Risk Factors. Iran J Public Health. 2018;47(10):1520-1528.

  • Prospective Studies Collaboration, “Body-mass index and cause-specific mortality in 900,000 adults: collaborative analyses of 57 prospective studies,” The Lancet, 2009; 373 (9669): 1083–1096.

  • K. M. Flegal, R. P. Troiano, E. R. Pamuk, R. J. Kuczmarski, and S. M. Campbell, “The influence of smoking cessation on the prevalence of overweight in the United States,” The New England Journal of Medicine, 1995; 333 (18): 1165–1170.

  • R. C. Klesges, A. W. Meyers, L. M. Klesges, and M. E. La Vasque, “Smoking, body weight, and their effects on smoking behavior: a comprehensive review of the literature,” Psychological Bulletin, 1989; 106 (2): 204–230.

  • D. Eisenberg and B. C. Quinn, “Estimating the effect of smoking cessation on weight gain: an instrumental variable approach,” Health Services Research, 2006; 41 (6): 2255– 2266.

  • H. Shimokata, D. C. Muller, and R. Andres, “Studies in the distribution of body fat. III. Effects of cigarette smoking,” Journal of the American Medical Association, 1989; 261(8): 1169–1173.

  • E. Barrett-Connor and K. T. Khaw, “Cigarette smoking and increased central adiposity,” Annals of Internal Medicine, 1989; 111(10): 783–787.

  • H. Komiya, Y. Mori, T. Yokose, and N. Tajima, “Smoking as a risk factor for visceral fat accumulation in Japanese men,” Tohoku Journal of Experimental Medicine, 2006; 208 (2): 123–132.

  • E.J.Jacobs,C.C.Newton,Y.Wangetal.,“Waistcircumference and all-cause mortality in a large US cohort,” Archives of Internal Medicine, 2010; 170(15): 1293–1301.

  • E. J. Boyko, W. Y. Fujimoto, D. L. Leonetti, and L. NewellMorris, “Visceral adiposity and risk of type 2 diabetes: a prospective study among Japanese Americans,” Diabetes Care, 2000; 23(4): 465–471.

  • B. H. Goodpaster, S. Krishnaswami, H. Resnick et al., “Association between regional adipose tissue distribution and both type 2 diabetes and impaired glucose tolerance in elderly men and women,” Diabetes Care, 2003; 26(2): 372–379,.

  • U.S. Department of Health and Human Services, How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease: A Report of the Surgeon General, Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Officeon Smoking and Health, Atlanta, Ga, USA, 2010.

  • R. J. Moffatt and S. G. Owens, “Cessation from cigarette smoking: changes in body weight, body composition, resting metabolism, and energy consumption,” Metabolism, 1991; 40(5): 465–470.

  • C. M. Ferrara, M. Kumar, B. Nicklas, S. McCrone, and A. P. Goldberg, “Weight gain and adipose tissue metabolism after smoking cessation in women,” International Journal of Obesity, 2001; 25(9): 1322–1326.

  • C. Filozof, M. C. Fern´andez Pinilla, and A. Fern´andez-Cruz, “Smoking cessation and weight gain,” Obesity Reviews, 2004; 5(2): 95–103.

  • WHO. Tobacco No.339; 2016.

  • R. Doll and R. Peto, “The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today,” Journal of the National Cancer Institute, 1981; 66(6): 1191– 1308.

  • R.Kahn, R.M.Robertson, R.Smith, and D.Eddy,“The impact of prevention on reducing the burden of cardiovascular disease,” Diabetes Care, 2008; 31(8): 1686–1696.

  • T. Bush, J. C. Lovejoy, M. Deprey, and K. M. Carpenter, “The effect of tobacco cessation on weight gain, obesity, and diabetes risk,” Obesity (Silver Spring), 2016; 24(9): 1834–1841.

  • (DK)N.B.o.H.Danskernes Sundhed. Den Nationale Sundhedsprofil 2013, Copenhagen: National Board of Health. 2014.

  • R.C. Klesges, A.W.Meyers, L.M.Klesges, and M.E.LaVasque, “Smoking, body weight, and their effects on smoking behavior: a comprehensive review of the literature,” Psychological Bulletin, 1989; 106(2); 204–230.

  • R.C.Klesgesand S.A.Shumaker,“Understandingtherelations between smoking and body weight and their importance to smoking cessation and relapse,” Health Psychology, 1992; 11(supplement): 1–3.

  • M. Komiyama, H. Wada, S. Ura et al., “Analysis of factors that determine weight gain during smoking cessation therapy,” PLoS ONE, 2013; 8(8): Article IDe72010.

  • A.C.Farley, P.Hajek, D.Lycett, and P.Aveyard, “Interventions for preventing weight gain after smoking cessation,” Cochrane database of systematic reviews (Online), 2012; 1 ; Article ID CD006219.

  • C. Filozof, M. C. Fernandez Pinilla, and A. Fernandez-Cruz, “Smoking cessation and weight gain,” Obesity Reviews, 2005; 5(2): 95–103.

  • G. Miyata, M. M. Meguid, M. Varma, S. O. Fetissov, and H. J. Kim, “Nicotine alters the usual reciprocity between meal size 74, 2001; 1(2): 169–176.

  • J.Audrain-Mcgovern and N.L.Benowitz, “Cigarette smoking, nicotine, and body weight,” Clinical Pharmacology and Therapeutics, 2011; 90(1): 164–168.

  • Beltowski J, Jamroz-Wisniewska A, Widomska S. Adiponectin and its role in cardiovascular diseases. Cardiovasc Hematol Disord Drug Targets 2008; 8:7-46.

  • Matsuzawa Y, Funahashi T, Kihara S, Shimomura I. Adiponectin and metabolic syndrome. Arterioscler Thromb Vasc Biol 2004; 24:29-33.

  • Havel PJ. Control of energy homeostasis and insulin action by adipocyte hormones: leptin, acylation stimulating protein, and adiponectin. Curr Opin Lipidol 2002; 13:51-59.

  • Kumada M, Kihara S, Sumitsuji S, Kawamoto T, Matsumoto S, Ouchi N, et al. Association of hypoadiponectinemia with coronary artery disease in men. Arterioscler Thromb Vasc Biol 2003; 23:85-89.

  • Pischon T, Girman CJ, Hotamisligil GS, Rifai N, Hu FB, Rimm EB. Plasma adiponectin levels and risk of myocardial infarction in men. JAMA 2004; 291:1730-1737.

  • 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.

  • Thamer C, Stefan N, Stumvoll M, Hring H, Fritsche A. Reduced adiponectin serum levels in smokers. Atherosclerosis 2005; 179:421-422.

  • Efstathiou SP, Skeva I, Dimas C, Panagiotou A, Parisi K, Tzanoumis L, et al. Smoking cessation increases serum adiponectin levels in an apparently healthy Greek population. Atherosclerosis 2009; 205:632-636.

  • Takefuji S, Yatsuya H, Tamakoshi K, Otsuka R, Wada K, Matsushita K, et al. Smoking status and adiponectin in healthy Japanese men and women. Prev Med 2007; 45:471-475.

  • Spranger J, Verma S, Göhring I, Bobbert T, Seifert J, Sindler AL, et al. Adiponectin does not cross the blood-brain barrier but modifies cytokine expression of brain endothelial cells. Diabetes 2006; 55:141-147.

  • Qi Y, Takahashi N, Hileman SM, Patel HR, Berg AH, Pajvani UB, et al. Adiponectin acts in the brain to decrease body weight. Nat Med 2004; 10:524-529.

  • Kubota N, Yano W, Kubota T, Yamauchi T, Itoh S, Kumagai H, et al. Adiponectin stimulates AMP-activated protein kinase in the hypothalamus and increases food intake. Cell Metab 2007; 6:55-68.

  • Wang-Youn Won, Chang-Uk Lee, Jeong-Ho Chae, Jung-Jin Kim, Chul Lee, and Dai-Jin Kim. Changes of Plasma Adiponectin Levels after Smoking Cessation. Psychiatry Investig 2014;11(2):173-178.

  • Mohd Hanaffi Siti Hajar, SanipZulkefli, ShaabanJuwita, MohdNoorNorhayati, MohdYusoffSitiSuhaila, AidaHanumGhulamRasool and MohamedYusoffHarmy. Metabolic, inflammatory, and oxidative stress markers in women exposed to second hand smoke. PeerJ. 2018; 6: e5758: 11. DOI: http://dx.doi.org/10.7717/peerj.5758.

  • J. S. Flier, “Hormone resistance in diabetes and obesity: insulin, leptin, and FGF21,” The Yale Journal of Biology and Medicine, 2012; 85(3): 405–414.

  • C. Bjørbæk, S. Uotani, B. da Silva, and J. S. Flier, “Divergent signaling capacities of the long and short isoforms of the leptin receptor,” The Journal of Biological Chemistry, 1997; 272(51): 32686–32695.

  • B. G. Phillips, M. Kato, K. Narkiewicz, I. Choe, and V. K. Somers, “Increases in leptin levels, sympathetic drive, and weight gain in obstructive sleep apnea,” American Journal of Physiology-Heart and Circulatory Physiology, 2000; 279(1): H234–H237.

  • I. Imayama and B. Prasad, “Role of leptin in obstructive sleep apnea,” Annals of the American Thoracic Society, 2017; 14(11): 1607–1621.

  • E. de Oliveira, E. G. Moura, A. P. Santos-Silva et al., “Neonatal nicotine exposure causes insulin and leptin resistance and inhibits hypothalamic leptin signaling in adult rat offspring,” Journal of Endocrinology, 2010; 206(1): 55–63.

  • J. L. Nobre, P. C. Lisboa, A. P. Santos-Silva et al., “Calcium supplementation reverts central adiposity, leptin, and insulin resistance in adult offspring programed by neonatal nicotine exposure,” Journal of Endocrinology, 2011; 210(3): 349– 359.

  • G. Targher, L. Zenari, G. Faccini, G. Falezza, M. Muggeo, and G. Zoppini, “Serum leptin concentrations in young smokers with type 1 diabetes,” Diabetes Care, 2001; 24(4): 793-794.

  • J. E. Reseland, H. H. Mundal, K. Hollung et al., “Cigarette smoking may reduce plasma leptin concentration via catecholamines,” Prostaglandins Leukotrienes and Essential Fatty Acids, 2005; 73(1): 43–49.

  • K. A. Perkins and C. Fonte, “Effects of smoking status and smoking cessation on leptin levels,” Nicotine & Tobacco Research, 2002; 4(4): 459–466.

  • Yi-Ting Sung, Cheng-Ting Hsiao, I-Jen Chang, Yu-ChihLin, and Chen-Yu Yueh. Journal of Diabetes Research 2016; Article ID 3961756: 7 pages http://dx.doi.org/10.1155/2016/3961756

  • Muhammad Zulhusni Suhaimi, Zulkefli Sanip, Hamid Jan Jan Mohamed, Harmy Mohamed Yusoff. Leptin and calorie intake among different nicotine dependent groups. Ann Saudi Med 2016; 36(6): 404-408. DOI: http://dx.doi.org/10.5144/0256-4947.2016.404

  • Effects of smoking cessation on serum leptin and adiponectin levels Maria Kryfti, Katerina Dimakou, Michail Toumbis, Zoe Daniil, Chryssi Hatzoglou and Konstantinos I. Gourgoulianis. Kryfti et al. Tobacco Induced Diseases 2015; 13:30 DOI: http://dx.doi.org/10.1186/s12971-015-0054-7

  • A.Chiolero,D.Faeh,F.Paccaud,andJ.Cornuz,“Consequences of smoking for bodyweight, body fat distribution, and insulin resistance,” The American Journal of Clinical Nutrition, 2008; 87(4): 801–809.

  • D.Bouros,A.Tzouvelekis,S.Anevlavisetal.,“Smokingacutely increases plasma ghrelin concentrations,” Clinical Chemistry, 2006; 52(4): 777–778.

  • YahiaA.Kaabi and Mohiealdeen A. Khalifa. Acute One-Cigarette Smoking Decreases Ghrelin Hormone in Saliva: A Pilot Study. International Journal of Endocrinology 2014; Article ID 575671: 4 pages http://dx.doi.org/10.1155/2014/575671

  • H.Lee,K.-H.Joe,W.Kimetal.,“Increased leptin and decreased ghrelin level after smoking cessation,”Neuroscience Letters, 2006; 409(1): 47–51.

  • B.-B. Li, Z.-B. Chen, B.-C. Li et al., “Expression of ghrelin in human salivary glands and its levels in saliva and serum in Chinese obese children and adolescents,” Archives of Oral Biology, 2011; 56(4): 389–394.

  • Y.-K. Shin, B. Martin, W. Kim et al., “Ghrelin is produced in taste cells and ghrelin receptor null mice show reduced taste responsivity to salty(NaCl) and sour(citric acid) tastants,”PLoS ONE, 2010; 5(9): e12729.


Abstract Views: 203

PDF Views: 0




  • Unraveling the Association of Tobacco Smoking (Nicotine) with Gut and Adipocyte Appetite Regulator Hormones–A Systematic Review

Abstract Views: 203  |  PDF Views: 0

Authors

U. S. Mahadeva Rao
Universiti Sultan Zainal Abidin, 20400 Terengganu, Malaysia
Harmy Bin Mohamed Yusoff
Universiti Sultan Zainal Abidin, 20400 Terengganu, Malaysia

Abstract


Lifestyle behaviour is the cause of about 70%–80% deaths in developing countries. Risk factors, such as smoking, alcohol consumption, physical inactivity, obesity, and poor nutrition are the major causes of mortality that are crucial for researchers and policymakers to improve health and reduce preventable deaths in the developing countries. In specific, cigarette smoking has an inverse implication with body weight or body mass index (BMI). Smoking cessation has been linked to weight gain indirectly mediated through gut and adipocyte appetite regulating hormones. This systematic review is achieved through MEDLINE search to collect the data which support this idea using PubMed, Google and MEDLINE databases.

Keywords


Association, Tobacco Smoking, Nicotine.

References