Fett- und Zuckerstoffwechselstörung durch Nikotin
Chronic stimulation of sympathic nerves by nicotine leads to increase of insuline resistance. This effect of active and passive smoking is supported by effects of nicotine on fat cells (lipolysis) in subcutaneous fat, where fat should be stored (instead of going to arteries).
From "Association between cigarette smoking and body composition among Austrian adults", dissertation by Fontes-Gasperin L. 2012, University of Vienna (Ernährungswissenschaften): Effects of nicotine on energy expenditure
Nicotine is a sympathomimetic agent, i.e. it activates the sympathetic nervous system (SNS) and stimulates the release of adrenaline and noradrenaline. Elevated circulating levels of these catecholamines promote lipolysis and increase plasma concentrations of FFA in smokers, contributing therefore to increased thermogenesis [Hellerstein et al., 1994; Audrain-Mcgovern and Benowitz, 2011]. It has been suggested that besides the lipolysis stimulation via catecholamine release, nicotine itself induces lipolysis by activating nicotinic cholinergic receptors in the adipose tissue [Andersson and Arner, 2001].
Page 22: Smoking and body fat distribution:
The mechanisms underlying the association between cigarette smoking and abdominal obesity remain to be elucidated, but a cluster of factors may be involved.
Hormonal and endocrine mechanisms are likely to modulate this association. Smoking influences the circulating levels of pituitary, adrenal, and sex steroid hormones [Kapoor and Jones, 2005; Tweed et al., 2012]. Compared to non-smokers, smokers were found to have higher circulating levels of cortisol [Steptoe and Ussher, 2006], which increased with the content of nicotine in cigarette smoking [Wilkins et al., 1982]. High levels of cortisol seem to have a key role in the development of visceral adiposity [Pasquali and Vicennati, 2000].
2.6.1. (Pages 24-25) Smoking and insulin resistance
It has been demonstrated that smoking is associated with an increased risk of developing T2DM [Rimm et al., 1995; Kawakami et al., 1997; Wilson et al., 1999; Sargeant et al., 2001; Maki et al., 2010; Teratani et al., 2012] and insulin resistance, as evidenced both by euglycaemic insulin clamp studies and by studies of glucose/insulin response to glucose loading [Targher et al., 1997; Benowitz, 2003; Berlin, 2009].
How cigarette smoking triggers these metabolic disturbances is not fully understood but it may involve hormonal regulation, altered inflammatory response and oxidative stress. Nicotine increases the plasma levels of catecholamines and other neurotransmitters, which act centrally and peripherally. Catecholamines are powerful antagonists of insulin action and leads to increased lipolysis [Hellerstein et al., 1994; Eliasson et al., 1994; Benowitz, 2003; Reseland et al., 2005; Bullen, 2008]. Elevated FFA and glycerol concentrations in the blood as a consequence of lipolysis also decreases the levels of circulating adiponectin, inducing insulin resistance and endothelial dysfunction [Van Gaal et al., 2006; Goossens, 2008]. Nicotine is also thought to promote increased release of corticosteroids and growth hormone, also contributing to insulin resistance [Benowitz, 2003; Tziomalos and Charsoulis, 2004]. Bergman and co-workers [Bergman et al., 2009] reported increased saturation of intramuscular TAG and diacylglycerols (DAG), together with increased insulin receptor substrate-1 Ser636 phosphorylation in smokers, compared with non-smokers. Smokers were also less insulin sensitive and, according to the authors, these metabolic differences could explain the decreased insulin action in smokers because of basal inhibition of insulin.
Cigarette smoking increases circulating levels of the inflammatory markers TNF-α, IL-6, and CRP. It also causes a dose-dependent increase in plasma intercellular adhesion molecule-1 (ICAM-1) [Fernandez-Real et al., 2003; Van Gaal et al., 2006; Bergmann and Siekmeier, 2009], thereby decreasing adiponectin levels and inducing insulin resistance [Van Gaal et al., 2006].