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):
2.5.3.1. 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].