Jurnal Sso
Jurnal Sso
Jurnal Sso
Review Article
Autonomic Nervous System in the Control of Energy Balance
and Body Weight: Personal Contributions
Copyright © 2013 G. Messina et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
The prevalence of obesity is increasing in the industrialized world, so that the World Health Organization considers obesity as
a “pandemia” in rich populations. The autonomic nervous system plays a crucial role in the control of energy balance and body
weight. This review summarizes our own data and perspectives, emphasizing the influence exerted by autonomic nervous system on
energy expenditure and food intake, which are able to determine the body weight. Activation of the sympathetic discharge causes
an increase in energy expenditure and a decrease in food intake, while reduction of food intake and body weight loss determines
a reduction of the sympathetic activity. On the other hand, pathophysiological mechanisms of the obesity involve alterations of
the sympathetic nervous system in accordance with the “Mona Lisa Hypothesis,” an acronym for “most obesities known are low in
sympathetic activity.” Furthermore, the parasympathetic influences on the energy expenditure are analyzed in this review, showing
that an increase in parasympathetic activity can induce a paradoxical enhancement of energy consumption.
of insulin sensitivity, creating a vicious cycle that may Lesion of lateral hypothalamus
contribute to the development of the metabolic syndrome
and hypertension. The cause of this overactivity is not clear,
but may be driven by certain adipokines [13]. Furthermore, Alteration of various pathways,
including orexinergic system
the postprandial activation of the peripheral sympathetic
nervous system is crucial to maintain energy balance. A
contribution of postprandial sympathetic activation to the
Ascending Descending
thermic effect of food is not always evident and depends on projections projections
the size and composition of the meal, with carbohydrates
having the clearest effect. Signals related to food intake from
various origins (e.g., gut, hepatoportal area, baroreceptors) Behavioral Increase in
are integrated in the brain and result in increased peripheral changes sympathetic activity
sympathetic outflow. It is of interest to emphasize the role of
diet composition (according to the life style of subjects) in the
level of sympathetic activation during the day in view of the Reduction of food intake
potential role of adrenergic overactivity in the pathogenesis
Scheme 1: Changes in eating behavior induced by lesion of the
of obesity and its metabolic syndrome [14].
lateral hypothalamus.
Although it is reported that low-frequency band (LF-
HRV) represents a noninvasive marker of sympathetic activ-
ity, there are recent studies which report that this assumption
is controversial. LF power may correlate more with baroreflex The firing rate of sympathetic nerves to interscapular
function and/or stress that with the cardiac sympathetic brown adipose tissue (IBAT) was monitored both before and
innervations [15, 16]. This vision should modify the interpre- after 5 g of food intake in 24 h fasted rats with a lesion of
tations about the sympathetic function in the pathophysiol- the ventromedial hypothalamus and in 24 h fasted rats with
ogy of the obesity. sham-lesion. The firing rate of nerves to IBAT increased
Since the incidence of body weight superior to normal after food intake in sham-lesioned rats. This increase was
values is increasing in the industrialized world, the World significantly reduced in the lesioned rats. These findings indi-
Health Organization considers obesity as a “pandemia” in cate that the sympathetic nervous system is involved in the
rich populations. Investigation into the mechanisms that con- postingestional activation of the sympathetic discharge, and
trol body weight give growing relevance to the possibilities reduction of this activation occurs when the ventromedial
of new strategies to reduce the incidences of overweight and hypothalamus is lesioned [20]. A long-term reduction of
obesity, which are frequently associated with metabolic and postingestional thermogenesis may contribute to the obesity
cardiovascular diseases. induced by this hypothalamic lesion through a decrease in
This review reports our evidences showing that the auto- energy expenditure induced by reduced sympathetic activity
nomic nervous system controls body weight by influencing (see Scheme 2). Since there is a close relationship between
food intake and energy consumption. The general research the sympathetic activity and food intake [19], a reduction
project was to test influence of the autonomic nervous system in the sympathetic response after food intake could induce
on energy balance under various conditions, which change an increase of total amount of ingested food. This reduction
the sympathetic and/or parasympathetic activities. may be another factor in the induction of obesity due
to ventromedial hypothalamic lesions. In other words, the
increased body weight may be caused by a reduction of satiety
signals and a decrease in postingestional energy expenditure.
2. Experimental Evidences The firing rate of the sympathetic nerves to interscapular
2.1. Animal Studies. The effect of intraperitoneal injection of brown adipose tissue and food intake were monitored in
lysine acetylsalicylate was tested on (1) food intake and (2) 24 h fasting male Sprague-Dawley rats before and after food
the sympathetic enhancement induced by lesion of the lateral presentation. Pyrogen (500 ng of prostaglandin E1 ) or saline
hypothalamus. Lysine acetylsalicylate modifies the aphagia by was injected into the lateral cerebral ventricle immediately
increasing food intake, and it reduces the enhancements of before food presentation. The increase in the sympathetic
the sympathetic discharge induced by the lateral hypothala- discharge due to prostaglandin E1 is associated with a
mic lesion [17]. The electrolytic lesion in the lateral hypotha- decrease in food intake [21]. The simultaneous measurement
lamus regulates body weight at a lower level. The lesioned rats of the sympathetic firing rate and food intake is the nicest
lose body weight at a faster rate than sham-lesioned controls demonstration of the feedback between the sympathetic
subjected to the same degree of food deprivation [18]. This nervous system and food intake. The sympathetic activity
experiment confirms that an increase in the sympathetic rises before food intake terminates. This implies that the rise
activity reduces food intake (see Scheme 1), in accord with in sympathetic discharge serves as an endogenous satiety
the findings of Bray [19]. On the other hand, these data show signal (see Scheme 3).
that an inhibitor of prostaglandin synthesis can modify the
aphagia induced by the lesion of the lateral hypothalamus, 2.2. Human Studies. Vegetative modulation, expressed as
throughout a reduction of the sympathetic discharge. heart rate variability (HRV) power spectral analysis, was
Neurology Research International 3
Reduction of
energy expenditure
Increase in body weight
Obesity
Scheme 4: Body weight gain during premenopausal age.
Scheme 2: Changes in energy expenditure induced by lesion of the
ventromedial hypothalamus.
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