The autonomic nervous system plays an important role in the regulation
of body processes in health and disease. Overfeeding and obesity (a d
isproportional increase of the fat mass of the body) are often accompa
nied by alterations in both sympathetic and parasympathetic autonomic
functions. The overfeeding-induced changes in autonomic outflow occur
with typical symptoms such as adiposity and hyperinsulinemia. There mi
ght be a causal relationship between autonomic disturbances and the co
nsequences of overfeeding and obesity. Therefore studies were designed
to investigate autonomic functioning in experimentally and geneticall
y hyperphagic rats. Special emphasis was given to the processes that a
re involved in the regulation of peripheral energy substrate homeostas
is. The data revealed that overfeeding is accompanied by increased par
asympathetic outflow. Typical indices of vagal activity (such as the c
ephalic insulin release during food ingestion) were increased in all o
ur rat models for hyperphagia. Overfeeding was also accompanied by inc
reased sympathetic tone, reflected by enhanced baseline plasma norepin
ephrine (NE) levels in both VMH-lesioned animals and rats rendered obe
se by hyperalimentation. Plasma levels of NE during exercise were, how
ever, reduced in these two groups of animals. This diminished increase
in the exercise-induced NE outflow could be normalized by prior food
deprivation. It was concluded from these experiments that overfeeding
is associated with increased parasympathetic and sympathetic tone. In
models for hyperphagia that display a continuously elevated nutrient i
ntake such as the VMH-lesioned and the overfed rat, this increased sym
pathetic tone was accompanied by a diminished NE response to exercise.
This attenuated outflow of NE was directly related to the size of the
fat reserves, indicating that the feedback mechanism from the periphe
ry to the central nervous system is altered in the overfed state.