Energy Metabolism 35brain that are known to modify feeding behavior,
specifi cally the paraventricular nuclei and the nigro-
striatal tract. These areas of the brain respond to
various neurotransmitters as well as sympathetic
nervous system activity. In general, food intake will
decrease as sympathetic nervous system activity
increases, and vice versa.
Circulating factors
After consumption of a meal, food is broken down
into its basic components (i.e., carbohydrate is broken
down to glucose, protein to amino acids, and fats or
triglycerides to glycerol and fatty acids) and the cir-
culating levels of some of these breakdown products
increase in the blood. Consequently, glucose, amino
acids, glycerol, and fatty acids are further metabo-
lized, primarily in the liver, or used for immediate
energy (e.g., in muscle or brain). There is evidence to
suggest that this resultant metabolism, especially in
the liver, may in turn regulate food intake. After meal
consumption, the circulating levels of nutrients fall
(within minutes for glucose, several hours for triglyc-
erides) and the feelings of hunger return. The link
from nutrient metabolism to central control of food
intake occurs through signals from the liver to the
brain via the vagus nerve. Thus, circulating factors
provide a link between the digestive system and the
central nervous system, which provides another
system for regulating food intake.
Signals from the periphery
Leptin is a hormone that is produced by fat cells
and communicates with the central nervous system
through leptin receptors in the hypothalamus. Reduced
production of leptin, or lack of sensitivity of the hypo-
thalamus to leptin, may regulate food intake and play
a key role in the etiology of rare forms of obesity in
humans. Leptin and the other peripheral hormones
with a central effect on appetite are divided into two
broad categories: (1) the so-called adiposity signals,
which are tonically active providing information on
body fat stores to the CNS and (2) the satiety signals
which are released in response to food intake and are
thought to be involved in short-term regulation of
energy intake. Currently known adiposity signals are
insulin, leptin, and adiponectin, which are considered
as long-acting signals reducing energy intake. Among
the satiety signals are the hunger hormone ghrelin,
which is secreted in the stomach, and the short-acting
gut- and pancreas-derived satiety signals CCK, peptide
YY (PYY), GLP-1, oxyntomodulin (OXM), and pan-
creatic polypeptide (PP). Many of the peripheral
satiety signals have receptors in the arcuate nucleus
(ARC) of the hypothalamus, which plays an impor-
tant role in appetite regulation. The ARC contains
neuropeptide Y (NPY)- and agouti-related peptide
(AgRP)-expressing neurons acting to stimulate food
intake along with the adjacent pro-opiomelanocortin
(POMC) and cocaine- and amphetamine-regulated
transcript (CART)-expressing neurons which inhibit
feeding. Besides the ARC, the nucleus of the solitary
tract (NTS) and the area postrema (AP) receive appe-
tite-regulating inputs from vagal afferents and circu-
lating factors and are connected to the hypothalamic
nuclei controlling food intake.External factors
Various nonphysiological or external factors are also
known to modify food intake, and these effects may
be mediated through the intrinsic factors described
above. Psychological factors such as depression may
lead to either increased or decreased food intake, or
changes in the consumption of specifi c types of foods.
Environmental factors are also important, the most
obvious being food availability. Even when food is
available, some of the specifi c properties of foods
make them more or less appealing, thereby modifying
food intake. Important physical characteristics of
food include taste, texture, color, temperature, and
presentation. Other cultural infl uences in the envi-
ronment, such as time of day, social factors, peer
infl uence, and cultural preferences, can also play a
role in infl uencing food intake.3.3 Energy expenditure
Concept of energy expenditure
The process of energy expenditure and the oxidation
or combustion of food for energy in the body is anal-
ogous to a woodstove that burns wood to release heat
in a controlled fashion. In this analogy, large chunks
of wood are fed to the stove and the wood is gradually
combusted in the presence of oxygen to release carbon
dioxide, water vapor, and heat. Similarly, in the body,
the food consumed is oxidized or combusted in the
presence of oxygen to release carbon dioxide, water,
and heat. When ingested food is used for energy,