Chapter 24
Nutrition, Metabolism, and Body Temperature Regulation
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24
calorie content and alert us to start eating or put down that fork?
Despite heroic research efforts, no such single receptor type has
been found.
It has been known for some time that the hypothalamus,
particularly its
arcuate nucleus
(
ARC
) and two other areas—the
lateral hypothalamic area
(
LHA
) and the
ventromedial nucleus
(
VMN
)—release several peptides that influence feeding behav-
ior. Most importantly, this influence ultimately reflects the ac-
tivity of two distinct sets of neurons—one set that promotes
hunger and the other that causes satiety:
Te NPY/AgRP group of ARC releases neuropeptide Y
(NPY) and agouti-related peptides, which collectively en-
hance appetite by stimulating the orexin-releasing second-
order neurons of the LHA (
Figure 24.23
, right side).
Te other neuron group in ARC consists of the POMC/
CAR± neurons, which suppress appetite by releasing the
peptides pro-opiomelanocortin (POMC) and cocaine- and
amphetamine-regulated transcript (CAR±). POMC and
CAR± act on the ventromedial nucleus, causing its neurons
to release CRH (corticotropin-releasing hormone), an im-
portant appetite suppressor.
Current theories of how feeding behavior and hunger are
regulated focus on several factors, most importantly (1) neu-
ral signals from the digestive tract, (2) bloodborne signals
related to body energy stores, and (3) hormones. ±o a smaller
degree, body temperature and psychological factors also play
a role.
All these factors appear to operate through feedback signals
to the feeding centers of the brain. Brain receptors include ther-
moreceptors, chemoreceptors (for glucose, insulin, and others),
and receptors that respond to a number of specific peptides
(leptin, neuropeptide Y, and others). Te hypothalamic nuclei
play an essential role in regulating hunger and satiety, but brain
stem areas are also involved. Sensors in peripheral locations
have also been suggested, with the liver and gut itself (alimen-
tary canal) the prime candidates. Controls of food intake come
in two varieties—short term and long term.
Short-Term Regulation of Food Intake
Short-term regulation of appetite and feeding behavior involves
neural signals from the GI tract, blood levels of nutrients, and
GI tract hormones. For the most part, the short-term signals
target hypothalamic centers via the solitary tract (and nucleus)
of the brain stem (Figure 24.23).
Neural Signals from the Digestive Tract
One way the brain
evaluates the contents of the gut depends on vagal nerve fibers
that carry on a two-way conversation between gut and brain.
For example, clinical tests show that ingesting protein produces
a 30–40% larger and longer response in vagal afferents than in-
gesting the same amount of glucose. Furthermore, activating
stretch receptors ultimately inhibits appetite, because GI tract
distension sends signals along vagus nerve afferents that sup-
press the appetite-enhancing or hunger center. Using these sig-
nals, together with others it receives, the brain can decode what
is eaten and how much.
cells cannot use this energy to do work, the heat warms the
tissues and blood and helps maintain the homeostatic body
temperature that allows metabolic reactions to occur efficiently.
Energy storage is an important part of the equation only during
periods of growth and net fat deposit.
When energy intake and energy output are balanced, body
weight remains stable. When they are not, weight is either
gained or lost. Unhappily for many people, the body’s weight-
controlling systems appear to be designed more to protect us
against weight loss than weight gain.
Obesity
How fat is too fat? What distinguishes a person who is obese
from one who is merely overweight? Let’s take a look.
Te bathroom scale, though it helps to determine degrees
of overweight, is an inaccurate guide because body weight tells
little of body composition. Dense bones and well-developed
muscles can make a fit, healthy person technically overweight.
Arnold Schwarzenegger, for example, has tipped the scales at a
he²y 257 lb.
Te official medical measure of obesity and body fatness is
the
body mass index (BMI)
, an index of a person’s weight rela-
tive to height. ±o estimate BMI, multiply weight in pounds by
705 and then divide by your height in inches squared:
BMI
5
wt(lb)
3
705/ht(inches)
2
Overweight is defined by a BMI between 25 and 30 and carries
some health risk. Obesity is a BMI greater than 30 and has a
markedly increased health risk.
Te most common view of obesity is that it is a condition
of excessive triglyceride storage. We bewail our inability to rid
ourselves of fat, but the real problem is that we keep refilling the
storehouses by downing too many calories. A body fat content
of 18–20% of body weight (males and females respectively) is
deemed normal for adults.
However it’s defined, obesity is perplexing and poorly under-
stood, and the economic toll of obesity-related disease is stag-
gering. Chronic low-grade systemic inflammation accompanies
obesity and contributes to insulin resistance and type 2 diabetes
mellitus. People who are obese also have a higher incidence of
atherosclerosis, hypertension, heart disease, and osteoarthritis.
Te U.S. is big and getting bigger, at least around its middle.
±wo out of three adults are overweight. Of that number, one
out of three is obese and one in twelve has diabetes. U.S. kids
are getting fatter too: 20 years ago, 5% were overweight; today
over 15% are and more are headed that way. Furthermore, be-
cause kids are opting for video games and nachos instead of tag
or touch football and an apple, their general cardiovascular fit-
ness is declining as well and health risks associated with excess
weight start frighteningly early.
A Closer Look
on pp. 942–943
discusses weight-control methods used by some obese people.
Regulation of Food Intake
Control of food intake poses difficult questions to researchers.
For example, what type of receptor could sense the body’s total
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