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OCR for page 1
Introduction:
Feed Intake
Control Mechanisms
INTRODUCTION
The control of feed intake and regulation of energy
balance are influenced by a number of factors. A regula-
tor of body energy content is apparently interfaced with
a controller of feed intake that maintains a balance of
energy input and output under normal conditions. How-
ever, under certain circumstances, the system can be
overridden and result in excessive weight gain or loss
(Baile and Forbes, 19741. Subsequently, either condition
could lead to metabolic disturbances and inefficient pro-
duction.
Feeding behavior can be influenced by several exter-
nal factors such as environmental conditions, sensory
cues, and nutrients in the diet. The internal milieu of an
animal, including gastrointestinal factors, hormones,
and metabolites, also plays a role in feeding behavior.
The primary site responsible for the integrated con-
trol of feed intake and energy balance is the central
nervous system (CNS), although the specific mecha-
nisms involved are not well understood. Peptides found
in the CNS have been shown to have a direct effect on
the control of metabolism, feed intake, and reproductive
behaviors. For instance, the onset of feeding may be
influenced by opioid peptides, and termination of feed-
ing may involve cholecystokinin. A number of CNS and
most likely peripheral receptor systems exist that pro-
vide information about the animal's metabolic state. A
coordinated feeding behavior is established via these
receptor systems and CNS centers.
Factors involved in the control of feed intake and en-
ergy balance are reviewed in this chapter. A comparison
is made between and within species regarding the
mechanisms that influence energy balance. The con-
trolling factors considered include those associated
with the gut and brain of the animal.
OVERVIEW OF CONTROL SYSTEMS
Several metabolic and sensory factors are known to
affect meal size and frequency. While meal size can vary
greatly, the total quantity eaten each day, for example,
must be controlled to maintain energy balance. The sig-
nals of satiety that control individual meal size must
have shorter time constants than the signals that regu-
late long-term energy balance. Feeding behavior is also
influenced by certain hormones and metabolites as well
as gastrointestinal factors. Understanding the mecha-
nisms involved in signaling the controller of feed intake
may lead to improved methods of animal production.
Digestive Tract
In ruminants it has been hypothesized that the
amount of forage eaten at a meal might be limited by the
capacity of the rumen (sampling, 1970~. When cattle
were offered feed for about 6 in/day, the weight of the
digesta of the rumen compared to that at the beginning
of feeding increased by 48 percent and dry matter in-
creased by 96 percent. Regardless of the range of feeds
or types of cattle tested, these increases were consis-
tent, supporting the idea that cattle eat until a certain
proportional change of ruminal distension is achieved.
Recent evidence suggests that the distension may be
detected by tension receptors with varying neural adap-
tation times that are thought to exist in the ruminant
stomach. These receptors have not been histologically
identified as yet. Grovum (1979) has reported that sheep
reduce feed intake in response to distension of the retic-
ulum, and thus, the sheep's reticulum may possess
stretch receptors that are sensitive to distension of the
gut after a meal.
Digestibility of the foods that ruminants consume can
1
OCR for page 2
2 Predicting Feed Intake
easily be related to the kinetics of digestion and its pas-
sage from the rumen (Waldo, 1969; Mertens, 1973~.
Forage intake is related to fiber digestion because it is
limited by the rate of disappearance of material from the
digestive tract (Conrad et al., 1964; Thorter and Min-
son, 1972; Mertens, 1973~. Mertens and Ely (1979
1982) have proposed a model of fiber disappearance
from the digestive tract in ruminants. They have sug-
gested that the ruminant's digestive process is divided
into rates of digestion, digestion lag, and potentially
digestible fraction. The retention time in the entire di-
gestive tract is influenced by level of intake, physical
characteristics of the diet, and rumination time. Specifi-
cally, their model suggests that maximum intake of di-
gestible dry matter is affected more by the proportion of
indigestible fiber and rate of passage than by the rate of
fiber digestion.
In general, increasing the level of feeding to twice
maintenance results in a 1 to 2 percent reduction in dry
matter digestibility of feed for the ruminant. This reduc-
tion can vary with the quality and grind of the feed. In
the pig, digestibility decreases with increases in level of
feeding but to a lesser extent than in ruminants (Mc-
Donald et al., 1973~.
Utilization of end products of digestion also differs
widely between ruminants and monogastric animals. Non-
ruminant herbivores, e.g., equines, absorb many prod-
ucts of digestion in the small intestine and utilize them
as a source of energy as efficiently as carnivores and om-
nivores (Roberts, 1975; Hansen et al., 1981~. Microbial
fermentation of ingesta in the equine cecum and large
colon can provide as much as 60 percent of the total di-
gestible energy available from the diet. This energy
source is in the form of short-chain volatile fatty acids
(VFAs). VFAs are the primary energy source in rumi-
nants, but are provided by fermentation in the rumen,
which is anterior to the small intestine. During and after
feeding the VFA concentrations in the rumen fluid and
blood increase (Chase et al., 1977~; these changes are
most obvious in sheep and cattle adapted to limited feed
access. During limited feed access smaller increases in
VFA concentrations occur during smaller spontaneous
meals. Large differences in VFA concentrations can exist
in various parts of the rumen for several hours after large
meals due to slow mixing within the rumen.
In ruminants acetate and propionate appear to play a
role in the control of meal size. Intraruminal injections
of either metabolite depress feed intake in cattle, sheep,
and goats (Baile and Mayer, 1970; Baile and Forbes,
19741. There are similarities that exist between the ef-
fects of acetate and propionate in that they can both
depress feed intake, but different receptors are thought
to exist for each in the ruminal area. It has been demon-
strated that there are chemoreceptors present in the
wall of the rumen that are sensitive to changes in pH but
not specifically to acetate (Harding and Leek, 1972~.
When infusions were made into the ruminal vein, pro-
pionate was most effective in depressing intake, sug-
gesting that propionate receptors are present in the wall
of that vein. Anil and Forbes' (1980a) work further sub-
stantiated that propionate depresses feed intake more
than acetate or butyrate. Sheep receiving a 3-h infusion
of sodium propionate into the portal vein ceased eating
30 min after the onset of the infusion until the end of
infusion. If the hepatic plexus was denervated, feeding
continued during portal propionate infusion, suggesting
that the liver is a major site for mediating the effect of
this VFA on feeding.
The question has been raised regarding the effects of
propionate infusions via the portal vein on blood compo-
sition. Results may be hampered by the uncertainty of
whether induced blood changes remain within the nor-
mal physiological levels. De Tong (1981) showed that the
change in VFA levels occurred in animals that were fed
once or twice daily. This scheduled feeding regime is
associated with large quantities of food eaten in a short
period of time and is different from those meals eaten by
animals on a free-feeding schedule. De long (1981) and
De Tong and coworkers (1981) infused isotonic or hyper-
tonic solutions of sodium salts of VFAs (acetate, propio-
Hate, n-butyrate, isobutyrate, or lactate) at a constant
rate for 4 h via portal vein catheters into free-feeding
adult goats. The results did not support the contention
that VFAs have a function in the control of feed intake,
and it was concluded that a role of the VFAs in the
control of feed intake did not involve blood concentra-
tion changes.
Ruminant feeding behavior can also be influenced by
changes in osmolarity of body fluids. Increases in rumen
fluid osmolarity from about 250 to 350 mOsM during
rapid eating of large meals can produce hypertonicity of
body fluids and result in dramatic circulatory and renal
changes. For instance, sheep can experience a rise in
systolic blood pressure and a reduction in plasma vol-
ume within 15 min of the initiation of rapid feeding
(Blair-West and Brook, 1969~. This is probably due to
the transfer of Na+ and water from body fluid to rumen
fluid. These mechanisms may cause ruminants as well
as other mammals not to eat if they are severely dehy-
drated (Utley et al., 1970~. Thus, water consumption
and changes in body fluids play a role in the control of
feed intake. However, in animals not deprived of water
or in which feed consumption is slow or feed is taken in
small meals, changes in the rumen or body fluid tonicity
are unlikely to limit feed intake.
Metabolites
Glucose has long been considered to be an integral
component of the feeding control system in monogastric
OCR for page 3
Introduction 3
animals. It has been shown that dramatically reduced
rates of glucose utilization associated with administra-
tion of glucose analogs or insulin-induced hypoglycemia
produce feeding and hunger, whereas increased glucose
utilization rates as well as hyperglycemia do not appear
to affect feeding (Baile and Mayer, 1969~. In the rumi-
nant, blood glucose concentration, arteriovenous differ-
ences in glucose concentration, and glucose utilization
rates generally decrease rather than increase with feed-
ing (Baile and Forbes, 19741. Thus, there is less evi-
dence that glucose utilization or concentration plays a
significant role in controlling feeding in the ruminant
(Baile and Della-Fera,1981~; in fact, there has been sub-
stantial evidence that supports the contrary.
Meal size was depressed in the pig by duodenal injec-
tions of isosmotic solutions of glucose and NaCl via im-
planted catheters (Houpt et al., 1983a,b). Injections
were made after the onset of alternate meals throughout
the day. Injections of 5 ml/kg of 5, 20, and 40 percent
glucose and 0.9, 3.25, and 6.5 percent NaCl equally de-
pressed the size of an ongoing meal proportionately
with respect to their hypertonicity. Neither intermeal
interval nor rate of eating changed to account for the
reduction of meal size; only meal duration decreased.
Such results are indicative of a possible duodenal os-
moreceptive system which may be involved in control-
ling the size of a meal.
In sheep, feeding of concentrate (feed that is more
calorically dense than average) can be reduced by high
physiological duodenal concentrations of lactate and
lactic acid. Receptors in the sheep's duodenum are par-
ticularly sensitive to these metabolites (Bueno, 19751.
This reduction in feeding may be a result of depressed
stomach motility or a feedback effect to the CNS from
the duodenal receptors.
Amino acids, e.g., lysine and glycine, may play a role
in the control of feeding (Baile and Martin, 1971~. In
sheep, plasma amino acid levels decline after a single
daily feeding but increase a few hours later, reaching
their maximum at about 24 h postmeal. Meal size of
ruminants is probably unrelated to the absorption of
amino acids since they are supplied primarily by the
small intestine several hours after ingestion. With re-
spect to amino acid imbalances or protein deficiencies,
the suckling (preruminant) lamb will decrease feed in-
take by one-half in response to a diet low in total protein
or void of either isoleucine or threonine (Rogers and
Egan, 1975~. Therefore, changes in plasma amino acid
levels do not appear to directly affect the feed intake of
ruminants fed a balanced diet.
The increase in free fatty acids (FFAs) associated
with starvation has been suggested to act as a signal to
induce feeding, despite the fact that FFAs increase not
only with energy depot mobilization but also with feed-
ing in animals adapted to a daily feeding schedule
(Chase et al., 1977~. Feed intake in sheep was depressed
by intraduodenal injections of long-chain fatty acids or
fats, but it remains unclear if depression in ruminoreti-
culum movements or changes in blood fatty acid compo-
sition was the cause (Titchen et al., 1966~. Thus, there is
insufficient evidence as to whether FFAs are a cause
rather than an effect of changes in feeding.
Hormones
Hormones considered for their possible role in con-
trolling feed intake include two of pancreatic origin,
glucagon and insulin. Experimental work with glucagon
was initiated in 1955 by Stunkard et al., in which intra-
venous infusions of glucagon brought about the sense of
satiety in humans. This work has been extended to
other species (Penick and Hinkle, 1961; VanderWeele
et al., 1979~. Glycogenolysis is the major metabolic
action of glucagon in the liver and was considered as the
mechanism of action for satiety (Geary et al., 19811. But
when glucagon was injected intraperitoneally and the
expected glycogenolysis occurred, it had no effect on
sham feeding (Geary and Smith, 1982a). Langhans et al.
(1982a) demonstrated that glucagon doses required to
reduce meal size produced changes in hepatic metabo-
lism that are also present at the end of normal meals,
e.g., reduced liver glycogen content; but in several in-
stances it has been shown that the hyperglycemic re-
sponse to glucagon is not sufficient to cause the satiety
response (Geary and Smith, 1982b). Some of the most
convincing evidence that supports glucagon's role as a
satiety factor is provided by Langhans et al. (1982b),
who showed that glucagon antibody injections in rats
cause increased feeding. Intraperitoneal injections of
rabbit antibodies against purified bovine pancreatic glu-
cagon or serum from nonimmunized rabbits were ad-
ministered at the beginning of the first meal of a dark
phase and after a 12-h fast. Feeding increased markedly
(63 percent) in these rats versus that in controls, as did
meal duration (74 percent). It was concluded that the
glucagon released during feeding was sequestered by
the antibody and thus removed a proposed essential
component for satiety.
McLaughlin et al. (1984) have demonstrated that fe-
male Zucker obese and lean rats decreased daily food
intake when immunized against pancreatic glucagon
(conjugated to bovine serum albumin). Over a 16-week
period, not only did food intake decrease 5.0 percent but
wei~ht ~ains decreased 9.4 percent as well. These
results appear contradictory to the hypothesized out-
come (Langhans et al., 1982a; McLaughlin et al., 1983a)
of increased food intake brought on by immunization
against glucagon. However, the observed decreases
may well be a consequence of an overcompensatory in
OCR for page 4
4 Predicting Feed Intake
crease in total (free and antibody-bound) serum gluca-
gon concentrations.
Over the last several decades the hypotheses regard-
ing insulin's involvement in the control of food intake
have varied. While hypoinsulinemia does not result in
anorexia, feeding can be induced by injections of insulin
but only after severe hypoglycemia occurs; yet insulin
can also be associated with overeating (Brandes, 1977~.
Hyperphagia and hyperinsulinemia, but not hypoglyce-
mia, often occur with the development of obesity
(Teanrenaud, 1979~. The causes for such associations
are not well understood, but insulin resistance is a com-
mon factor. Acute and persistent changes in plasma in-
sulin concentration may have opposing effects on
feeding. Porte and Woods (1981) proposed that insulin
may be a body adiposity signal. Factors that influence
the control of food intake may be classified into two
categories: (1) factors that cause feeding behavior to
change independent of body stores and (2) factors that
are sensitive to the size of the adipose mass. The second
category involves insulin as the hormone that signals
meal feeding to maintain energy balance. This proposal
is based on the observations that the plasma insulin con-
centration increases with the severity of adiposity.
Since levels of insulin fluctuate frequently within a 24-h
period, it is likely that some means is essential for ob-
taining an integrated response with a relatively slow
time constant. Porte and Woods (1981) hypothesized
that insulin in the cerebrospinal fluid (CSF) may possess
such a means. Concentrations of CSF insulin change
with plasma concentrations but at a much slower rate,
with a half-life of hours as opposed to minutes.
Further evidence in support of this hypothesis is pro-
vided by continuous lateral ventricular injections of in-
sulin in the baboon over a 14-day period, resulting in a
reduction in food intake and body weight (Woods et al.,
1979~. Similar glucagon injections had no effect, which
suggests that the response was caused by a specific
peptide. However, many studies have demonstrated
that insulin and glucagon have influential roles in con-
trolling feeding behavior and in the regulation of energy
balance. Still, much remains to be done toward proving
the association of CSF insulin and energy balance regu-
lation and glucagon's role in feeding before these two
pancreatic hormones can be considered as satiety sig-
nals.
Insulin's effectiveness as a satiety hormone has also
been investigated in swine (Anika et al., 1980~. Follow-
ing a 4-h fast, doses of insulin (0.05,0.13, and 0.25 U/kg)
delivered via intrajugular catheters produced a depres-
sion of feed intake compared to that in controls. Other
doses (0.03,0.5, and 1.0 U/kg) of insulin did not produce
similar effects during the first 10-min feeding period.
However, significant depression of feeding did occur in
the second 10-min period with the higher doses (0.13,
0.25, and 0.5 U/kg). Anika et al. (1980) suggest that
prandially released insulin, whether released by the
action of cholecystokinin or glucose absorption, for ex-
ample, may be influential in bringing a meal to an end.
An interrelationship between insulin and growth hor-
mone (GH) during lipogenesis has been noted by Gra-
ham (1967~. A high insulin: GH plasma ratio is required
for lipogenesis, and this ratio occurs in sheep after
meals scheduled at 3-h intervals, whereas lipolysis is
stimulated by a low insulin: GH ratio. A decline in the
insulin:GH ratio might be expected to occur at the start
of a meal if a shortage of absorbed energy triggers lipol-
ysis and feeding. Driver has observed peaks of GH ev-
ery 2 to 4 h in sheep with free access to food, and he
noted that spontaneous feeding did not occur when the
GH concentration was high (Driver and Forbes, 1978;
Driver et al., 1979~. Forbes (1980a,b) suggested that
elevated plasma GH levels do not directly inhibit feed-
ing but that this provides evidence for a link between the
initiation of feeding and a deficit of energy-yielding me-
tabolites.
Brain
The hypothalamus is directly and indirectly involved
in the control of systems and variations of body energy
content. The center controlling energy balance in the
brain is classically the ventromedial nuclear region of
the hypothalamus (VMH). Stimulation of this satiety
center inhibits feeding (Hetherington and Ranson,
1939~. If complete or partial lesions are made in the
entire area, they usually produce an immediate hyper-
phagia and weight gain that eventually stabilizes at a
higher set point and the hyperphagia subsides. Contro-
versy exists over whether VMH lesions induce hyper-
phagia since some studies have shown that damage to
the proximal catecholaminergic pathways can influence
feeding. However, these pathways do not synapse in the
VMH (Ahlskog and Hoebel, 1973; Gold, 1973~.
Much of the early work on the role that the brain plays
in controlling feed intake was conducted on rats, but
other species, i.e., ruminant and nonruminant domestic
animals, have been considered as well. Baile et al.
(1968a,b) demonstrated that goats with bilateral lesions
of the lateral hypothalamic area became temporarily
aphagic and adipsic, and lesions of the ventromedial
area produced hyperphagia and substantial weight
gain. Aphagia and adipsia can also be induced by lesions
of the lateral area of the hypothalamus in swine (Khalaf
and Robinson, 1972) and sheep (Tarttelin and Bell,
1968~.
In the chicken the hypothalamus is also the site of
many food-regulatory effector functions. Several physi
OCR for page 5
Introduction
ological changes have been noted to occur in the chicken
when electrolytic lesions are made, but only those rele-
vant to feed intake will be considered here. Some hypo-
thalamic lesions produce aphagia (Feldman et al., 1957),
and hyperphagia accompanies functional castration,
but no hyperphagia has occurred in permanently cas-
trated males and females (Snapir et al., 1969~. Properly
placed lesions normally produced increases in body
weight as a result of the production and accumulation of
excess fat. However, occasionally no effect results. A
typical hypothalamic obesity can be demonstrated in
the chicken with basomedial hypothalamic (BMH) le-
sions (Robinzon et al., 1977a). Placement of bilateral
septal lesions by intracranial injection of 6-hydroxydo-
pamine in geese produced a significant increase in feed
intake (Snapir et al., 1976~. In contrast to the hypotha-
lamic obesity brought about by BMH lesions, septally
lesioned geese and cocks did not develop obesity but
were hyperphagic (Snapir et al., 1976; Robinzon et al.,
1978~. These results with geese are similar to those ob-
tained from bulbectomized chickens, in which a marked
increase in feed intake occurred without obesity (Robin-
zon et al., 1977b).
Thus, lesions of the hypothalamus produce a number
of effects related to the control of feed intake in both
ruminant and monogastric animals. However, there are
probably differences in the feedback and receptor sys-
tems involved in energy balance for each type.
The route via which information travels from the sen-
sor of energy balance to the hypothalamus is not clear,
although the bloodstream has been suggested as a possi-
ble pathway for such communication. Hervey (1959)
noted metabolic adaptations that occurred in parabiotic
pairs of rats. When the VMH of one partner of a pair was
lesioned, it became obese while the other partner be-
came thin and died apparently from inanition. It has
been suggested that the nonlesioned hypothalamus of
the one partner responded to the total positive energy
balance of both rats by reducing its food intake. Subse-
quently, only its own body weight was affected and not
that of the obese rat. More recently, parabiotic rats have
been used to demonstrate the existence of endogenous
factors that separately control feed intake and metabo-
lism of body fat. Kasser et al. (1984) have shown that the
hypothalamic tissue pentose phosphate pathway can be
uniquely altered, supporting the concept of an eminent
role for CNS metabolism in controlling feed intake. It is
clear that the hypothalamus plays a primary and critical
function in the regulation of energy balance in animals.
Other Factors
Factors other than those previously mentioned can
affect feeding behavior. Sensory cues of olfaction and
taste can influence the selection and consumption of
various foods for most species. Ruminant Animals are
capable of utilizing a variety of waste products as feed-
stuffs. However, many of these products are unpalata-
ble and not utilized to their fullest extent. Olfactory cues
can influence whether or not a meal will be initiated, and
taste may affect the length of that meal. It appears that
species variability does exist with regard to taste prefer-
ences. However, most species exhibit a preference for
sweet tastes (Hellenkant,1978~. Although palatable fla-
vors can increase feed intake in many species (Baldwin,
1978), only a few flavors have been tested systemati-
cally (Zivkovic, 1978; McLaughlin et al., 1983a).
Ammonium ions, i.e., urea, whether injected or used
as a diet supplement, are also effective in controlling
feeding. Baile (cited in Conrad et al., 1977) demon-
strated that ammonium infusions into the rumen failed
to reduce rumen motility until lethal levels had been
added. Conrad et al. (1977) found that an intraruminal
injection of an ammonium load in goats during sponta-
neous meals reduced meal length, rate of eating, and
meal frequency. They also reported that when urea was
added to the diets of cows, the first meal length, as well
as meal size, was decreased, but total feed intake was
unaffected since the number of spontaneous meals in-
creased. Thus, those physiological factors that limit
meal length with urea in the rations are undefined, yet
they are important considerations in the successful
feeding of cows in situations where eating time is lim-
ited.
Other factors that can affect feed intake are tempera-
ture and environmental conditions. Growth or lactation
in an animal can be reduced by heat stress in some spe-
cies, but the critical temperatures at which effects be-
come noticeable vary within and between species.
Feeding can be inhibited by extreme heat loads, but it
has been postulated that this may be a stress-related
response as opposed to a normal satiety signal. How-
ever, most species do have a uniform milk production
rate and feed efficiency over a relatively wide range of
conditions.
Sex hormones are also influential in determining
amounts of feed eaten by animals. When weight gain is
induced in rats by progesterone, the increase in feed
intake is more variable than the weight gain. In fact,
when feed is restricted to the control intake, progester-
one treatment produces two-thirds of the additional en-
ergy storage that occurs in free-fed rats (Hervey and
Hervey, 1967), thus indicating a decreased energy ex-
penditure.
Estrogen has been suggested as a factor that can af-
fect feed intake by acting on an area of known sensitiv-
ity in the anterior hypothalamus (AH) which sends
projections to the VMH (Kennedy and Mitra, 1963;
OCR for page 6
6 Predicting Feed Intake
Kennedy, 1964~. More recently, Wade and Zucker
(1970a,b) have demonstrated that estradiol can act di-
rectly on the VMH. The result was a depression of feed
intake, which was apparently an estrogen-induced
action; however, this depression was not observed in
weanling rats under 40 days of age unless they were
hypophysectomized.
They concluded that before puberty pituitary hor-
mones blocked the VMH restraint on intake. There
must be other sites of action involved in estrogen's ef-
fects on feed intake since estrogens are capable of stim-
ulating eating in rats that have access to exercise
wheels. This occurs indirectly by stimulating locomo-
tive activity, hence increasing energy expenditure, and
lesions of the AH block this locomotor action of estro-
gen. High levels of estrogens are generally considered
to inhibit growth which in turn can depress feed intake.
Tarttelin (1968) has also reported depressed feed intake
coinciding with estrus in the ewe. Growth and intake do
not appear to be affected by estrogens in the prepuber-
tal rat, but after puberty estrogens do have an effect on
intake (Wade and Zucker, 1970a,b).
Diethylstilbestrol (DES) has been used as a feed addi-
tive or as an ear implant for stimulating weight gains
and improving feed efficiency of growing and finishing
ruminants (Riggs, 1958; National Research Council,
19631. It has also been reported by Trenkle (1969) that
estrogenic compounds, e.g., DES, produce only a slight
increase in feed intake.
Other steriods, e.g., dehydroepiandrosterone
(DHEA), a 17-ketosteroid, can produce a decrease in
weight gain without affecting feed intake in lean mice
and yellow obese mice that have hypertrophic adipose
tissue (Yen et al., 1977; Cleary et al., 1982~. Not only was
body weight reduced but the feed efficiency ratio, fat
cell number, and size of the fat cell were significantly
decreased (Cleary et al., 19841.
In the Leghorn cock testosterone propionate (TP) is
effective in inducing hypophagia and, in turn, reducing
carcass fat content, while DES increased adiposity
markedly through hyperphagia. Injections of the com-
bined steroids (TP and DES) produced only moderate
obesity (Snapir et al., 1983~. The results suggest that TP
may decrease feed intake and lipogenesis, whereas
DES has the opposite effect.
REGULATORY PEPTIDES
Other hormones are involved in the regulation of en-
ergy balance and control of feeding behavior, including
peptides of the gastrointestinal (GI) tract and brain. For
years knowledge of GI hormones was limited to the exis-
tence of three or four, but now many GI peptides are
known to exist. Many of their actions remain undefined,
however. While advances have been made in the area of
regulatory peptides within the last decade, much re-
mains to be discovered with respect to synthesis, re-
lease, and actions of the various forms of the peptides.
One GI hormone for which there is evidence for a role in
controlling feed intake is cholecystokinin (CCK).
Cholecystokinin
Gibbs et al. (1973) showed that CCK is capable of
inhibiting feed intake. Studies have revealed that sham-
fed fistulated rats decreased feed intake following intra-
peritoneal or intravenous (IV) injections of CCK, and
the observed percentage of inhibition of feed intake was
dose dependent (Lorenz et al., 1979~.
The specificity of CCK has been clearly demonstrated
by comparing the effects of closely related peptides. A
sulfate group present on the seventh amino acid, tyro-
sine, can influence the actions and receptor-binding af-
finities of CCK-active peptides (Steigerwalt and
Williams, 1981) and is necessary for the satiety effect
(Ondetti et al., 1970~. The desulfated CCK is far less
active than the sulfated form; for example, Lorenz et al.
(1979) reported the potency of desulfated CCK-8 to be
10 times less than that of the sulfated form in inhibiting
feeding.
Over the last decade the effects of CCK on the feeding
behavior of food-producing animals have been studied.
Intraportal injections of CCK in pigs proved to be more
effective in inhibiting intake than intrajugular injec-
tions, whereas intraperitoneal injections were signifi-
cantly less effective than injection at either intravenous
site (Anika et al., 1981~. In comparison, peripherally
administered CCK produced very little or no effect on
feed intake in sheep (Baile and Grovum, 1974; Anil and
Forbes, 1980b). However, if a small dose of an impure
CCK-33 preparation was injected intrajugularly over a
296-min period, a decrease of 40 percent in intake oc-
curred within the first 10 min of injection. This decrease
did not persist over subsequent time periods, despite
the continuation of the injection (Grovum, 1981~. In
chickens intravenous injections of CCK-8 or caerulein
decreased feeding within the first 10 min of injection
and then normal feed intake resumed (Savory and Gen-
tle, 1980~. Feeding was also shown to decrease after
administration of a CCK-33 preparation in a different
test system (Snapir and Glick, 1978~.
There are variations in the effects of CCK between
species. Effects of CCK may vary due to interspecies
rate of digestion. In chickens, for instance, feed first
passes through the crop and gizzard, delaying the ar-
rival of the ingesta to the intestines and, in turn, delay-
ing the release and effect of intestinal CCK. Savory and
OCR for page 7
Introduction 7
Gentle (1980) proposed that meals that were greater
than 6 min in length could be influenced by CCK re-
leased from the duodenum as a result of the newly in-
gested food reaching that part of the intestinal tract. In
sheep there is also a delay of intestinal digestion since
food is held in the rumen, subjected to microbial diges-
tion, and then slowly passed to the intestines. There-
fore, GI CCK may not work as a satiety agent in sheep
and chickens by the same route as in other animals, such
as pigs. These characteristics should be considered
when evaluating the effectiveness of gut hormones on
feeding behavior.
Despite the finding that exogenous administration of
CCK results in decreased feed intake in several species,
little conclusive evidence exists that supports the fact
that CCK is essential for satiety to occur. Recently,
McLaughlin et al. (1985) used antibodies (AB) to CCK to
sequester endogenous CCK to determine the effect on
feed intake. Zucker lean rats were autoimmunized using
a conjugated CCK-8. Both average daily feed intake and
weight gain increased in immunized rats versus con-
trols. Sequestering of CCK released during a meal in-
creased meal size, and in those animals that developed
significant endogenous CCK-AB titers daily feed intake
and weight gain increased. These data provide strong
evidence that CCK may play a role in satiety.
Several other experimental approaches have been
used to demonstrate that endogenous CCK might medi-
ate intestinal satiety. Some amino acids, in particular
l-phenylalanine, in the lumen of the small intestine
causes CCK to be released. If infused intragastrically in
monkeys, I-phenylalanine decreased feed intake,
whereas d-phenylalanine was ineffective (Gibbs et al.,
1976~. Evidence exists for a negative feedback control
of CCK release by trypsin in the lumen (Brande and
Morgan, 1981~. Oral administration of a trypsin inhibi-
tor causes a decrease in trypsin activity and decreases
CCK content in the intestinal mucosa (implying CCK
release). This inhibitor also increases the secretion of
pancreatic enzymes, a known effect of CCK. Brande
and Morgan (1981) suggest that by changing the level of
trypsin activity in the gut it is possible to alter the
amount of CCK released. Other work indicates that
trypsin inhibitors decrease feed intake in rats and that
trypsin supplements can increase intake (McLaughlin
et al., 1983b,c).
Numerous studies have demonstrated the presence of
CCK peptides in the brain of both mammalian and non-
mammalian species. At least five forms of CCK are
known to exist: a component larger than CCK-39, a
component similar to CCK-39, CCK-12, CCK-8, and
CCK-4. Of these forms CCK-8 is the predominant form
in the brain (Rehfeld, 1978; Rehfeld et. al., 1979; Golter-
mann et al., 1980~. There appears to be a specificity of
regional distribution of CCK peptides and receptors in
the brain. The highest concentration of CCK and its
receptors occurs in the cortex; however, significant
quantities of CCK-8 have been located in the hippocam-
pus, periaqueductal gray, and dorsomedial hypothala-
mus as well (Rehfeld, 1978; Saito et al., 1980; Beinfeld
et al., 1981~.
Evidence that supports the role of brain CCK peptides
in satiety has been obtained from experiments in which
lateral ventricular (LV) injections of CCK were made in
sheep (Della-Fee and Baile, 1979; Della-Fera et al.,
1981) and pigs (Parrott and Baldwin, 1981~. Significant
decreases in feeding occurred when fasted sheep were
administered as little as 0.01 pmol of CCK-8/min.
Larger doses of 2.5 pmol of CCK-8/min or greater sup-
pressed all feed intake during 3-h injection periods
(Della-Fee and Baile, 1979~. With respect to fasted
pigs, feed intake also decreased in a dose-dependent
manner. In both species CCK-8 affected only feed intake
without affecting water intake or body temperature
(Della-Fee and Baile, 1980a; Parrott and Baldwin,
19811. Amounts of CCK-8 required to induce this re-
sponse were similar between species.
Experiments in which CCK antiserum was injected
into the LV of sheep provide the strongest evidence for
CCK's involvement in satiety (Della-Fee et al., 1981~.
Significant increases in feed intake occurred during in-
jection of antiserum versus injection of normal control
serum. The pattern of increased feed intake may have
been related to an inhibition of satiety as opposed to the
stimulation of hunger, since typical postmeal intervals
did not occur during injection of CCK antiserum but did
occur with the control. The early onset of increased
feeding in association with injections of CCK antiserum
indicated that CCK antibody may have been effective by
sequestering CCK in the CSF. CCK may have been re-
leased into the CSF prior to interaction with the recep-
tors that mediate the satiety effect; thus, it is possible
that CCK is transported via CSF to its sites of uptake or
action (Della-Fee et al., 1981~.
In experiments with chickens, in which 4-week-old
broilers were injected intracerebroventricularly with
doses of 100 and 150 ng, CCK-8 reduced feed intake
over a period of 60 and 105 min, respectively. Feed in-
take was reduced by 87 percent for the first 15 min
postinjection of 150 ng of CCK-8 (Denbow and Myers,
1982~. This decrease was nearly fourfold greater with
less than one-third the amount injected intravenously by
Savory and Gentle (1980~. In the latter studies subjects
were 12- to 17-week-old hens and thus larger in body
mass. When injected with 40 times the amount of CCK-
8 used by Denbow and Myers (1982), feed intake was
only reduced by approximately 45 percent.
The mechanism of action of CCK's central effect on
OCR for page 8
{3 Predicting Feed Intake
feeding behavior is not yet clearly defined. The problem
is complex in that centrally administered CCK can pro-
duce changes in GI function (Della-Fee and Baile,
1980a,b; Bueno et al., 1983) and secretion of specific
hormones (Della-Fee and Baile, 1981~. The possibility
exists that the effects of brain CCK may be mediated
through the release of other brain peptides such as calci-
tonin (Care et al., 1971) or neurotransmitters such as
norepinephrine (McCaleb and Myers, 1980~. Clearly,
much more information is required to propose a unifying
hypothesis for these actions of CCK.
Opioid Pep tides
Recently, evidence has been generated that indicates
a role for certain brain peptides such as neurohormones
or neurotransmitters in hunger and satiety. Opioid pep-
tides have been implicated in several bodily functions
and processes (Terenius, 1978; Margules et al., 1979;
Amir et al., 1980), including feeding and ingestive be-
havior (Morley, 1980~. An opiate receptor system has
been suggested as a component in initiation of hunger in
the ruminant (Baile et al., 1981~.
A broad spectrum of opiate agonists and antagonists
have been tested to determine the mechanisms involved
and the classiest of opiate receptors responsible for
opiate-induced feeding. Feeding can be stimulated in
sheep receiving injections ICV of opioid peptides; e.g.,
an enkephalin analog can stimulate satiated sheep to eat
(Baile et al., 19811. Opiate antagonists, such as nalox-
one, can suppress feeding in sheep (Baile et al., 1981;
Bueno et al., 1983), guinea pigs (Schulz et al., 1980),
rabbits (Sanger and McCarthy, 1981), and mice (Holtz-
man, 1974~. Naloxone-injected IV in combination with
an LV injection of enkephalamide eliminates the feed-
ing responses of enkephalamide (Bueno et al., 1983~.
In yet another series of experiments, IV injections of a
similar enkephalin analog (Tyr-D-Ala-Gly-Phe-NtCH33-
~-PheNH2-HOAc) stimulated feeding in satiated sheep
(approximately 50-kg body weight). An approximate
14-fold increase of peptide was required for this re-
sponse versus the amount of analog used in the LV study
(12.25 versus 0.92 ma) (Baile et al., 19811. The findings
from these LV studies are indicative of the fact that CNS
is a likely site of action for opioid peptides, but it remains
to be shown where the IV-injected peptides act.
Another opioid peptide associated with the hunger
component of feed intake is 3-endorphin. Increased
plasma 3-endorphin concentrations have been shown to
be related to hunger (McLaughlin and Baile, 1985~.
They postulated that if rats were immunized against
,B-endorphin, antibodies would sequester h-endorphin
and produce a decrease in feed intake and body weight.
In fact, rats autoimmunized against ,6-endorphin in
creased feed intake and body weight. It is not clear if
these responses are due to a decreased free concentra-
tion or an increased total concentration of plasma
h-endorphin. Increased production of other proopicorti-
cotropin cleavage products, e.g., adrenocorticotropic
hormone, in these rats may contribute to the observed
increases in feed intake, body weight, and pituitary size.
On the basis of various studies showing that different
opiate agonists bind different classes of receptors with
varying affinities, some tentative conclusions concern-
ing specific receptor systems involved in feeding can be
drawn. It appears that kappa- and mu-opiate receptors
may be particularly important in the hyperphagic re-
sponse since opiates that are relatively specific for ei-
ther of these types of receptors are highly effective in
inducing feeding (Larrson and Rehfeld, 1979; Yim et al.,
1980; Morley and Levine, 1981~.
In an effort to test the differential roles that opiate
receptor subtypes play in feed intake, Della-Fera et al.
(1983) tested D-alanine (2D A~a) dynorphin (dyn)-17 and
dye-13, and dye-17. Feed intake was increased during a
60-min LV injection in sheep. Dyn-,B had no effect,
whereas (2D A~a 5I eu) enkephalin (DADL) decreased feed
intake. Della-Fera et al. (1983) suggested that since dyn-
A and DADL act on receptors other than kappa and
delta, that exclusivity may not exist for their action at
the receptor level.
The specific sites of opiate receptors involved in the
feeding responses and the mechanism of opiate action
responsible for eliciting feeding remain unknown. Some
evidence does exist, however, for an interaction be-
tween opiates and dopamine in the nigrostriatal path-
way (Urwyler and Tabakoff, 1981~. It has also been
suggested that glucose levels are important in regulat-
ing the sensitivity of the opiate receptors involved in
feeding (Morley et al., 1983~. Thus, opiate peptides may
contribute to the onset of feeding under certain condi-
tions.
THE ROLE OF FEED INTAKE IN THE
REGULATION OF ENERGY BALANCE
The mechanisms involved in receiving information
from the periphery and then processing it centrally to
produce an appropriate response are not adequately de-
fined. Factors such as GI conditions, hormones, and
metabolites act on receptor systems which essentially
transduce analog information (e.g., concentration) into
neuronal units. Due to the changes in individual neuro-
nal firing that interface with a detector cell and spike a
potential generator, e.g., temperature receptor
(Edinger and Eisenman, 1970), as well as the number of
OCR for page 9
Introduction 9
detector neuron units that are influenced, subsequent
changes in the output of a single type of detector system
may occur (see Figure 1-11. The final result of such a
system is a transformation of analog to digital informa-
tion (firing rate x number of cells influenced).
The analog information, including sensory inputs, is
evaluated and integrated primarily in the hypothalamic
area that initiates the appropriate behavior. Specific hy-
pothalamic areas that appear to be important compo-
nents in the control of feeding and the regulation of
energy balance have been identified. For example, stim-
ulating the VMH generally has an inhibitory effect on
feeding, and lesions in this area can result in hyperpha-
gia and obesity (Hoebel and Teitelbaum, 1966~. The
lateral hypothalamus appears to be responsible for the
initiation of feeding, with lesions of this area resulting in
aphagia and weight loss (Teitelbaum, 1961~.
FACTORS CONTROLLING FEEDING BEHAVIOR
,
Not only do specific brain areas have an influence on
feeding but neural transmitters have been identified as
having roles in eliciting and suppressing feeding behav-
iors (P;aile and Forbes, 1974~. When injected into spe-
cific sites of the hypothalamus of sheep, several putative
neurotransmitters, such as norepinephrine, elicited
feeding (Baile, 1974~. Other experiments on sheep and
cattle have shown that several neurotransmitters (Baile
et al., 1974b; Forbes and Baile, 1974; Simpson et al.,
1975), prostaglandins (Baile et al., 1974a), and certain
Ca+ + and Mg+ + concentration shifts (Seoane and Baile,
1973, 1975) elicit large meals in satiated animals.
In addition to the factors previously discussed, other
factors are involved in feeding behavior and energy bal-
ance regulation. The effects of diet dilution can have an
influential role on feed intake. Conrad et al. (1964) did a
comprehensive study on the effect of availability of en
negative effects on Fl of feedback
from adipose tissue may be less potent
BRAI N CCK
in farm animals than other species. +
~ Y
- ~: ~Am ~ x~ ~ ~ As ~ ~ 1 1 ~ l~'~ ~ ~ l~ ~' , ~ ~ ~
= ~ ,-~ w~ ~ ~\
- & HORT~NOALE~,ORECEPTORS
~ GUT RESPONSE ~ ''; LAD ~ ^/ ~ ~
V F. A = erase 9teS° ~: ~ ~ Envi~ j ~ Olfaction
propionatet; ~ MUSCLES ; ) ~Taste & other
Progesterone e.g. C ~PAL / ~Hyperthermia
(estrogenic cmpds (e.g. ) D ES
~ F I ~ in ruminants
fermentation in ~i( )~°
ruminants occurs
prior to sm. intestine
~ I\
,.
glucose utilization may be more important
in controlling Fl in mono
gastrics vs. ruminants
FIGURE 1-1 Factors controlling feeding behavior. Several factors that influence the control of feeding behavior in the ruminant
are summarized. Some differences that exist between species are indicated. The abbreviations and their meanings are: CCK,
cholecystokinin; DES, diethylstilbestrol; DHEA, dehydroepiandrosterone; FFA, free fatty acids; FI, feed intake; FSH, follicle-
stimulating hormone; GH, growth hormone; GRF, growth hormone-releasing factor; HYPO, hypothalamus; IGF, immunoglobulin
factor; LH, luteinizing hormone; LPL, lipoprotein lipase; PIT, pituitary; PRL, prolactin; VFA, volatile fatty acids; and VMH,
ventromedial hypothalamus.
OCR for page 10
JO Predicting Feed Intake
ergy from feeds on feed intake in dairy cows. In their
study, which examined rations varying in roughage and
concentrate content, a number of assumptions were
made in accounting for variation between cows. Yet
they demonstrated that lactating cows compensate for
the dilution of digestible energy (DE) if digestibility of
dry matter of the feed was above 67 percent. A relation-
ship between minimum calorie density of diet fed to
dairy cows and milk production indicates that the
greater the milk production, the more dense the re-
quired diet (Bull et al., 1976~. These examples illustrate
that lactating cows, like sheep and growing cattle, are
capable of controlling intake to maintain a constant DE
level, provided that the diet has a DE concentration
above the critical point. This critical point is variable,
depending upon the physiological demands for sub-
strate.
The lipostatic hypothesis suggests that for mature
animals to maintain a relatively stable body weight, feed
intake must be controlled to regulate total body fat con-
tent (Kennedy, 1953~. The mechanisms responsible for
body fat regulation are not completely understood.
Studies in which parabiotic rats were used suggest that
a bloodborne factor influences a central control mecha-
nism of the state of the peripheral energy stores (Her-
vey, 1959~. The central control system then modifies
feed intake to compensate for shifts in energy balance
away from equilibrium. In addition, it is not adequately
understood how the state of the lipid depot may influ-
ence energy balance regulation in the ruminant. It may
be related to the selection for certain traits of the animal,
i.e., the "finish" which is in part related to fatness that
varies among species and breeds of animals. Such dif-
ferences may be the result of changes in the level at
which fat depots are regulated. There is evidence that
fat ruminants consume less than thin ones and may reg-
ulate their fat depots (Baile and Forbes, 1974; Paguay et
al., 19791. From the evidence that exists it appears that a
humoral factor may be one link between lipid depots and
the CNS. The level of intake of digestible energy has
been shown to be related more closely to weight of body
fat than to feed quality (Lee, 1974; Blaxter, 1976~. This
implies that some physical effect of fat on intake is not
sufficient to explain its physiological effects. Forbes
(1980a) suggested two ways, unrelated to the set-point
theory for body weight, in which fat and fattening might
influence the homeostatic balance of energy. First,
there is a limit to the rate at which adipose tissue is able
to synthesize triglycerides. Smaller amounts of the
available excess energy are taken up by adipose tissue
as this limit is approached. Those receptors that are
sensitive to energy availability recognize the excess and
depress intake. Second, the decrease in metabolite up-
take by adipose tissue may exert a negative feedback on
the energy-sensing centers causing a decline in feed
intake.
Substances derived from the ingested feed increase
protein and fat synthesis which in turn generate
negative-feedback signals to the CNS energy balance
regulator. One such substance is a protein deposition
promoter, somatomedin. The energy balance regulator
provides an input to the controller of hunger and satiety,
and thus shifts in the body energy status are reflected by
changes in feeding behavior. Deficits in body energy
stores modulate the controller to increase meal size and
meal frequency, whereas decreases occur during en-
ergy surfeit. This substrate uptake is then modulated in
the various tissues, i.e., by lipoprotein lipase in adipose
tissue and somatomedin in muscle tissue. Consequently,
lipoprotein lipase and somatomedin are potential candi-
dates that influence the feedback signal for this energy
balance regulator.
It appears that the negative effects on feeding of the
feedback from adipose tissue are less potent in domestic
farm animals than in other species because of elevated
levels of body fat achieved after extended ad libitum
feeding (Blaxter, 19761. Forbes (1977) has suggested
that this may be related to past selection for fast growth
rates without great consideration for carcass composi-
tion and a decrease in sensitivity of satiety neurons in
the hypothalamus.
SUMMARY
Changes in peripheral or central factors can modify
normal feed intake and influence the systems that con-
trol hunger and satiety with subsequent effects on pro-
duction performance. Depending upon environmental
conditions under which species evolved, differences ex-
ist among feeding behaviors. Among the numerous fac-
tors, hormones have received special attention,
although the proposed relets) of any particular hormone
has varied over time. Several classes of hormones have
been considered in this chapter; among them are GI,
pancreatic, and brain peptides (see Table 1-1~. Of these
classes, a few have obtained notable recognition for
their likely roles in the control of feeding. Glucagon of
pancreatic origin appears to be involved in satiety. An-
other pancreatic hormone considered for its role in the
control of feeding is insulin. Recently, some evidence
points to the possibility that CSF insulin-like factors
provide an integrated link between the metabolic state
of the adipose tissue and the brain structures involved in
the control of feeding. Thus, these may be primary hor-
mones for the maintenance of energy balance or body
weight.
Studies with two classes of peptides, CCK and opiate
OCR for page 11
Introduction 1 1
TABLE 1-1 Summary of Factors Influencing Food Intake
Effect
Factor
Sensory
Olfaction
Taste
Temperature
Brain
Controls food intake
Controls food intake
Controls food intake
Hypothalamus Controls energy balance
Pituitary Controls energy balance
Metabolites and hormones
Somatomedin Affects muscle and cartilage
Glucose Little control of food intake in ruminants; greater control in monogastrics
GH Decreases insulin: GHa; initiates feeding
Insulin Decreases insulin: GH; initiates feeding
Glucagon Undefined
FFA Undefined
Amino acids None in ruminants
Digestion
Meal size Tension receptors detect rumen distension
Diet digestibility Duodenal receptors detect absorbed nutrients in sheep
Feeding frequency Affects rate of ingesta passage
H2O intake Controls food intake
Fermentation pH Affects chemoreceptors in rumen wall
Urea
Urea, ammonium chloride, and Shortens meal length in goats
ammonium lactate (injections)
Urea (as feed additive) Decreases length of first meal and meal size, but total intake remains unchanged because
spontaneous meal number increases in cows
Acetate Reduces meal size in cattle, sheep, and goats
Lactate (sodium lactate injections) Reduces meal size in goats
Propionate Reduces intake; shows evidence of propionate receptors in ruminal vein walls
Sex hormones
Estrogenic compounds Increase food intake in ruminants
Progesterone Affects other ovarian hormones
DHEAb Decreases weight gain without affecting food intake in mice
PRLC Affects lactation and other physiological responses
ASHY Affects lactation and other physiological responses
LHe Affects lactation and other physiological responses
aGH, growth hormone.
bDHEA, dehydroepiandrosterone.
CPRL, prolactin.
ASH, follicle-stimulating hormone.
eLH, luteinizing hormone.
peptides, have shown that these may play a role in con-
trolling feed intake. CCK, an intestinal and brain hor-
mone, appears to act as a satiety agent. The brain
opiates are most likely involved in the transmission of
information concerned with the interaction of feeding
and maintenance of energy balance. Thus, their func-
tions may be interrelated. Other peptides, such as soma-
tomedins, influence growth of nonadipose tissues and
may also act on energy balance regulators with a result-
ing decrease in feeding behavior.
Clearly, then, the CNS and its pathways play a pri
mary role in the control of feeding behavior and the
regulation of energy balance. The specific actions or
components of the associated physiological systems and
the interfaces of information remain inadequately de-
fined. Until recently, the emphasis of research has fo-
cused primarily on changes in gastric functions as well
as the metabolite responses associated with feeding.
Now interest has shifted to the influential role of the
CNS and various means of modifying voluntary feed
intake. With the greater understanding of control sys-
tems, it appears likely that feeding behavior and the
OCR for page 12
12 Predicting Feed Intake
level at which body energy content is maintained in
adult animals, or the rate at which it increases in grow
ing animals, can be modified. Such modifications could
lead to improved bioenergetic efficiencies and reduced
management demands. In addition, certain metabolic
diseases could be prevented if the hunger drive was
stimulated sufficiently to compensate for the lacking
nutrient supply. These modifications may lead to im
proved efficiencies and allow greater food and fiber pro
duction from animals.
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Representative terms from entire chapter:
food intake
