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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

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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

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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

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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

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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;

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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

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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

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{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

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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.

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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

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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

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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. REFERENCES Ahlskog, J. E., and B. G. Hoebel. 1973. Hyperphagia resulting from selective destruction of an ascending noradrenergic pathway in the rat brain. Fed. Proc. 31:397. Amir, S., Z. W. Brown, and Z. Amit. 1980. The role of endorphins in stress: Evidence and speculations. Neurosci. Biobehav. Rev. 4:77. Anika, S. M., T. R. Houpt, and K. A. Houpt.1980. Insulin as a satiety hormone. Physiol. Behav.25:21. Anika, S. M., T. R. Houpt, and K. A. Houpt. 1981. Cholecystokinin and satiety in pigs. Am. J. Physiol. 240:R310. Anil, M. H., and J. M. Forbes. 1980a. Feeding in sheep during intra- portal infusions of short-chain fatty acids and the effect of liver denervation. J. Physiol.298:407. Anil, M. H., and J. M. Forbes. 1980b. Effects of insulin and gastroin- testinal hormones on feeding and plasma insulin levels in sheep. Horm. Metab. Res. 12:234. Baile, C. A. 1974. Putative neurotransmitters in the hypothalamus and feeding. Fed. Proo. 33:1166. Baile, C. A., and M. A. Della-Fera.1981. Nature of hunger and satiety control systems in ruminants. J. Dairy Sci. 64:1140. Baile, C. A., and M. J. Forbes.1974. Control of feed intake and regula- tion of energy balance in ruminants. Physiol. Rev. 54:160. Baile, C. A., and W. L. Grovum. 1974. Pentagastrin, secretin, chole- cystokinin, and caerulin in feeding in sheep. Proceedings of the Fourth International Food and Fluid Intake Conference, Jerusalem, Israel. Baile, C. A., and F. H. Martin. 1971. Hormones and amino acids as possible factors in the control of hunger and satiety in sheep. J. Dairy Sci. 54:897. Baile, C. A., and J. Mayer.1969. Depression of feed intake of goats by metabolites injected during meals. Am. J. Physiol.217:1830. Baile, C. A., and J. Mayer. 1970. Hypothalamic centres: feedbacks and receptor sites in the short-term control of feed intake. P.254 in Third International Symposium on the Physiology of Digestion and Metabolism in the Ruminant, A. T. Phillipson, ed. Newcastle-upon- Tyne, England: Oriel Press. Baile, C. A., A. W. Mahoney, and C. L. McLaughlin.1968a. Hypotha- lamic hyperphagia in goats and some observations of its effect on glucose utilization rate. J. Dairy Sci. 52:101. Baile, C. A., A. W. Mahoney, and J. Mayer.1968b. Induction of hypo- thalamic aphagia and adipsia in goats. J. Dairy Sci. 51:1474. Baile, C. A., F. H. Martin, J. M. Forbes, R. L. Webb, and W. Kings- bury. 1974a. 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