Abstract
Changes in plasma concentrations of GH and insulin in response to feeding and stimulation with GH-releasing hormone (GHRH) or GH-releasing peptide (GHRP-6, a ligand for endogenous GH secretagogue receptors) were compared between 3-week-old (milk-fed) and 12-week-old (concentrate and hay-fed) calves. Feeding of a milk-replacer diet in 3-week-old animals significantly increased the basal (prefeeding) concentrations of GH, insulin and glucose in plasma, whereas feeding of concentrate and hay in 12-week-old animals did not cause a significant change in these traits. However, in the animals maintained on a milk-replacer diet until 12 weeks of age, postprandial plasma GH concentrations and AUC (area under the curve) were not different from those in the age-matched weaned group. The venous injection of either GHRH (0.25 μg/kg) or GHRP-6 (2.5 μg/kg) significantly increased plasma GH concentrations in both 3- and 12-week-old animals, but GH AUC was significantly greater in 3-week-old than in 12-week-old animals. Insulin concentration was transiently but significantly increased by the injection of GHRP-6 only in 12-week-old animals, the AUC being greater in 12-week-old than 3-week-old animals. From these results, we conclude that postprandial levels of plasma GH and insulin concentrations are altered after weaning and by aging, and that the quality of diets or development of the neuroendocrine functions in the digestive–pituitary system may be involved in this alteration.
Introduction
Weaning, after birth, is the most drastic event that neonates have to experience, because they are obliged to change feedstuffs from liquid milk to solid particles, even if it occurs gradually. This means that weaning has to change the digestive and metabolic functions to meet the change in the quality of the diet. We recently found that weaning abolished leptin expression in the rumen and abomasum in calves. Similarly, the expression of CCKa and CCKb receptors in the foregut of calves was also suppressed after weaning (Yonekura et al. 2002). In addition, when calves were fed a milk-replacer diet until 13 weeks of age, leptin expression in the epithelium of the rumen and abomasum was still detected throughout (Yonekura et al. 2002), and carbonic anhydrase activity and ion secretion in the parotid gland also remained at preweaning levels (Kitade et al. 2002). With regard to glucose metabolism, when veal calves were fed milk without solid feed, such as concentrates or roughage, plasma glucose and insulin concentrations were greater than those of weanlings (Blum & Hammon 1999).
For the ruminant, growth hormone (GH), as well as insulin, as in other domestic animals, is indispensable for the control of the metabolism and function of bone, liver, skeletal and cardiac muscles, adipose tissue, reproductive organs and various other tissues or organs (Simmen et al. 1998, Clark & Rogol 1999). The somatotropic axis principally consists of hypothalamic (growth hormone-releasing hormone (GHRH) and somatostatin (SRIF)) and peripheral hormones, such as ghrelin and leptin, and insulin-like growth factor-I (IGF-I). Pituitary GH secretion, which alters in a pulsatile manner in all of the animal species studied so far, is mainly stimulated by two hormones (GHRH and ghrelin (or GH secretagogues: GHS)), whereas it is suppressed by SRIF (Lamberts 1999, Tannenbaum & Epelbaum 1999) and IGF-I (Katoh et al. 2004). The responsiveness to GHRH in the bovine fetus pituitary cells seems greater than that in adult cells, since the basal GH release was age-dependently reduced in ovine pituitary cells isolated at different ages and the maximum release was obtained in a 70-day-old fetus (Blanchard et al. 1988). Therefore, it is likely that GH secretion in response to GHRH stimulation declines with the aging process, although it is not known how the response to GHRP changes and why basal GH levels decline in an age-dependent manner.
Weaning is a critical point for neonates because not only do they have to change diets but also the endocrine system has to adapt to this change. In the present study, therefore, we observed changes in the secretion of GH and insulin in response to feeding and stimulation with GHRH and GHS (GH-releasing peptide: GHRP-6) in 3-week-old (milk-fed) and 12-week-old (concentrate and hay-fed) calves. We also compared the endocrine responses to feeding between the animals maintained on a milk-replacer diet until 12 weeks of age and those of weaned, age-matched control animals.
Materials and Methods
Animals
Holstein calves were treated according to ‘Guiding Principles for the Care and Use of Animals in the Field of Physiological Sciences’ (Physiological Society of Japan), and the present experiment was approved by the Animal Care Committee of Tohoku University.
Four to six male calves for each experiment were fed with their dams for 1 week after birth to ensure sufficient intake of colostrum before starting the experimental feeding. In experiments 1 and 3, the animals were fed a milk-replacer diet until 4 weeks of age, milk-replacer and calf-starter diets after 4 weeks of age, and then calf starter and hay from 7 to 13 weeks of age, as described in our previous reports (Kitade et al. 2002, Yonekura et al. 2002). In experiment 2, the animals were fed only a milk-replacer diet until 12 weeks of age. All calves were fed twice daily at 1000 and 1600 h.
Experimental design
Experiment 1: effects of feeding At 3 and 12 weeks of age, at 1 day before blood sampling, calves were fitted with a catheter (type V-1; Top, Tokyo, Japan) in the left jugular vein under local anesthesia. The catheter was filled with sterile iso-osmotic sodium citrate (3.8% w/v) solution before and throughout the sampling. The blood sampling (4 ml each) was done every 15 min from 30 min before to 90 min after feeding (0930–1130 h). Animals were fed a milk-replacer diet (2000 ml) at the age of 3 weeks and, at 12 weeks of age, had free access to a calf-starter diet and hay for 30 min twice daily at 1000 and 1600 h. Blood samples were centrifuged at 8000 g for 15 min, and blood plasma was divided into three portions and stored at −30 °C until analysis.
Experiment 2: effects of feeding in animals maintained on a milk-replacer diet Five calves were maintained on a milk-replacer diet until 12 weeks of age, as previously described (Kitade et al. 2002, Yonekura et al. 2002). Another five animals were weaned at 7 weeks old and fed until 12 weeks of age, as age-matched controls. They were subjected to blood sampling at 12 weeks of age, as described in experiment 1.
Experiment 3: effects of venous injection of GHRH or GHRP-6 At the ages of 3 and 12 weeks, on the same day as for experiment 1, blood sampling (4 ml each) was conducted every 15 min for 90 min after the venous injection of hGHRH (0.25 μg/kg body mass) or GHRP-6 (2.5 μg/kg body mass) (1130–1400 h). The dose of GHRH (Peptide Research Institute, Osaka, Japan) was determined from our previous report (Matsunaga et al. 1997), whereas the dose of GHRP-6 (Peptide Research Institute) employed was 10 times greater than that of GHRH, because the potency of GHRP for GH-releasing activity has been found to be 10-fold less than that of GHRH (Ohata et al. 1997). The morning feed was given at 1000 h, but the afternoon feed was given after the final sample had been taken. The sampling and storage method of blood plasma was the same as described for experiment 1.
Analyses
The plasma concentrations of GH, insulin and IGF-I were measured by RIA, as previously described (Kuhara et al. 1991). The glucose concentration was determined by the glucose oxidase method, using a commercial kit (Glucose CII-Test; Wako Pure Chemicals, Osaka, Japan).
Statistics
The data at each sampling time were expressed as the mean± s.e.m. For the GH and insulin secretion curve data, AUC (area under the curve) was calculated and expressed as ng per min/ml and μU per min/ml, respectively.
The significance of the differences was determined by paired t-test to analyze the data within each hormone concentration curve, and by Student’s t-test between two groups (Zar 1984).
Results
Experiment 1: effects of feeding
Feeding of a milk-replacer diet in the 3-week-old group significantly increased the basal GH concentration, the peak value being 45.3 ± 7.5 ng/ml (n=6) at 60 min after feeding. In contrast, feeding of concentrate and hay in the 12-week-old group did not cause a significant change in GH concentrations (n=4). Consequently, there were significant differences between the two groups for 15–90 min after feeding. The AUC of GH for the 3-week-old group was significantly greater than that for the 12-week-old group (5547.9 ± 563.3 vs 1547.5 ± 404.1 ng per min/ml respectively; P=0.0009), as shown in Fig. 1B.
Plasma insulin concentration levels before feeding were significantly greater for the 12-week-old group than for the 3-week-old group, as shown in Fig. 2A (4.1±1.1 vs 16.1±2.3 μU/ml at 0 min respectively; P=0.0008). Feeding caused a significant increase in insulin concentrations in the 3-week-old group, the peak value being 34.1±4.7 μU/ml at 75 min after feeding. For the 12-week-old group, a nonsignificant increase in plasma insulin concentrations was noted after feeding. However, the AUC of insulin was still greater for the 12-week-old group than for the 3-week-old group (3033.5±424.5 vs 1637.7±105.0 μU per min/ml respectively; P=0.0088), as shown in Fig. 2B.
As depicted in Fig. 3, the prefeeding glucose level was significantly greater for the 12-week-old group than for the 3-week-old group (78.6±3.6 vs 56.1±5.5 mg/dl at 0 min respectively; P=0.0166). Feeding caused a significant increase in the 3-week-old group (from 55.1±6.2 to 89.3±3.5 mg/dl) only at 90 min after feeding.
IGF-I concentrations in plasma sampled just before feeding were slightly greater for the 12-week-old group than for the 3-week group (29.7±4.2 vs 20.4±3.9 ng/ml respectively; P=0.1390; not shown).
Experiment 2: effects of feeding in the animals maintained on a milk-replacer diet
The GH levels in the animals maintained on a milk-replacer diet until 12 weeks of age were not significantly different from that of the age-matched, weaned animals (Fig. 4A). Therefore, there was no significant difference in the GH AUC between the age-matched control group (n=5) and the group maintained on milk replacer (n=5) (1147.5±531.1 vs 1557.7±326.8 ng per min/ml respectively; P=0.1797; not shown).
In contrast, the postprandial insulin level of the group maintained on a milk-replacer diet drastically and significantly increased after feeding (Fig. 4B). The insulin AUC was, therefore, significantly greater for the group maintained on a milk-replacer diet than for the control group (11250.4±1750.3 vs 3125.2±375.6 μU per min/ml respectively; P=0.0001; not shown).
As also shown in Fig. 4C, there were no significant changes in postprandial glucose levels in the weaned control group. However, the glucose level of the group maintained on a milk-replacer diet significantly increased, and was significantly greater (P=0.0004) than that of the control group at 30–90 min after feeding (Fig. 4C).
Plasma concentrations of IGF-I before feeding were significantly greater in the group maintained on a milk-replacer diet than those of the control group (57.0±7.8 vs 31.4±4.3 ng/dl respectively; P=0.0017).
Experiment 3: effects of injection of GHRH or GHRP-6
The GH levels during the preinjection period were significantly greater in the 3-week-old group than those in the 12-week-old group, as shown in Fig. 5. The GHRH injection (0.25 μg/kg) significantly increased the GH level by 151 and 139 ng/ml respectively, for the 3-week and 12-week groups. Similarly, the GHRP-6 injection (2.5 μg/kg) also significantly increased the GH level, by 85 and 82 ng/ml respectively, for the 3-week and 12-week groups. The AUC for 3-week-old animals was greater than that for 12-week-old animals in both cases.
The injection of GHRH slightly increased (Fig. 6A), but GHRP-6 injection significantly increased (Fig. 6B) the insulin level of the 12-week-old group. The insulin AUC for GHRH and GHRP-6 injection for the 12-week-old group was significantly greater than that for 3-week-old group (P< 0.01).
Plasma glucose concentration was not significantly changed by the injection of GHRH or GHRP-6 (not shown).
Discussion
The present study clearly demonstrated that postprandial changes in plasma GH concentrations in 3-week-old (preweaning) calves are different from those in 12-week-old (postweaning) calves. Feeding commonly reduces plasma GH levels, as shown in sheep (Bassett 1974a,b, Driver & Forbes 1981, Trenkle 1989, Thomas et al. 1991, Matsunaga et al. 1998, 1999), calves (Moseley et al. 1988) and humans (Merimee & Fineberg 1974, Ishizuka et al. 1983, Jaffe et al. 1998), although it seemed to increase with feeding in lambs (Driver & Forbes 1981), steers (Moseley et al. 1988) and rats (Tannenbaum et al. 1976). Feeding-induced reductions in plasma GH levels become more apparent in adult animals under restricted feeding or at low feeding frequency during the day, because these conditions are known to raise basal GH levels and pulse amplitude (Thomas et al. 1990, 1991), and to reduce SRIF synthesis in the hypothalamus of sheep (Thomas et al. 1991, Henry et al. 2001). Feeding also reduces GHRH-induced GH release, and the response is mimicked by the anticipation of being fed, by distension of the rumen with a water-filled balloon, and sham-feeding (Trenkle 1989).
In the present study, the postprandial increase in GH levels shown in the milk-fed preweaning animals was abolished at 12 weeks of age, even though they were maintained on a milk-replacer diet. Therefore, the post-prandial GH increase shown in preweaning animals seems to be dependent on age-associated processes. A significantly greater IGF-I concentration for the 12-week-old animals maintained on the milk-replacer diet may have caused a greater inhibitory feedback action on GH release from the pituitary gland than in age-matched, weaned animals, as suggested by in vitro results with goat anterior pituitary cells (Katoh et al. 2004). In a previous study (Hammon & Blum 1997), however, postprandial GH response was not dependent on plasma IGF-I levels.
In the present study, basal and GHRH- or GHRP-stimulated GH secretion was greater for 3-week-old than for 12-week-old animals. We used GHRH as a central GH stimulant released from the hypothalamus and GHRP as a peripheral stimulant. In previous reports (Blanchard et al. 1988, Silverman et al. 1989), the basal GH release was age-dependently reduced in ovine pituitary cells isolated at different ages, and the maximum GH release was obtained in a 70-day-old fetus (term=147 days), in response to administration of GHRH and somatostatin. This and our preliminary study (Katoh & Obara 2001) indicate that bovine somatotrophs differentiate and possess GHRH receptors and the relevant intracellular signaling system at an early state of gestation, and that GH secretion in response to GHRH stimulation declines with the aging process in this species.
The mechanism underlying the difference in post-prandial GH levels between pre- and postweaning animals has yet to be clarified. It is known that ingested milk directly comes down into the omasum by passing through the reticular (esophageal) groove in preweaning, milk-fed animals (Ruckebusch 1988). The efferent limb of the groove-opening reflex contains cholinergic parasympathetic fibers, the transmitter of which is vasoactive intestinal peptide (VIP) (Reid et al. 1991). Therefore, the digestive tract is apparently able to detect and respond to the chemical and physical quality of diets, and to change a neural reflex to control GH secretion. Alternatively, Plouzek et al.(1988) reported that hypophysial stalk transection reduced the GH increase induced by GHRH stimulation, but feeding further reduced the GHRH-induced response in calves. These findings imply that the postprandial reduction in GH level is partly mediated by peripheral factors, as well as by the central nervous system. We postulated a physiologic role of short-chain fatty acids produced by microbes in the forestomachs (the reticulorumen), and have shown their involvement in the inhibitory mechanism for the postprandially reduced GH levels (Matsunaga et al. 1998, 1999, Katoh et al. 1999, Ishiwata et al. 2000, Katoh & Obara 2001). In addition, we recently demonstrated that leptin mRNA expression was increased by addition of acetate to the medium of primary cultured bovine anterior pituitary cells (Yonekura et al. 2003). Leptin is known as an inhibitor of GH secretion induced by GHRH in sheep pituitary cells (Roh et al. 1998).
It has been shown that feeding is accompanied by a reciprocal increase in peripheral plasma insulin, glucagon and SRIF concentrations (Bassett 1974b, Matsunaga et al. 1999). In the present study, the postprandial insulin response was greater in preweaning than that in postweaning animals, although basal levels were significantly greater in postweaning than in preweaning animals. It is likely that the postprandial increase in insulin concentration was due to milk ingestion in preweaning calves because the milk replacer contained a high concentration of proteins and fats as ingredients (24% proteins and 21% fats). Milk feeding caused hyperinsulinemia and hyperglycemia in the group maintained on a milk-replacer diet, as shown in the present experiment (Fig. 4) and a previous study (Blum & Hammon 1999). Higher basal glucose levels may be, at least in part, due to higher SGLT-1 expression in the small intestine and also to higher hepatic gluconeogenesis in milk-fed animals. This is likely because lambs maintained on a milk-replacer diet showed no reduction in SGLT-1 expression relative to age-matched animals (Lescal-Matys et al. 1993).
In 12-week-old calves, the GHRP-6 injection transiently but significantly increased plasma insulin concentrations. This may be caused by the direct action of GHRP on β cells, because rat pancreatic islets have been shown to synthesize ghrelin and GHS receptors (Guan et al. 1997), and ghrelin increases insulin release (Adeghate & Ponery 2002). This is not always the case in the human, however, because ghrelin has been shown to cause hyperglycemia and insulin suppression (Svensson et al. 1998, Broglio et al. 2001).
In conclusion, the feeding of milk in 3-week-old calves significantly increased plasma concentrations of GH, insulin and glucose, whereas feeding of concentrate and hay in 12-week-old animals did not cause a significant change in these parameters. However, feeding-induced GH secretion in the animals maintained on a milk-replacer diet until 12 weeks of age was not different from that in the age-matched, weaned group. The difference in postprandial responses may be explained by aging, by the difference in processes accompanied by quality of diets, or by altered neuroendocrine functions in the digestive–pituitary axis.
Postprandial changes in plasma GH concentrations (A) and GH AUC (B) in 3-week-old (n=6) and 12-week-old (n=4) calves. Animals were given a milk-replacer diet at 3 weeks of age, or concentrate and hay at 12 weeks of age. The values are represented as the mean ± s.e.m. Open symbols indicate a significant difference from the prefeeding level. *P< 0.05; **P< 0.01; ***P< 0.001.
Citation: Journal of Endocrinology 183, 3; 10.1677/joe.1.05898
Postprandial changes in plasma insulin concentrations (A) and insulin AUC (B) in 3-week-old (n=6) and 12-week-old (n=4) calves. Animals were fed as in Fig. 1. The values are represented as the mean±s.e.m. Open symbols indicate a significant difference from the prefeeding level. **P< 0.01; ***P< 0.001.
Citation: Journal of Endocrinology 183, 3; 10.1677/joe.1.05898
Postprandial changes in plasma glucose concentrations in 3-week-old (n=6) and 12-week-old (n=4) calves. Animals were fed as in Fig. 1. The values are represented as the mean±s.e.m. Open symbols indicate a significant difference from the prefeeding level. *P< 0.05.
Citation: Journal of Endocrinology 183, 3; 10.1677/joe.1.05898
Postprandial changes in plasma GH (A), insulin (B) and glucose (C) concentrations in weaned (n=5) or milk-fed (n=5) animals at 12 weeks of age. Unweaned, milk-fed animals were fed a milk-replacer diet until 12 weeks of age, whereas weaned (control) animals were fed concentrate and hay. The values are represented as the mean± s.e.m. Open symbols indicate a significant difference from the prefeeding level. *P< 0.05; **P< 0.01; ***P< 0.001.
Citation: Journal of Endocrinology 183, 3; 10.1677/joe.1.05898
Changes in plasma GH concentrations (A and B) and AUC (C) in response to the intravenous administration of GHRH (0.25 μg/kg) (A) or GHRP-6 (2.5 μg/kg) (B) in 3-week-old (n=6) and 12-week-old (n=4) calves. The animals were fed as in Fig. 1, and given either GH stimulant 2 h after feeding. The values are represented as the mean± s.e.m. Open symbols indicate a significant difference from the preweaning level. *P< 0.05; ** P< 0.01.
Citation: Journal of Endocrinology 183, 3; 10.1677/joe.1.05898
Changes in plasma insulin concentrations (A and B) and AUC (C) in response to the intravenous administration of GHRH (0.25 μg/kg) (A) or GHRP-6 (2.5 μg/kg) (B) in 3-week-old (n=6) or 12-week-old (n=4) calves. The animals were fed as in Fig. 1, and given either GH stimulant 2 h after feeding. The values are represented as the mean±s.e.m. Open symbols indicate a significant difference from the preweaning level. *< 0.05; **P< 0.01; ***P< 0.001.
Citation: Journal of Endocrinology 183, 3; 10.1677/joe.1.05898
This paper incorporates part of the master’s thesis by G. Furukawa submitted to Tohoku University in 2002. We thank Dr M.T. Rose (University of Wales, Aberystwyth, UK) for his kind advice on this paper and Dr A.F. Parlow for the ovine GH and antibodies to ovine GH and IGF-I provided by NIDDK (USA). The authors declare that there is no conflict of interest that would prejudice the impartiality of this scientific work.
References
Adeghate E & Ponery AS 2002 Ghrelin stimulates insulin secretion from the pancreas of normal and diabetec rats. Journal of Neuroendocrinology 14 555–560.
Bassett JM 1974a Early changes in plasma insulin and growth hormone levels after feeding in lambs and adult sheep. Australian Journal of Biological Science 27 157–166.
Bassett JM 1974b Diurnal patterns of plasma insulin, growth hormone, corticosteroid and metabolite concentrations in fed and fasted sheep. Australian Journal of Biological Science 27 167–181.
Blanchard MM, Goodyer CG, Charrier J & Barenton B 1988 In vitro regulation of growth hormone (GH) release from ovine pituitary cells during fetal and neonatal development: effects of GH-releasing factor, somatostatin, and insulin-like growth factor I. Endocrinology 122 2114–2120.
Blum JW & Hammon H 1999 Endocrine and metabolic aspects in milk-fed calves. Domestic Animal Endocrinology 17 219–230.
Broglio F, Arvat E, Benso A, Gottero C, Muccioli G, Papotti M, Van der Lely AJ, Deghenghi R & Ghigo E 2001 Ghrelin, a natural GH secretagogue produced by the stomach, induces hyperglycemia and reduces insulin secretion in humans. Journal of Clinical Endocrinology and Metabolism 86 5083–5086.
Clark PA & Rogol AD 1999 Somatic growth and its regulation. In Handbook of Physiology, Sec. 7, Vol. 5: Hormonal Control of Growth, pp 37–72. Vol. Ed. JL Kostyo. American Physiological Society. New York: Oxford University Press.
Driver PM & Forbes JM 1981 Episodic growth hormone secretion in sheep in relation to time of feeding, spontaneous meals and short term fasting. Journal of Physiology 317 412–424.
Guan XM, Yu H, Palyha OC, McKee KK, Feighner SD, Sirinathsinghji DJ, Smith RG, van der Ploeg LTH & Howard AD 1997 Distribution of mRNA encoding the growth hormone secretagogue receptor in brain and peripheral tissues. Brain Research: Molecular Brain Research 48 23–29.
Hammon H & Blum JW 1997 The somatotropic axis in neonate calves can be modulated by nutrition, growth hormone, and long-R3-IGF-I. American Journal of Physiology – Endocrinology and Metabolism 273 E130–E138.
Henry BA, Rao A, Tilbrook AJ & Clarke IJ 2001 Chronic food-deprivation alters the expression of somatostatin and growth hormone-releasing hormone in the ovariectomized ewe. Journal of Endocrinology 170 R1–R6.
Ishiwata H, Nagano M, Sasaki Y, Chen C & Katoh K 2000 Short-chain fatty acids inhibit the release and content of growth hormone in anterior pituitary cells of the goat. General and Comparative Endocrinology 118 400–406.
Ishizuka B, Quigley ME & Yen SSC 1983 Pituitary hormone release in response to food ingestion: evidence for neuroendocrine signals from gut to brain. Journal of Clinical Endocrinology and Metabolism 57 1111–1116.
Jaffe CA, Ocampo-Lim B, Guo W, Krueger K, Sugahara I, DeMottfriberg R, Ermann M & Barkan A 1998 Regulatory mechanisms of growth hormone secretion are sexually dimorphic. Journal of Clinical Investigation 102 153–164.
Katoh K & Obara Y 2001 Developmental and nutritional control of the somatotropic axis in the ruminant. Asian-Australasian Journal of Animal Science 14 (Special Issue) 91–99.
Katoh K, Ohata Y & Ishiwata H 1999 Suppressing effects of short-chain fatty acids on growth hormone (GH)-releasing hormone-induced GH release in isolated anterior pituitary cells of goats. Domestic Animal Endocrinology 17 85–93.
Katoh K, Shimoguchi R, Ishiwata H & Obara Y 2004 Rapid suppressing action of insulin-like growth factor-I (IGF-I) on GH release from anterior pituitary cells of goats. Domestic Animal Endocrinology 26 177–188.
Kitade K, Takahashi K, Yonekura S, Katsumata N, Furukawa, G, Osuga S, Nishita T, Katoh K & Obara Y 2002 Effects of nutritional conditions around weaning on carbonic anhydrase activity of the parotid gland and ruminal and abomasal epithelia of Holstein calves. Journal of Comparative Physiology B 172 379–385.
Kuhara T, Ikeda S, Ohneda A & Sasaki Y 1991 Effects of intravenous infusion of 17 amino acids on the secretion of GH, glucagon, and insulin in sheep. American Journal of Physiology 260 E21–E26.
Lamberts SWJ 1999 Introduction. In Growth Hormone Secretagogues, pp 1–4. Eds E Ghigo, M Boghen, FF Casanueva & C Dieguez. Amsterdam: Elsevier.
Lescale-Matys L, Dyer J, Scott D, Freeman TC, Wright EM & Shirazi-Beechey SP 1993 Regulation of the ovine intestinal Na+/glucose co-transporter (SLT-1) is dissociated from mRNA abundance. Biochemical Journal 291 435–440.
Matsunaga N, Goka T, Nam KT, Oda S, Ohneda A & Sasaki Y 1997 Inhibition of GH releasing factor (GRF)-induced GH secretion by intraruminal infusion of volatile fatty acids (VFA) in sheep. Endocrine Journal 44 133–140.
Matsunaga N, Wakiya M, Roh SG, Hirota M, He ML, Hidaka S & Hidari H 1998 Effect of cholinergic blockade on inhibited GH secretion by feeding and intraruminal SCFA infusion in sheep. American Journal of Physiology 274 E45–E51.
Matsunaga N, Arakawa NT, Goka T, Nam KT, Ohneda A, Sasaki Y & Katoh K 1999 Effects of ruminal infusion of volatile fatty acids on plasma concentration of growth hormone and insulin in sheep. Domestic Animal Endocrinology 17 17–27.
Merimee TJ & Fineberg SE 1974 Growth hormone secretion in starvation: a reassessment. Journal of Clinical Endocrinology and Metabolism 39 385–338.
Moseley WM, Alaniz GR, Claffin WH & Krabill LF 1988 Food intake alters the serum growth hormone response to bovine growth hormone-releasing factor in meal-fed Holstein steers. Journal of Endocrinology 117 253–259.
Ohata Y, Maruyama Y, Katoh K & Sasaki Y 1997 Growth hormone release induced by an amino acid mixture from primary cultured anterior pituitary cells of goats. Domestic Animal Endocrinology 14 99–107.
Plouzek CA, Molina JR, Hard DL, Vale WW, Rivier J, Trenkle A & Anderson LL 1988 Effects of growth hormone-releasing factor and somatostatin on growth hormone secretion in hypophysial stalk-transected beef calves. Proceedings of the Society for Experimental and Biological Medicine 189 158–167.
Reid AM, Post EJ & Titchen DA 1991 Control of the reticulo-omasal oriffice and related structures in the ruminant stomach. In Physiological Aspects of Digestion and Metabolism in Ruminants, pp 33–48. Eds T Tsuda, Y Sasaki & R Kawashima. San Diego, CA: Academic Press.
Roh SG, Clarke IJ, Xu RW, Goding JW, Loneragan K & Chen C 1998 The in vitro effect of leptin on basal and growth hormone-releasing hormone-stimulated growth hormone secretion from the ovine pituitary gland. Neuroendocrinology 68 361–364.
Ruckebusch Y 1988 Motility of the gastro-intestinal tract. In The Ruminant Animal, pp 64–107. Ed. DC Church. Englewood Cliffs, NJ: Prentice-Hall.
Silverman BL, Bettendorf M, Kaplan SL, Grumbach MM & Miller WL 1989 Regulation of growth hormone (GH) secretion by GH-releasing factor, somatostatin, and insulin-growth factor I in ovine fetal and neonatal pituitary cells in vitro. Endocrinology 124 84–89.
Simmen FA, Badinga L, Green ML, Kwak I, Song S & Simmen CM 1998 The porcine insulin-like growth factor system: at the interface of nutrition, growth and reproduction. Journal of Nutrition 128 315S–320S.
Svensson J, Lonn L, Jansson JO, Murphy G, Wyss D, Krupa D, Cerchio K, Polvino W, Gertz B, Boseaus I, Sjostrom L & Bengtsson BA 1998 Two-month treatment of obese subjects with the oral growth hormone (GH) secretagogue MK-677 increases GH secretion, fat-free mass, and energy expenditure. Journal of Clinical Endocrinology and Metabolism 83 362–369.
Tannenbaum GS & Epelbaum J 1999 Somatostatin. In Handbook of Physiology, sec. 7, vol. 5: Hormonal Control of Growth, pp 221–266. Vol. Ed. JL Kostyo. American Physiological Society. New York: Oxford University Press.
Tannenbaum GS, Martin JB & Colle E 1976 Ultradian growth hormone rhythm in the rat: effects of feeding, hyperglycemia, and insulin-induced hypoglycemia. Endocrinology 99 720–727.
Thomas GB, Mercer JE, Karalis T, Rao A, Cummins JT & Clarke IJ 1990 Effect of restricted feeding on the concentrations of growth hormone (GH), gonadotropins, and prolactin (PRL) in plasma, and on the amounts of messenger ribonucleic acid for GH, gonadotropin subunits, and PRL in the pituitary glands of adult ovariectomized ewes. Endocrinology 126 1361–1367.
Thomas GB, Cummins JT, Francis H, Sudbury AW, McCloud PI & Clarke IJ 1991 Effect of restricted feeding on the relationship between hypophysial portal concentrations of growth hormone (GH)-releasing factor and somatostatin, and jugular concentrations of GH in ovariectomized ewes. Endocrinology 128 1151–1158.
Trenkle A 1989 Influence of feeding on growth hormone secretion and response to growth hormone-releasing factor in sheep. Journal of Nutrition 119 61–65.
Yonekura S, Kitade K, Furukawa G, Takahashi K, Katsumata N, Katoh K & Obara Y 2002 Effects of aging and weaning on mRNA expression of leptin and CCK receptors in the calf rumen and abomasum. Domestic Animal Endocrinology 22 25–35.
Yonekura S, Senoo T, Kobayashi Y, Yonezawa T, Katoh K & Obara Y 2003 Effects of acetate and butyrate on the expression of leptin and short-form leptin receptor in bovine and rat anterior pituitary cells. General and Comparative Endocrinology 133 165–172.
Zar JH 1984 Biostatistical Analysis. Englewood Cliffs, NJ: Prentice-Hall.
