The Effect of Feeding on Plasma Immunoreactive ACTH andB-EndorphinLevels in Newborn Infant M. Gemelli, R. Manganaro1, Fr. DeLuca1, C. Imperatore , G. Costa and C. Mami1 Institute of Clinica Pediatrica and Institute of Farmacologia, University of Messina, Messina, Italy
In order to clarify whether an interaction between endogenous opioids and feeding occurs at birth, we studied Beta-endorphin (B-EP) and ACTH plasma levels in response to a feed of 10% glucose, or formula, in 120 healthy full-term infants. Neither postprandial B-EP nor ACTH increases were found at the 24 th hour or on the fourth day of life. B-EP physiology in newborn infants seems to be different from adults. Key words
During the first days of life glucose homeostasis is precarious and the basal and postfeeding plasma levels of several gastrointestinal regulatory peptides show dramatic changes (Aynsley-Green 1983). In the newborn infant it is known that the basal plasma levels of ACTH and B-EP are elevated only in the first day of life (Facchinetti, Bagnoli, Bracci and Genazzani 1982; Gemelli, Mami, Manganaro, De Luca, Saja and Costa 1988), but the plasma B-EP response to feeding has not been studied. In order to clarify whether the interaction between endogenous opioids and feeding occurs at birth, we studied ACTH and B-EP plasma levels in response to a feed of 10 % glucose, or formula, at the 24th hour and on the 4th day of life.
ACTH — Beta-Endorphin — Newborn Infant Material and Methods Introduction Endogenous opioid peptides have been shown to be widely distributed in tissues other than the central nervous system and pituitary. ACTH has been found in the myenteric plexus, in epithelial cells of small intestine and in pancreatic islets {Larson 1977). B-LPH (B-lipotropin) was detected in human colon (Odell, Wolf sen, Bachelot and Hirose 1979) and B-EP (Beta-Endorphin) in the gastrointestinal tract and pancreas (Orwall and Kendall 1980; Bruni, Waikins and Yen 1979; Matsumura, Saito and Fuijino 1982a). This extensive distribution suggests that opioids may be involved in peripheral functions in addition to those in the central nervous system (Lala, Boulox, Tamburrano and Gale 1987). In man, plasma BEP increases after the ingestion of glucose or a standard meal (Matsumura, Fukuda, Saito and Mori 1982b; Getto, Fullerton and Carlson 1984; Scavo, Facchinetti, Barletta, Petraglia, Buzzetti, Monaco, Giovannini and Genazzani 1987) and the administration of pharmacological doses of B-EP raises insulin levels
(ReidzndLYenim). These data indicate that circulating B-EP may play a role in modulation of glucose homeostasis through an interaction with opiate receptors in the gastrointestinal tract or pancreas (Lala et al. 1987; Giugliano, Torella, Lefebvre and D'Onofrio 1988). Horm.metab.Res.24(1992)39-41 © Georg Thieme Verlag Stuttgart -New York
After informed consent of the parents, 120 full-term newborn infants delivered vaginally after spontaneous labor were studied. Their gestational age ranged between 38 and 41 weeks and neonatal weight between 2800 and 3700 g. Their 1 min Apgar score was > 8 and no pathological conditions were present during the perinatal period. Each infant in the study contributed only two venous blood samples taken at the same time as blood required for routine clinical purposes. Infants were studied at the 24th hour (n = 60) or on the fourth (n = 60) day of life. Blood samples were collected just before and 5,20 or 60 minutes after the ingestion of a feed of 10% glucose or formula which contains 67 Kcal/100 ml. At each time period 20 blood samples were taken. The food volume was 20 ml at the 24th hour and 40 ml on the 4th day of life in accordance with hospital practice. Blood samples were immediately put in chilled heparinized tubes containing 500 KIU Trasylol, kept on ice and centrifuged within a few minutes, at 4 °C. Plasma was stored at — 30 °C and assays performed within 1 month. ACTH was measured by radioimmunoassay performed according to a modification of the method of Rees, Cook, Kendall, Allen, Kromer, Ratcliffe and Knight (1971). P-EP was measured by New England Nuclear B-endorphin radioimmunoassay Kit after plasma extraction with SEPPAK CI8 Columns (Waters Associates, Milford, NA) as previously described (Gemelli et al. 1988). The used B-EP antiserum had 20% cross reactivity with B-lipotropin.
Received: 2 Oct. 1990
Accepted: 23 June 1991
Downloaded by: University of British Columbia. Copyrighted material.
Summary
Horm. metab. Res. 24 (1992)
M. Gemelli, R. Manganaro, Fr. De Luca, C. Imperatore, G. Costa and C. Mami
Fig. 1 Plasma levels (mean±SD) of ACTH ( 0 - 0 ) and B-EP (•-•) on the 1st day of life after a formula (Fig. 1) or 10% glucose (Fig. 2) feed, and on the 4th day of life after a formula (Fig. 3) or 10% glucose (Fig. 4) feed. 20 samples were taken at each time period.
Intra- and interassay coefficients of variation were respectively less than 3.1% for ACTH and less than 3.5 % for B-EP. The statistical analysis of data was performed with two-way analysis of variance and with the Student's t-test. Results The Figures 1—4 show the basal and post-feeding plasma levels of ACTH and |3-EP in newborn infants at the 24th hour and on the fourth day of life. The mean (+ SD) basal plamsa concentrations of ACTH were 59.58 + 10.85 pg/ml at the 24th hour and 57.96 ± 12.56 pg/ml on the fourth day of life. The mean (+ SD) basal plasma concentrations of B-EP were 16.45 + 3.12 pmol/1 at the 24th hour and 17.09 + 3.47 pmol/1 on the foruth day of life. In both age groups, no change in plasma ACTH or B-EP concentrations occurred after the feeding.
Discussion B-EP has been intensely studied as a plasma marker for acute stress. In adults, plasma concentrations of BEP have been shown to increase in parallel with ACTH during pregnancy and labor (Csontos, Rust, Hollt, Mahr, Kroner and Teschemacher 1970), electroconvulsive therapy (Cork, Misiaszek, Finley, Hameroff and Scherer 1982), hypoglycemia (Nakao, Nakai, Jingami, Oki, Fukata and Imura 1979), surgery (Oyama, Tamigushi, Ishihara, Matsuki, Maeda, Murakawa and Kudo 1979) and exercise (Gambert, Garthwaite and Hagen 1980). The pituitary represents the main source of circulating levels of these peptides which derived from a common precursor, the proopiomelanocortin (POMC) (Guillemin, Vargo, Rossier, Minick, Ling, Rivier, Vale and Bloom 1977). In infants, it has been demonstrated that a strong stimulus for plasma P-EP and ACTH release is hypoxemia (Wardlaw, Stark, Baxi and Andrew 1979). In fact, high
Downloaded by: University of British Columbia. Copyrighted material.
40
Feeding, A CTA and |3 -Endorphin in Newborn Infants
Horm. metab. Res. 24 (1992)
41
Getto, C. J., D. T. Fullerton, I. H. Carlson: Plasma immunoreactive Bendorphin response to glucose ingestion in human obesity. Appetite 5: 329-334 (1984) Giugliano, D., R. Torella, P. J. Lefebvre, F. D'Onofrio: Opioid peptides and metabolic regulation. Diabetologica 31: 3—15 (1988) Guillemin, R., T. M. Vargo, J. Rossier, J. Minick, N. Ling, C. Rivier, W. Vale, F. Bloom:B-endorphinand adrenocorticotropin are secreted concomitantly by the pituitary gland. Science 197: 1367-1369 (1977) Lala, A., P. Boulox, G. Tamburrano, E. Gale: Opioid peptides and glucose metabolism. J. Endocrinol. Invest. 10:95—104(1987) Larson, L. I.: Corticotropin-like peptides in central nerves and in endocrine cells of gut and pancreas. Lancet 2:1321 — 1323(1977) In adults, the source of the postprandial inLeRoith, D., I. M. Spitz, R. Ebert, Y. Liel, S. Odes, W. Creutzfeldt: crease of plasma P-EP levels is the gastrointestinal tract and its Acid-induced gastric inhibitory polypeptide secretion in man. J. Clin. Endocrinol. Metab. 51: 1385-1389(1980) release is stimulated by gastric acid (Matsumura et al. 1982b). Lucas, A., T. E. Adrian, S. R. Bloom, A. Aynsley-Green: Plasma secreThe lack of P-EP response to feeding in infants may be due tion in neonates. Acta Paediatr. Scand. 69:205-210(1980) both to gastrointestinal immaturity of P-EP release mechanism Lucas, A., D. L. Sarson, S. R. Bloom, A. Aynsley-Green: Developmenor to deficit of gastric acid output demonstrated also by us in tal aspects of gastric inhibitory polypeptide (GIP) and its possible infants {Magazzii, Gemelli, Pustorino, Turiano, Arrigo, Barberole in the insular axis in neonates. Acta Paediatr. Scand. 69: 321 — rio, Conti Nibali, Sferlazzas and Ferrau 1981). The latter hy325 (1980) pothesis is more likely since the post-feeding release of other Magazzii, G., M. Gemelli, S. Pustorino, S. Turiano, M. Arrigo, G. Barberio, S. Conti Nibali, C. Sferlazas, O. Ferrau: Gastrinemia e gut hormones which is also stimulated by duodenal acidificasecrezione acida gastrica durante i primi 5 giorni di vita. Min. Ped. tion, such as secretin and GIP (gastric inhibitory polypeptide), 33: 11-16(1981) is not present in the neonate (Lucas, Adrian, Bloom and AynMatsumura, M., S. Saito, M. Fuijino: Effects of solution of low ph and sley-Green 1980; LeRoith, Spitz, Ebert, Liel, Odes and Creutztaurocholate on release of B-endorphin-like immunoreactivity feldt 1980; Lucas, Sarson, Bloom and Aynsley-Green 1980). from duodenal mucosa in vitro. Regul. Peptides 3: 173-181 (1982a) Matsumura, M., N. Fukuda, S. Saito, M. Mori: Effect of a test meal, It is known that the hormonal and metabolic duodenal acidification and tetragastrin on the plasma concenresponses to feeding in neonate are different from those in tration of B-endorphin like immunoreactivity in man. Regul. Pepadult, and the transmission of signal from the gut to pancreas tides 4: 173-181 (1982b) islets, the so-called entero-insular axis, is blocked (AynsleyNakao, K, Y. Nakai, H. Jingami, S. Oki, J. Fukata, H. Imura: SubGreen 1983). Since P-EP modulates also pancreatic islet horstantial rise of plasma B-endorphin levels after insulin-induced hymone secretin (Lata et al. 1987), it could have a part in the enpoglycemia in human subjects. J. Clin. Endocrinol. Metab. 49: tero-insular axis regulation. If this is true the lack of p-EP re838-841 (1979) Odell, W. D., A. R. Wolfsen, I. Bachelot, F. M. Hirose: Ectopic producsponse to feeding, observed in the neonate could be an attempt tion of lipotropinby cancer. Am. J. Med. 66:631—638 (1979) to prevent excessive insulin release, which may disturb the preOrwall, E. S., J. C. Kendall:B-endorphinand adrenocorticotropin in carious glucose homeostasis present at this age. extrapituitary sites: gastrointestinal tract. Endocrinology 107: 438-442(1980) Further investigation of the development of Oyama, T, K. Tanigushi, H. Ishihara, A. Matsuki, A. Maeda, T the P-EP response to feeding could contribute suggestions on Murakawa, T. Kudo: Effects of enflurance anesthesia and surgery on endocrine function in man. Br. J. Anesth. 51:141 — 148(1979) the physiological significance of the postprandial P-EP gut reRees, L. H., D. M. Cook, J. W. Kendall, C. F. Allen, R. M. Kromer, J. G. lease. Ratcliffe, R. A. Knight: A radioimmunoassay for rat plasma ACTH. Endocrinology 89:254-258 (1971) References Reid, R., S. S. C. Yen: B-endorphin stimulates the secretion of insulin and glucagon in humans. J. Clin. Endocrinol. Metab. 52: 592—594 Aynsley-Green, A.: Hormones and postnatal adaptation to enteral (1983) nutrition. J. Pediatr. Gastroenterol. Nutr. 2:418 -427 (1983) Sankaran, K., K. W. Hindmarsh, V. Watson: Perinatal asphyxia and Bruni, J. F., W. B. Watkins, S. S. C. Yen: p-endorphin in the human plasmaB-endorphins.(Abstract) Pediatr. Res. 18: 382A (1984) pancreas. J. Clin. Endocrinol. Metab. 49:645-651 (1979) Scavo, D., F. Facchinetti, C. Barletta, F. Petraglia, R. Buzzetti, M. Cork, R. C, J. Misiszek, J. Finley, S. R. Hameroff, K. Scherer: Effect of Monaco, C. Giovannini, R. Genazzani: Plasma P-endorphin in reelectroconvulsive therapy on plasma beta endorphin (Abstract) sponse to oral glucose tolerance test in obese patients. Horm. Anesthesiology 57: A301 (1982) Metabol. Res. 19: 204-207 (1987) Csontos, K., M. Rust, V. Hollt, U. Mahr, W. Kromer, H. J. Tesche- Wardlaw, S. L., R. I. Stark, L. Baxi, G. Andrew: Plasma P-endorphin macher: Elevated plasma B-endorphin levels in pregnant women and B-lipotropin in the human fetus at delivery: Correlation with and their neonates. Life Sci. 25:835-844(1970) arterial pH and p02. I. Clin. Endocrinol. Metab. 49: 888-891 Facchinetti, F., F. Bagnoli, R. Bracci, R. Genazzani: Plasma opioids in (1979) the firsthoursoflife. Pediatr. Res. 16:95-98(1982) Gambert, S. R., T. L. Garthwaite, T. C. Hagen: Running increases plasma beta endorphin (EP) in man. (Abstract) Clin. Res. 28: 720A(1980) Requests for reprints should be addressed to: Gemelli, M., C. Mami, R. Manganaro, Fr. De Luca, A. Saja, G. Costa: Correlation between plasma levels of ACTH and p-endorphin. J. Prof. Marina Gemelli Endocrinol. Invest. 11:395-398 (1988) Istituto di Clinica Pediatrica Universita di Messina, Policlinico 1-98100 Messina (Italy)
Downloaded by: University of British Columbia. Copyrighted material.
plasma levels of these peptides have been found at birth (Facchinetti et al. 1982) and in neonates with hypoxic-ischemic encephalopathy associated with ongoing hypoxemia {Sankaran, Hindmarsh and Watson 1984). The significant correlation between B-EP and ACTH plasma levels found by us in the neonate (Gemelli et al. 1988) suggests a common source and a same secretory process for these peptides in normal adult and infant. Now, the unchanged post-feeding levels of ACTH and |3-EP found by us during the first four days of life indicate differences from the adult pattern in peripheral release of P-EP.
In order to clarify whether an interaction between endogenous opioids and feeding occurs at birth, we studied Beta-endorphin (B-EP) and ACTH plasma levels in response to a feed of 10% glucose, or formula, in 120 healthy full-term infants. Neither postprandial B-EP nor ACTH increases were found at the 24 th hour or on the fourth day of life. B-EP physiology in newborn infants seems to be different from adults. Key words
During the first days of life glucose homeostasis is precarious and the basal and postfeeding plasma levels of several gastrointestinal regulatory peptides show dramatic changes (Aynsley-Green 1983). In the newborn infant it is known that the basal plasma levels of ACTH and B-EP are elevated only in the first day of life (Facchinetti, Bagnoli, Bracci and Genazzani 1982; Gemelli, Mami, Manganaro, De Luca, Saja and Costa 1988), but the plasma B-EP response to feeding has not been studied. In order to clarify whether the interaction between endogenous opioids and feeding occurs at birth, we studied ACTH and B-EP plasma levels in response to a feed of 10 % glucose, or formula, at the 24th hour and on the 4th day of life.
ACTH — Beta-Endorphin — Newborn Infant Material and Methods Introduction Endogenous opioid peptides have been shown to be widely distributed in tissues other than the central nervous system and pituitary. ACTH has been found in the myenteric plexus, in epithelial cells of small intestine and in pancreatic islets {Larson 1977). B-LPH (B-lipotropin) was detected in human colon (Odell, Wolf sen, Bachelot and Hirose 1979) and B-EP (Beta-Endorphin) in the gastrointestinal tract and pancreas (Orwall and Kendall 1980; Bruni, Waikins and Yen 1979; Matsumura, Saito and Fuijino 1982a). This extensive distribution suggests that opioids may be involved in peripheral functions in addition to those in the central nervous system (Lala, Boulox, Tamburrano and Gale 1987). In man, plasma BEP increases after the ingestion of glucose or a standard meal (Matsumura, Fukuda, Saito and Mori 1982b; Getto, Fullerton and Carlson 1984; Scavo, Facchinetti, Barletta, Petraglia, Buzzetti, Monaco, Giovannini and Genazzani 1987) and the administration of pharmacological doses of B-EP raises insulin levels
(ReidzndLYenim). These data indicate that circulating B-EP may play a role in modulation of glucose homeostasis through an interaction with opiate receptors in the gastrointestinal tract or pancreas (Lala et al. 1987; Giugliano, Torella, Lefebvre and D'Onofrio 1988). Horm.metab.Res.24(1992)39-41 © Georg Thieme Verlag Stuttgart -New York
After informed consent of the parents, 120 full-term newborn infants delivered vaginally after spontaneous labor were studied. Their gestational age ranged between 38 and 41 weeks and neonatal weight between 2800 and 3700 g. Their 1 min Apgar score was > 8 and no pathological conditions were present during the perinatal period. Each infant in the study contributed only two venous blood samples taken at the same time as blood required for routine clinical purposes. Infants were studied at the 24th hour (n = 60) or on the fourth (n = 60) day of life. Blood samples were collected just before and 5,20 or 60 minutes after the ingestion of a feed of 10% glucose or formula which contains 67 Kcal/100 ml. At each time period 20 blood samples were taken. The food volume was 20 ml at the 24th hour and 40 ml on the 4th day of life in accordance with hospital practice. Blood samples were immediately put in chilled heparinized tubes containing 500 KIU Trasylol, kept on ice and centrifuged within a few minutes, at 4 °C. Plasma was stored at — 30 °C and assays performed within 1 month. ACTH was measured by radioimmunoassay performed according to a modification of the method of Rees, Cook, Kendall, Allen, Kromer, Ratcliffe and Knight (1971). P-EP was measured by New England Nuclear B-endorphin radioimmunoassay Kit after plasma extraction with SEPPAK CI8 Columns (Waters Associates, Milford, NA) as previously described (Gemelli et al. 1988). The used B-EP antiserum had 20% cross reactivity with B-lipotropin.
Received: 2 Oct. 1990
Accepted: 23 June 1991
Downloaded by: University of British Columbia. Copyrighted material.
Summary
Horm. metab. Res. 24 (1992)
M. Gemelli, R. Manganaro, Fr. De Luca, C. Imperatore, G. Costa and C. Mami
Fig. 1 Plasma levels (mean±SD) of ACTH ( 0 - 0 ) and B-EP (•-•) on the 1st day of life after a formula (Fig. 1) or 10% glucose (Fig. 2) feed, and on the 4th day of life after a formula (Fig. 3) or 10% glucose (Fig. 4) feed. 20 samples were taken at each time period.
Intra- and interassay coefficients of variation were respectively less than 3.1% for ACTH and less than 3.5 % for B-EP. The statistical analysis of data was performed with two-way analysis of variance and with the Student's t-test. Results The Figures 1—4 show the basal and post-feeding plasma levels of ACTH and |3-EP in newborn infants at the 24th hour and on the fourth day of life. The mean (+ SD) basal plamsa concentrations of ACTH were 59.58 + 10.85 pg/ml at the 24th hour and 57.96 ± 12.56 pg/ml on the fourth day of life. The mean (+ SD) basal plasma concentrations of B-EP were 16.45 + 3.12 pmol/1 at the 24th hour and 17.09 + 3.47 pmol/1 on the foruth day of life. In both age groups, no change in plasma ACTH or B-EP concentrations occurred after the feeding.
Discussion B-EP has been intensely studied as a plasma marker for acute stress. In adults, plasma concentrations of BEP have been shown to increase in parallel with ACTH during pregnancy and labor (Csontos, Rust, Hollt, Mahr, Kroner and Teschemacher 1970), electroconvulsive therapy (Cork, Misiaszek, Finley, Hameroff and Scherer 1982), hypoglycemia (Nakao, Nakai, Jingami, Oki, Fukata and Imura 1979), surgery (Oyama, Tamigushi, Ishihara, Matsuki, Maeda, Murakawa and Kudo 1979) and exercise (Gambert, Garthwaite and Hagen 1980). The pituitary represents the main source of circulating levels of these peptides which derived from a common precursor, the proopiomelanocortin (POMC) (Guillemin, Vargo, Rossier, Minick, Ling, Rivier, Vale and Bloom 1977). In infants, it has been demonstrated that a strong stimulus for plasma P-EP and ACTH release is hypoxemia (Wardlaw, Stark, Baxi and Andrew 1979). In fact, high
Downloaded by: University of British Columbia. Copyrighted material.
40
Feeding, A CTA and |3 -Endorphin in Newborn Infants
Horm. metab. Res. 24 (1992)
41
Getto, C. J., D. T. Fullerton, I. H. Carlson: Plasma immunoreactive Bendorphin response to glucose ingestion in human obesity. Appetite 5: 329-334 (1984) Giugliano, D., R. Torella, P. J. Lefebvre, F. D'Onofrio: Opioid peptides and metabolic regulation. Diabetologica 31: 3—15 (1988) Guillemin, R., T. M. Vargo, J. Rossier, J. Minick, N. Ling, C. Rivier, W. Vale, F. Bloom:B-endorphinand adrenocorticotropin are secreted concomitantly by the pituitary gland. Science 197: 1367-1369 (1977) Lala, A., P. Boulox, G. Tamburrano, E. Gale: Opioid peptides and glucose metabolism. J. Endocrinol. Invest. 10:95—104(1987) Larson, L. I.: Corticotropin-like peptides in central nerves and in endocrine cells of gut and pancreas. Lancet 2:1321 — 1323(1977) In adults, the source of the postprandial inLeRoith, D., I. M. Spitz, R. Ebert, Y. Liel, S. Odes, W. Creutzfeldt: crease of plasma P-EP levels is the gastrointestinal tract and its Acid-induced gastric inhibitory polypeptide secretion in man. J. Clin. Endocrinol. Metab. 51: 1385-1389(1980) release is stimulated by gastric acid (Matsumura et al. 1982b). Lucas, A., T. E. Adrian, S. R. Bloom, A. Aynsley-Green: Plasma secreThe lack of P-EP response to feeding in infants may be due tion in neonates. Acta Paediatr. Scand. 69:205-210(1980) both to gastrointestinal immaturity of P-EP release mechanism Lucas, A., D. L. Sarson, S. R. Bloom, A. Aynsley-Green: Developmenor to deficit of gastric acid output demonstrated also by us in tal aspects of gastric inhibitory polypeptide (GIP) and its possible infants {Magazzii, Gemelli, Pustorino, Turiano, Arrigo, Barberole in the insular axis in neonates. Acta Paediatr. Scand. 69: 321 — rio, Conti Nibali, Sferlazzas and Ferrau 1981). The latter hy325 (1980) pothesis is more likely since the post-feeding release of other Magazzii, G., M. Gemelli, S. Pustorino, S. Turiano, M. Arrigo, G. Barberio, S. Conti Nibali, C. Sferlazas, O. Ferrau: Gastrinemia e gut hormones which is also stimulated by duodenal acidificasecrezione acida gastrica durante i primi 5 giorni di vita. Min. Ped. tion, such as secretin and GIP (gastric inhibitory polypeptide), 33: 11-16(1981) is not present in the neonate (Lucas, Adrian, Bloom and AynMatsumura, M., S. Saito, M. Fuijino: Effects of solution of low ph and sley-Green 1980; LeRoith, Spitz, Ebert, Liel, Odes and Creutztaurocholate on release of B-endorphin-like immunoreactivity feldt 1980; Lucas, Sarson, Bloom and Aynsley-Green 1980). from duodenal mucosa in vitro. Regul. Peptides 3: 173-181 (1982a) Matsumura, M., N. Fukuda, S. Saito, M. Mori: Effect of a test meal, It is known that the hormonal and metabolic duodenal acidification and tetragastrin on the plasma concenresponses to feeding in neonate are different from those in tration of B-endorphin like immunoreactivity in man. Regul. Pepadult, and the transmission of signal from the gut to pancreas tides 4: 173-181 (1982b) islets, the so-called entero-insular axis, is blocked (AynsleyNakao, K, Y. Nakai, H. Jingami, S. Oki, J. Fukata, H. Imura: SubGreen 1983). Since P-EP modulates also pancreatic islet horstantial rise of plasma B-endorphin levels after insulin-induced hymone secretin (Lata et al. 1987), it could have a part in the enpoglycemia in human subjects. J. Clin. Endocrinol. Metab. 49: tero-insular axis regulation. If this is true the lack of p-EP re838-841 (1979) Odell, W. D., A. R. Wolfsen, I. Bachelot, F. M. Hirose: Ectopic producsponse to feeding, observed in the neonate could be an attempt tion of lipotropinby cancer. Am. J. Med. 66:631—638 (1979) to prevent excessive insulin release, which may disturb the preOrwall, E. S., J. C. Kendall:B-endorphinand adrenocorticotropin in carious glucose homeostasis present at this age. extrapituitary sites: gastrointestinal tract. Endocrinology 107: 438-442(1980) Further investigation of the development of Oyama, T, K. Tanigushi, H. Ishihara, A. Matsuki, A. Maeda, T the P-EP response to feeding could contribute suggestions on Murakawa, T. Kudo: Effects of enflurance anesthesia and surgery on endocrine function in man. Br. J. Anesth. 51:141 — 148(1979) the physiological significance of the postprandial P-EP gut reRees, L. H., D. M. Cook, J. W. Kendall, C. F. Allen, R. M. Kromer, J. G. lease. Ratcliffe, R. A. Knight: A radioimmunoassay for rat plasma ACTH. Endocrinology 89:254-258 (1971) References Reid, R., S. S. C. Yen: B-endorphin stimulates the secretion of insulin and glucagon in humans. J. Clin. Endocrinol. Metab. 52: 592—594 Aynsley-Green, A.: Hormones and postnatal adaptation to enteral (1983) nutrition. J. Pediatr. Gastroenterol. Nutr. 2:418 -427 (1983) Sankaran, K., K. W. Hindmarsh, V. Watson: Perinatal asphyxia and Bruni, J. F., W. B. Watkins, S. S. C. Yen: p-endorphin in the human plasmaB-endorphins.(Abstract) Pediatr. Res. 18: 382A (1984) pancreas. J. Clin. Endocrinol. Metab. 49:645-651 (1979) Scavo, D., F. Facchinetti, C. Barletta, F. Petraglia, R. Buzzetti, M. Cork, R. C, J. Misiszek, J. Finley, S. R. Hameroff, K. Scherer: Effect of Monaco, C. Giovannini, R. Genazzani: Plasma P-endorphin in reelectroconvulsive therapy on plasma beta endorphin (Abstract) sponse to oral glucose tolerance test in obese patients. Horm. Anesthesiology 57: A301 (1982) Metabol. Res. 19: 204-207 (1987) Csontos, K., M. Rust, V. Hollt, U. Mahr, W. Kromer, H. J. Tesche- Wardlaw, S. L., R. I. Stark, L. Baxi, G. Andrew: Plasma P-endorphin macher: Elevated plasma B-endorphin levels in pregnant women and B-lipotropin in the human fetus at delivery: Correlation with and their neonates. Life Sci. 25:835-844(1970) arterial pH and p02. I. Clin. Endocrinol. Metab. 49: 888-891 Facchinetti, F., F. Bagnoli, R. Bracci, R. Genazzani: Plasma opioids in (1979) the firsthoursoflife. Pediatr. Res. 16:95-98(1982) Gambert, S. R., T. L. Garthwaite, T. C. Hagen: Running increases plasma beta endorphin (EP) in man. (Abstract) Clin. Res. 28: 720A(1980) Requests for reprints should be addressed to: Gemelli, M., C. Mami, R. Manganaro, Fr. De Luca, A. Saja, G. Costa: Correlation between plasma levels of ACTH and p-endorphin. J. Prof. Marina Gemelli Endocrinol. Invest. 11:395-398 (1988) Istituto di Clinica Pediatrica Universita di Messina, Policlinico 1-98100 Messina (Italy)
Downloaded by: University of British Columbia. Copyrighted material.
plasma levels of these peptides have been found at birth (Facchinetti et al. 1982) and in neonates with hypoxic-ischemic encephalopathy associated with ongoing hypoxemia {Sankaran, Hindmarsh and Watson 1984). The significant correlation between B-EP and ACTH plasma levels found by us in the neonate (Gemelli et al. 1988) suggests a common source and a same secretory process for these peptides in normal adult and infant. Now, the unchanged post-feeding levels of ACTH and |3-EP found by us during the first four days of life indicate differences from the adult pattern in peripheral release of P-EP.
