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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma concentrations of glucose, alanine, and glucagon were measured after 24 hour fasting in newborn and infant sheep and in response to infusion of alanine alone and concurrently with theophylline. The plasma glucagon response to alanine was minimal in newborn sheep; in contrast, alanine produced a brisk response in plasma glucagon concentration in infant sheep. Glucose concentrations were unchanged in both groups. Theophylline enhanced blood glucagon and glucose responses to alanine in newborn animals but had minimal effects on the response of the infant sheep. These data, considered with earlier data in fetal sheep, suggest a progressive maturation of pancreatic islet alpha-cell glucagon secretion in the sheep during the postnatal period and suggest that the blunted glucagon response observed in the neonate is related to immaturity of the glucagon secretion mechanisms rather than deficient synthesis of the hormone. This immaturity may be related to impaired synthesis and/or enhanced degradation of cyclic adenosine monophosphate (cAMP) or to diminished responsiveness to cAMP.
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PMID:Effects of fasting and theophylline on alanine-stimulated glucagon secretion in neonatal and infant sheep. 17 57

Insulin release was studied in vitro using pieces of pancreas from rabbits of between 24 days gestational age and 6 weeks postnatal age. When allowance was made for the fraction of pancreas which was endocrine, 16-5mM-glucose caused increasing stimulation of insulin release as development advanced and 3-3 mM-glucose caused a similar rate of secretion at all ages. Secretion was not significantly influenced by insulin destruction in the incubation medium. Glucagon (5 mug/ml) did not stimulate insulin secretion from 24-day foetal pancreas but did so postnatally. Theophylline (1 mmol/1) stimulated insulin release at all ages and was equipotent on 24-day foetal pancreas in 3-3 or 16-5 mM-glucose. The stimulation of insulin release from 24-day foetal pancreas by 1 mM-theophylline occurred in the absence of extracellular glucose, pyruvate, fumarate and glutamate and in the presence of mannoheptulose and 2-deoxyglucose (each 3 mg/ml). Adrenaline (1 mumol/1) and diazoxide (250 mug/ml) abolished or attenuated the stimulation of insulin release by glucose, leucine plus arginine or theophylline from 24-day foetal, 1 day and 6 weeks postnatal pancreas. The stimulation of insulin release from 6-week-old pancreas by 1mM-barium was blocked by adrenaline and diazoxide but the effect became less with increasing immaturity. The experimental results illustrate some of the ways in which insulin secretion by the rabbit beta cell changes as a function of development and draw attention to the importance of glucose and cyclic adenosine monophosphate in this process.
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PMID:Development of pathways of insulin secretion in the rabbit. 109 Jun 94

This is the first study investigating hormone secretion by the isolated perfused pancreas of the aged Fischer 344 rat. Nutrient-induced release of insulin, glucagon, and somatostatin in overnight-fasted rats aged 2, 10, 18, 24, and 30 mo was studied. After an equilibration period, the pancreas was perfused for 20 min with buffer A (containing 4.2 mM glucose plus a 3.5 mM mixture of amino acids) then for 20 min with buffer B (containing 8.3 mM glucose and 7.0 mM amino acids). When stimulated by buffer B, the amount of insulin secreted increased (P less than 0.05) from immaturity (2 mo) to adulthood (10-18 mo) because of growth of the organ. From adulthood to very old age an equal amount of insulin was released in all groups during the last 19 min of perfusion with buffer B. Fasting blood glucose levels remained constant throughout life, whereas pancreatic insulin stores and plasma insulin levels rose, reaching peak values at 18 mo. The alpha-cell appeared to be deemphasized relative to the beta-cell during development but not thereafter, as indicated by the findings that from immaturity to adulthood pancreatic glucagon stores expanded less than insulin stores and that glucagon release significantly decreased. Only minor changes in somatostatin release from the delta-cells were observed after the rat reached adulthood. We conclude that the endocrine secretory response of the pancreas is well maintained throughout life in the Fischer 344 rat.
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PMID:Hormone secretion by isolated perfused pancreas of aging Fischer 344 rats. 167 Sep 77

In the neonatal period of the rat, pancreatic thyrotropin-releasing hormone content decreases and the sensitivity of insulin secretion to glucose increases. In adult rat islets, TRH inhibits glucose-induced insulin release. The aim of this study was to investigate whether a high TRH content and release can be part of the explanation for the functional immaturity of neonatal islets. For that purpose, we have measured the tissue content and the secretion of immunoreactive insulin, glucagon, somatostatin and TRH in islets from 21.5-day-old rat fetuses cultured for up to one week. Insulin, glucagon and somatostatin content increased during one week of culture in the presence of 11.1 mmol/l glucose. The TRH content decreased during culture, but did not equal adult values. Insulin, glucagon and somatostatin responses to glucose were present after one week of culture. Glucose had no effect on TRH release in cultured fetal islets, but inhibited TRH release in adult islets. We conclude that glucose can stimulate insulin secretion without inhibiting TRH release, but that a decrease in islet TRH content and a sensitization of TRH secretion to glucose may be important in the full maturation of fetal pancreatic islets.
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PMID:Insulin, glucagon, somatostatin, and thyrotropin-releasing hormone content and secretion by perifused fetal rat islets during culture. 197 58

Glucagon and its second messenger, cAMP, are known to rapidly block expression of the L-type pyruvate kinase gene and to stimulate expression of phosphoenolpyruvate (PEP) carboxykinase gene in the liver in vivo. The respective roles, however, of hyperglucagonemia, insulinopenia, and carbohydrate deprivation in the inhibition of L-type pyruvate kinase gene expression during fasting are poorly understood. In addition, the long-term effects of physiological hyperglucagonemia on expression of the two genes are not known. In this study, we investigate the effects of long-term physiological hyperglucagonemia and insulinopenia induced by suckling (which provides a high-fat, low-carbohydrate diet) on expression of the two genes in the liver of normal newborn rats. We show that transcription of the L-type pyruvate kinase gene is inhibited at birth and remains low during the whole suckling period, whereas transcription of the PEP carboxykinase gene is maximal in the neonate, and then decreases despite very high levels of plasma glucagon during suckling. In contrast to the adult, however, in which L-type pyruvate kinase gene expression in the liver is blocked by cAMP and stimulated by carbohydrates, the regulation of L-type pyruvate kinase gene expression in the newborn undergoes a developmental maturation: the inhibitory effect of glucagon is never complete in developing rat liver and the stimulatory effect of glucose could not be detected during suckling, due to either hyperglucagonemia, immaturity of the gene regulatory system, or both.
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PMID:In vivo regulation of glycolytic and gluconeogenic enzyme gene expression in newborn rat liver. 283 19

High plasma concentrations of C-terminal immunoreactive glucagon (IRG) have been found during early life in several mammalian species. We have analyzed the plasma IRG of 12 h to 60 day-old dogs in terms of the 4 peaks (IRG greater than 20,000, IRG9000, IRG3500 and IRG2000) obtained by gel filtration on Bio-Gel P-30. Significant changes with age and in response to administered agents were confined to IRG9000 and IRG3500. IRG9000 was 9-fold higher in 12-36 h old dogs than in adults (108 +/- 24 pg/ml pancreatic glucagon equivalents v. 12 +/- 3 pg/ml, mean +/- SEM) and showed a decline to 2-fold higher (27 +/- 5 pg/ml) at 31-60 days. IRG3500 was higher than in the adult only during the first 36 h of life (36 +/- 5 pg/ml v. 15 +/- 3 pg/ml). Arginine infusion (0.5 g/kg over 15 min) caused an increase in plasma levels of both IRG9000 and IRG3500 in the newborn, whereas in adult dogs only IRG3500 was increased. Insulin injection (0.2 U/kg intravenously) causing a marked hypoglycemia had no significant effect on the plasma level of any IRG component in newborn dogs. Dihydrosomatostatin infusion (10 micrograms/kg bolus +/- 90 micrograms/kg over 30 min) caused a decrease in both IRG9000 and IRG3500. The increased basal level and secretory response to arginine of IRG9000 in newborn dogs may reflect an immaturity of the A cells, whereby more of this component, which may represent a precursor of pancreatic glucagon, is secreted than in the adult. The immature A cells also appear to have an impaired secretory response to hypoglycemia.
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PMID:Plasma glucagon-immunoreactive components in early life in dogs. 286 2

The ontogeny of insulin, glucagon, PP and somatostatin in the mammalian fetal pancreas has been examined in recent years largely by immunocytochemistry and in some instances by radioimmunoassay. Complete ontogenic data are available only for the rat, human, pig and sheep. Figure 3 compares the time of appearance of the endocrine cell-types within the fetal pancreas when the periods of gestation of the four species are converted to a uniform scale. The striking ontogenic difference in the rat probably reflects the immaturity of the rodent fetus at birth compared with the human, pig and sheep. In the fetal pancreas, differences in cell number of glucagon and PP cells in the dorsal and ventral lobes become apparent from an early gestational period. Factors responsible for the functional and structural maturation of the fetal pancreatic endocrine cells and the processes involved in pancreatic organogenesis are poorly understood. Studies in these areas would have clinical implications since it may be possible in the future to employ agents for selective replication of fetal beta-cells for transplantation in patients with Type I diabetes, bearing in mind that such cells must have the capacity to respond to normal stimuli and repressors when transplanted. The presence of the other islet cell-types may be obligatory for these appropriate responses. This would require a more complete knowledge of those factors which produce the normal selectivity of the four hormonal cell-types.
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PMID:Ontogenic development of peptide hormones in the mammalian fetal pancreas. 289 13

When compared to adults, muscle mass in children is lower and the relative development of aerobic and anaerobic pathways is different. The main consequences are the following: 1) The aerobic metabolism, evaluated by measurement of maximal oxygen uptake (VO2max), is either the same as in adults or more developed when VO2 max is related to body mass or lean body mass. 2) The maximal anaerobic power developed during force-velocity test and Wingate test is lower than in adults even if it is expressed by total or lean body mass unit. Blood lactate concentration is also lower. This immaturity of the anaerobic metabolism, especially the "lactic pathway" may result from lower anaerobic enzyme activities (lactico-dehydrogenase, phosphofructokinase, etc) and glycogen content. During puberty, "lactic metabolism" starts to develop significantly, simultaneously with muscle mass. It has been suggested that sexual hormones (testosterone in boys, oestrogens in girls) and other factors, such as growth factors, are implicated in this phenomenon. During this period, the aerobic metabolism remains unchanged. In prepubertal children there is neither aerobic nor anaerobic specialization: the highest anaerobic performance is associated with the highest VO2 max. Moreover, it seems that before puberty, bioenergetic profile is not modified by training. 3) Despite a high VO2 max, performance in endurance events is not as high in children as in adults because of a lower running economy. Cardiovascular responses are characterized by higher maximal and infra-maximal heart rates, and lower systolic stroke volume and arterial blood pressures than in adults. During prolonged exercise, the hormonal adaptations for energy substrate utilization is quite different from adults: a lower decrease in insulin and increase in catecholamines and glucagon in response to exercise could be responsible for a less effective regulation of glycemia with a risk of hypoglycemia. Therefore, an adequate carbohydrate intake is recommended.
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PMID:[Physiology of muscular exercise in children]. 784 28

Six extragonadal teratomas that contained pancreatic tissue were retrieved from archival material at the University of Minnesota Hospital, Minneapolis. The neuroendocrine cells were studied immunohistochemically for insulin, glucagon, somatostatin, pancreatic polypeptide, vasoactive intestinal polypeptide, gastrin, chromogranin, and synaptophysin. Pancreatic tissue from autopsies of 10 stillbirths (20 to 40 weeks' gestational age) was evaluated similarly. The features of the teratomatous pancreatic tissue were compared with those of the fetal pancreata and with data from previous studies of normal pancreatic development and adult pancreata. The pancreatic tissue in all six teratomas contained abundant mature islets that contained beta, alpha, delta, and pancreatic polypeptide cells; however, they also showed widespread nesidioblastosis with the same cell types, resembling third-trimester fetal and neonatal pancreata. Increased proportions of alpha and delta cells were observed in three and five cases (relative to those of adult tissue), respectively, providing further evidence of immaturity. Two cases showed a lack of alpha cells. None of the teratomas contained pancreatic cells that were positive for vasoactive intestinal polypeptide or gastrin. Mechanisms that regulate neuroendocrine cell differentiation in the normal pancreas also seem to operate in the teratomatous pancreas; they may eventuate in features similar to those of the late fetal and neonatal pancreas. Abnormal differentiation in teratomas may result in deficient hormone production.
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PMID:Immunohistochemical characterization of teratomatous and fetal neuroendocrine pancreas. 831 55

Glucagon-like peptide 2 (GLP-2) is a hormone produced primarily in the distal intestine, stimulated by enteral nutrients, and playing diverse roles in the intestinal adaptation and growth. We aimed to investigate whether GLP-2 may play a role in the development of feeding intolerance which is a common problem in preterm newborns resulting from the intestinal immaturity. The study included 20 term and 28 preterm neonates. Of preterm babies, 13 showed feeding intolerance fulfilling at least one of the following criteria: abdominal distension, increased gastric residual volume and presence of bile in the gastric aspirate. The plasma GLP-2 levels measured prior to enteral feeding (fasting level) and at 60 min after the beginning of the feeding (post-pradial level) were correlated with of clinical parameters. There was no statistical difference between GLP-2 levels of overall preterm babies and those of term newborns. However, preterm neonates with feeding intolerance showed significantly lower levels of GLP-2 and increased duration to achieve full enteral feeding and hospitalization. It is suggested that GLP-2 plays a significant role in the regulation of feeding in newborns and that preterm babies with low levels of GLP-2 carry a risk for development of feeding intolerance. It may, therefore, be of relevance to investigate the therapeutic and prophylactic effects of GLP-2 administration in the preterm babies.
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PMID:The relationship between glucagon-like peptide 2 and feeding intolerance in preterm infants. 1849 38


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