Effect of Glucose Priming on Insulin Response in the Premature Infant

Grasso, Sebastiano; Distefano, Giuseppe; Messina, A; Vigo, R. Carmona; Reitano, G

doi:10.2337/diab.24.3.291

Cited by 9 publications

(7 citation statements)

References 5 publications

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“…These results show that the response of human fetal pancreatic tissue to glucose matures over a period of many months, corresponding to a time span from early in the second trimester of fetal life to 15 weeks after the birth of an infant. Our findings are similar to those reported in the clinical situation with no release of insulin in response to glucose before 25 weeks of age [3,4], sluggish release of insulin in both pre-term and terminfants [6][7][8], and a doubling of the insulinogenic response to glucose between 1 and 6 months of age [9]. A similar time-dependent maturation of response to glucose has also been recorded in animals, especially the fetal rat [11], and in pancreatic tissue removed from the fetal rat and cultured in vitro [12][13].…”

Section: Discussionsupporting

confidence: 91%

“…It is known that the ability of the pancreas to respond to glucose is sluggish at birth for full-term infants [6,7] and improves in a matter of 24 h after birth [7]. A similar initial sluggish response is seen with pre-term infants and does not improve within days after birth [7,8]. It is not until at least 1 month and, possibly 6 months of age, that a maximal response to glucose occurs in these infants [9].…”

mentioning

confidence: 98%

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Maturation of the response of human fetal pancreatic expiants to glucose

1985

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The release of insulin from the human pancreas in response to glucose is known to be either poor or absent in the fetus, whereas in the infant and adult, the response is much greater. The maturation of this response was examined systematically in this study using pancreases that were initially obtained at 14-20 weeks gestation and maintained either in culture alone or by passaging them in diabetic nude mice. Stimulation with glucose was carried out in vitro using tissue of ages ranging from 14 to 58 weeks. A response to glucose was initially seen at 25 weeks and this dramatically increased in the fetal tissue that had reached an age of 55 weeks or more. One of the nude mice used for passage developed normoglycaemia and when the pancreatic implant of age 52 weeks was removed, diabetes recurred. Our findings support the idea of the use of human fetal pancreatic tissue in the treatment of diabetes mellitus.

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Section: Discussionsupporting

confidence: 91%

mentioning

confidence: 98%

Maturation of the response of human fetal pancreatic expiants to glucose

1985

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“…Previous studies on fetal carbohydrate metabolism have been confined to either animals {Hay and Sparks 1985; Battaglia and Meschia 1986) or human fetuses born preterm {Grasso, Massina, Saporito and Reitano 1968;Grasso, Distefano, Messina, Vigo and Reitano 1975) and at term {Spellacy, Buhi, Bradley and Holsinger 1973;Metzger, Rodeck, Freinkel, Price and Young 1985). The technique of fetal blood sampling has allowed the opportunity to study fetal glucose concentration in normal {Forestier, Daffos, Rainaut, Bruneau and Trivin 1987) and abnormal pregnancies {Nicolini et al 1989).…”

Section: Discussionmentioning

confidence: 99%

Effects of Fetal Intravenous Glucose Challenge in Normal and Growth Retarded Fetuses

Nicolini¹,

Hubinont²,

Santolaya³

et al. 1990

Horm Metab Res

104

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Fetal intravenous glucose challenge test (0.75 g/kg of estimated fetal weight) was performed at 26-33 weeks gestation in 9 patients undergoing fetal blood sampling (FBS) by ultrasound guided needling from the umbilical vein. The indication for FBS was rapid karyotyping for fetal malformations in 5 (control group) and severe intrauterine growth retardation in the remaining 4 (IUGR group). Fetal blood samples were taken before the glucose infusion and after 1, 3, 5, 10 and 15 min; glucose and insulin were assayed on each occasion and acid-base balance at 0 and 5 min. Basal fetal pO2, pH, glucose and insulin were lower in the IUGR group than in controls. Following the glucose challenge, fetal glucose levels were similar in the two groups, but in the IUGR group the latter part of the glucose curve was characterized by a slower and delayed return to basal levels. In control fetuses the insulin response following the glucose challenge peaked at 3 min while in IUGR no change in insulin concentration was detected. Fetal pO2 did not change in either group; the median change in fetal pH was significantly different between the two groups (controls: +0.01; IUGR: -0.04; P less than 0.05) and there was a significant correlation between basal pO2 and the change in fetal pH (r = 0.79) (P less than 0.02). These results support the concept of a low energy state in IUGR. Fetal glucose supplementation in IUGR is unlikely to be of benefit and may even exacerbate underlying acidosis.

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“…We have previously shown that if an infusion of glucose administered for 120 minutes precedes the acute injection of glucose, the latter becomes a potent stimulus of insulin secretion. 7 However, in the same study the priming with 2.5 gm. of glucose and the successive rapid infusion of glucose (2.5 gm.)…”

Section: Discussionmentioning

confidence: 82%

“…On the other hand, recent studies showed that in preterm neonates the unresponsiveness to glucose can be reversed. 7 When glucose is injected into them acutely it is a poor stimulant of insulin secretion, but if a small infusion of glucose precedes the acute injection of glucose, the latter becomes a potent stimulus of insulin secretion.…”

mentioning

confidence: 99%

Effect of Priming of Amino Acids on Insulin and Growth Hormone Response in the Premature Infant

et al. 1978

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Glucose, alpha-amino nitrogen, serum insulin, and HGH were studied in preterm infants during the first 24 hours of life. Glucose infusion (1.25 gm.) resulted in a slight elevation of serum insulin. When this amount of glucose was infused during the last 30 minutes of a two-and-a-half-hour infusion of a mixture of essential amino acids, there was a rapid and striking increase in serum insulin. However, this increase was not associated with a faster glucose disposal rate. The administration of this mixture of amino acids doubled the basal level of alpha-amino nitrogen, and during the first two hours, before glucose infusion, it caused a significant rise of serum insulin and HGH. In both cases glucose caused an increase of HGH secretion that was not significantly different in the two groups of infants.

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Effect of Glucose Priming on Insulin Response in the Premature Infant

Cited by 9 publications

References 5 publications

Maturation of the response of human fetal pancreatic expiants to glucose

Maturation of the response of human fetal pancreatic expiants to glucose

Effects of Fetal Intravenous Glucose Challenge in Normal and Growth Retarded Fetuses

Effect of Priming of Amino Acids on Insulin and Growth Hormone Response in the Premature Infant

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