2004
DOI: 10.1542/peds.113.3.537
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Both Relative Insulin Resistance and Defective Islet β-Cell Processing of Proinsulin Are Responsible for Transient Hyperglycemia in Extremely Preterm Infants

Abstract: These data suggest that 1) preterm neonates are sensitive to changes in plasma glucose concentration, but proinsulin processing to insulin is partially defective in hyperglycemic preterm neonates; 2) hyperglycemic neonates are relatively resistant to insulin because higher insulin levels are needed to achieve euglycemia in this group compared with normoglycemic neonates. These results also show that insulin infusion is beneficial in extremely preterm infants with transient hyperglycemia.

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Cited by 151 publications
(110 citation statements)
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“…This supports the existing data that suggest hepatic glucose production, pancreatic beta cell response and insulin sensitivity are physiologically related and developmentally regulated. 3,[17][18][19] Contrary to previous reports, sepsis and postnatal steroid exposure during the first 2 weeks of life were not associated with hyperglycemia, although a trend existed with postnatal steroid exposure. The lack of association with steroids may be due to the small number of euglycemic patients or to the change in clinical practice of using lower dexamethasone doses and shorter regimens.…”
Section: Discussioncontrasting
confidence: 70%
“…This supports the existing data that suggest hepatic glucose production, pancreatic beta cell response and insulin sensitivity are physiologically related and developmentally regulated. 3,[17][18][19] Contrary to previous reports, sepsis and postnatal steroid exposure during the first 2 weeks of life were not associated with hyperglycemia, although a trend existed with postnatal steroid exposure. The lack of association with steroids may be due to the small number of euglycemic patients or to the change in clinical practice of using lower dexamethasone doses and shorter regimens.…”
Section: Discussioncontrasting
confidence: 70%
“…The known mechanisms responsible for hyperglycaemia specific to extremely premature infants are related to their reduced ability to produce insulin [11]; defective beta-cell processing of pro-insulin (which is 10-16 times less active than insulin) to insulin [12]; an inability to suppress hepatic glucose production in response to glucose infusion [13]; and, finally, a decreased uptake of glucose secondary to a limited mass of insulin-sensitivity tissues (e.g. : muscle and adipose tissue) [14].…”
Section: Introductionmentioning
confidence: 99%
“…They have impaired glucose tolerance attributed to insufficient processing of pro-insulin by the immature pancreas, and decreased sensitivity of the liver to insulin, leading to continuous glucose production despite hyperglycemia. 1,2 The relationship between hyperglycemia and morbidity (e.g., intraventricular hemorrhage, which could be mediated by changes in osmolal concentration) 3 and mortality in this population is still not clearly defined. In this month's Journal of Perinatology, Kao et al 4 and Blanco et al 5 describe multivariate analyses of this relationship in large samples of ELBW infants from single-site centers.…”
mentioning
confidence: 99%