Gluconeogenesis in very low birth weight infants receiving total parenteral nutrition

Citation
Al. Sunehag et al., Gluconeogenesis in very low birth weight infants receiving total parenteral nutrition, DIABETES, 48(4), 1999, pp. 791-800
Citations number
67
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
DIABETES
ISSN journal
00121797 → ACNP
Volume
48
Issue
4
Year of publication
1999
Pages
791 - 800
Database
ISI
SICI code
0012-1797(199904)48:4<791:GIVLBW>2.0.ZU;2-F
Abstract
Very low birth weight (VLBW) infants are dependent on total parenteral nutr ition (TPN) to prevent hypoglycemia and provide a sufficient energy intake. However, diminished tolerance for parenteral glucose delivered at high rat es frequently provokes hyperglycemia. We hypothesized that when their gluco se supply is reduced to prevent hyperglycemia, VLBW infants can maintain no rmoglycemia via gluconeogenesis from glycerol and amino acids. Twenty infan ts born at 27 +/- 0.2 (mean +/- SE) gestational weeks and having a birth we ight of 996 +/- 28 g, received lipids (1.6 +/- 0.1 mg.kg(-1).min(-1)), prot ein (2.2 0.1 mg.kg(-1).min(-1)), and glucose (3.1 +/- 0.1 mg.kg(-1).min(-1) [17.1 +/- 0.2 mu mol.kg(-1).min(-1)]) parenterally over a period of 8-12 h on day 5.0 +/- 0.2 of life. Gluconeogenesis was estimated using [U-C-13]gl ucose (n = 8) or [2-C-13] glycerol (n = 6) and mass isotopomer distribution analysis (MIDA), or (H2O)-H-2 (n = 6) and the rate of deuterium incorporat ion in carbon 6 of glucose. Blood glucose averaged 3.0 +/- 0.1 mmol/l; plas ma glucose appearance rate (glucose Ra), 28.8 +/- 1.1 mu mol.kg(-1).min(-1) ; and glucose production rate (GPR), 10.7 +/- 1.0 mu mol.kg(-1).min(-1) The [U-C-13]glucose and [2-C-13]glycerol tracers provided similar estimates of gluconeogenesis, averaging 28 +/- 2 and 26 +/- 2% of glucose Ra and 72 +/- 5 and 73 +/- 9% of GPR, respectively. Glycerol contributed 64 +/- 5% of to tal gluconeogenesis. Gluconeogenesis measured by (H2O)-H-2, which does not include the contribution from glycerol, was comparable to the nonglycerol f raction of gluconeogenesis derived by the [2-C-13]glycerol MIDA. We conclud e that in VLBW infants receiving TPN, normoglycemia was maintained during r educed glucose infusion by glucose production primarily derived from glucon eogenesis, and that glycerol was the principal gluconeogenic substrate.