| Stimulation of gluconeogenesis by intravenous lipids in preterm infants: response depends on fatty acid profile. | |
| | |
MedLine Citation:
|
PMID: 16291574 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
In preterm infants, both hypo- and hyperglycemia are a frequent problem. Intravenous lipids can affect glucose metabolism by stimulation of gluconeogenesis by providing glycerol, which is a gluconeogenic precursor, and/or free fatty acids (FFA), which are stimulants of the rate of gluconeogenesis. In 25 preterm infants, glucose production and gluconeogenesis were measured using stable isotope techniques during a 6-h infusion of glucose only, glucose plus glycerol, or glucose plus an intravenous lipid emulsion. Two lipid emulsions differing in FFA composition were used: Intralipid ( approximately 60% polyunsaturated FFA) and Clinoleic (approximately 60% monounsaturated FFA). The rate of glucose infusion was 22 micromol x kg(-1) x min(-1) in all groups. During the study infusion, the FFA concentrations were higher in both lipid groups vs. the glycerol group (P < 0.001). Compared with baseline, the glucose production rate increased in the Intralipid group, whereas it decreased in the other groups (P = 0.002) due to a significant increase in gluconeogenesis in the Intralipid group (P = 0.016). The plasma glucose concentration was significantly higher during Intralipid infusion vs. the other groups (P = 0.046). Our conclusion was that Intralipid enhanced glucose production by increasing gluconeogenesis in preterm infants. This can be ascribed to the stimulatory effect of FFA in addition to any effect of glycerol alone. The lack of stimulation of gluconeogenesis in the Clinoleic vs. the Intralipid group suggests that different classes of fatty acids exert different effects on glucose kinetics in preterm infants. |
| | |
Authors:
|
Anne A M W van Kempen; Saskia N van der Crabben; Mariëtte T Ackermans; Erik Endert; Joke H Kok; Hans P Sauerwein |
Related Documents
:
|
6804294 - Branched-chain amino acids and alanine as indices of the metabolic control in type 1 (i... 6382374 - Differential response of plasma glucose, amino acids and nonesterified fatty acids to i... 1928334 - In vivo evidence for hepatic autoregulation during ffa-stimulated gluconeogenesis in no... 1765054 - Thermogenic effect of adrenaline: interaction with insulin. 6421424 - Human ultralente insulin. 1986904 - Impact of a camp experience on choice of coping strategies by adolescents with insulin-... |
Publication Detail:
|
Type: Comparative Study; Journal Article Date: 2005-11-15 |
Journal Detail:
|
Title: American journal of physiology. Endocrinology and metabolism Volume: 290 ISSN: 0193-1849 ISO Abbreviation: Am. J. Physiol. Endocrinol. Metab. Publication Date: 2006 Apr |
Date Detail:
|
Created Date: 2006-03-14 Completed Date: 2006-05-02 Revised Date: 2006-11-15 |
Medline Journal Info:
|
Nlm Unique ID: 100901226 Medline TA: Am J Physiol Endocrinol Metab Country: United States |
Other Details:
|
Languages: eng Pagination: E723-30 Citation Subset: IM |
Affiliation:
|
Metabolism Unit, Department of Endocrinology and Metabolism, Emma Children's Hospital, Amsterdam, The Netherlands. A.vanKempen@amc.uva.nl |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Fat Emulsions, Intravenous
/
administration & dosage Fatty Acids, Nonesterified / blood, metabolism Female Gluconeogenesis / drug effects*, physiology Glucose / biosynthesis* Humans Infant, Newborn Infant, Premature / blood, metabolism* Insulin / blood, metabolism Kinetics Lipids / administration & dosage* Male Triglycerides / blood, metabolism |
| Chemical | |
Reg. No./Substance:
|
0/Fat Emulsions, Intravenous; 0/Fatty Acids, Nonesterified; 0/Lipids; 0/Triglycerides; 11061-68-0/Insulin; 50-99-7/Glucose |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Atrial natriuretic peptide stimulates lipid mobilization during repeated bouts of endurance exercise...
Next Document: Protection against cisplatin-induced nephrotoxicity by a carbon monoxide-releasing molecule.