Document Detail

Metabolic effects of free fatty acids during endotoxaemia in a porcine model--free fatty acid inhibition of growth hormone secretion as a potential catabolic feedback mechanism.
MedLine Citation:
PMID:  20195947     Owner:  NLM     Status:  MEDLINE    
Critical illness and severe inflammation are catabolic states characterised by breakdown of tissue and protein stores, by increased levels of free fatty acids, and by insulin resistance. These metabolic features contribute to morbidity and mortality. Growth hormone and insulin are the two major anabolic hormones. The present study was designed to test whether increased levels of free fatty acids (i) inhibit growth hormone secretion and (ii) induce insulin resistance during acute endotoxin exposure in a porcine model of critical illness. We studied 20 pigs for 6 h during combined anaesthesia and endotoxin infusion and a hyperinsulinaemic glucose clamp to control glucose, insulin, and free fatty acid concentrations. Pigs were randomised to two different continuous infusion rates of Intralipid resulting in different, sustained, and elevated free fatty acid concentrations (1.63 mmol l(-1) vs. 0.58 mmol l(-1), p=0.0002). Concomitantly, we observed reduced growth hormone concentrations in the group with high free fatty acid concentrations (3.5 ng ml(-1) vs. 6.6 ng ml(-1), p<0.003). No difference in insulin sensitivity, measured as the glucose infusion rate necessary to maintain euglycaemia, was observed. We conclude that high levels of free fatty acids reduce circulating growth hormone concentrations in porcine endotoxaemia; this probably constitutes a negative feedback mechanism whereby growth hormone induced-stimulation of free fatty acids release inhibit growth hormone secretion. This mechanism may further contribute to protein loss in critical illness. We found no evidence that the increment of plasma free fatty acids between groups contribute to insulin resistance in critical illness.
M Buhl; J Gjedsted; A Granfeldt; P Ø Larsen; O Schmitz; E Tønnesen; N Møller
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Publication Detail:
Type:  Journal Article     Date:  2010-03-01
Journal Detail:
Title:  Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme     Volume:  42     ISSN:  1439-4286     ISO Abbreviation:  Horm. Metab. Res.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-05-04     Completed Date:  2010-07-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0177722     Medline TA:  Horm Metab Res     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  348-52     Citation Subset:  IM    
Copyright Information:
Georg Thieme Verlag KG Stuttgart-New York.
Medical Department M (Endocrinology and Diabetes), Aarhus University Hospital, Aarhus, Denmark.
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MeSH Terms
Endotoxemia / metabolism*
Endotoxins / pharmacology
Epinephrine / blood
Fatty Acids, Nonesterified / pharmacology*
Feedback, Physiological / physiology*
Glucagon / blood
Glucose / pharmacology
Growth Hormone / antagonists & inhibitors*,  metabolism*
Hydrocortisone / blood
Hypoglycemic Agents / pharmacology
Insulin / pharmacology
Insulin Resistance
Lipopolysaccharides / pharmacology
Norepinephrine / blood
Reg. No./Substance:
0/Endotoxins; 0/Fatty Acids, Nonesterified; 0/Hypoglycemic Agents; 0/Lipopolysaccharides; 11061-68-0/Insulin; 50-23-7/Hydrocortisone; 50-99-7/Glucose; 51-41-2/Norepinephrine; 51-43-4/Epinephrine; 67924-63-4/endotoxin, Escherichia coli; 9002-72-6/Growth Hormone; 9007-92-5/Glucagon

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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