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Insulin and metabolic substrates during human sepsis
Rusavy and colleagues recently endeavoured to dissect out the metabolic effects of insulin in patients with severe sepsis, in the setting of normoglycaemia. Twenty stable patients were studied 3–7 days after admission using a euglycaemic clamp at two supraphysiological insulin levels. Increased dose...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2004
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC522846/ https://www.ncbi.nlm.nih.gov/pubmed/15312202 http://dx.doi.org/10.1186/cc2883 |
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author | Finney, Simon J |
author_facet | Finney, Simon J |
author_sort | Finney, Simon J |
collection | PubMed |
description | Rusavy and colleagues recently endeavoured to dissect out the metabolic effects of insulin in patients with severe sepsis, in the setting of normoglycaemia. Twenty stable patients were studied 3–7 days after admission using a euglycaemic clamp at two supraphysiological insulin levels. Increased doses of exogenous insulin caused preferential use of glucose as a metabolic substrate, while total energy expenditure remained constant. Consequently, hyperinsulinaemia reduced tissue oxygen demand and catabolism of protein in patients with sepsis; the benefits of these effects are not proven. The effects of insulin at different time points in sepsis were not examined. |
format | Text |
id | pubmed-522846 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2004 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-5228462004-10-17 Insulin and metabolic substrates during human sepsis Finney, Simon J Crit Care Commentary Rusavy and colleagues recently endeavoured to dissect out the metabolic effects of insulin in patients with severe sepsis, in the setting of normoglycaemia. Twenty stable patients were studied 3–7 days after admission using a euglycaemic clamp at two supraphysiological insulin levels. Increased doses of exogenous insulin caused preferential use of glucose as a metabolic substrate, while total energy expenditure remained constant. Consequently, hyperinsulinaemia reduced tissue oxygen demand and catabolism of protein in patients with sepsis; the benefits of these effects are not proven. The effects of insulin at different time points in sepsis were not examined. BioMed Central 2004 2004-05-25 /pmc/articles/PMC522846/ /pubmed/15312202 http://dx.doi.org/10.1186/cc2883 Text en Copyright © 2004 BioMed Central Ltd |
spellingShingle | Commentary Finney, Simon J Insulin and metabolic substrates during human sepsis |
title | Insulin and metabolic substrates during human sepsis |
title_full | Insulin and metabolic substrates during human sepsis |
title_fullStr | Insulin and metabolic substrates during human sepsis |
title_full_unstemmed | Insulin and metabolic substrates during human sepsis |
title_short | Insulin and metabolic substrates during human sepsis |
title_sort | insulin and metabolic substrates during human sepsis |
topic | Commentary |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC522846/ https://www.ncbi.nlm.nih.gov/pubmed/15312202 http://dx.doi.org/10.1186/cc2883 |
work_keys_str_mv | AT finneysimonj insulinandmetabolicsubstratesduringhumansepsis |