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Vascular and metabolic effects of adrenaline in adipose tissue in type 2 diabetes

OBJECTIVE: The aim was to investigate adipose tissue vascular and metabolic effects of an adrenaline infusion in vivo in subjects with and without type 2 diabetes mellitus (T2DM). DESIGN: Clinical intervention study with 1-h intravenous adrenaline infusion. SUBJECTS: Eight male overweight T2DM subje...

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Autores principales: Tobin, L, Simonsen, L, Galbo, H, Bülow, J
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3461355/
https://www.ncbi.nlm.nih.gov/pubmed/23446661
http://dx.doi.org/10.1038/nutd.2012.19
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author Tobin, L
Simonsen, L
Galbo, H
Bülow, J
author_facet Tobin, L
Simonsen, L
Galbo, H
Bülow, J
author_sort Tobin, L
collection PubMed
description OBJECTIVE: The aim was to investigate adipose tissue vascular and metabolic effects of an adrenaline infusion in vivo in subjects with and without type 2 diabetes mellitus (T2DM). DESIGN: Clinical intervention study with 1-h intravenous adrenaline infusion. SUBJECTS: Eight male overweight T2DM subjects and eight male weight-matched, non-T2DM subjects were studied before, during and after an 1-h intravenous adrenaline infusion. Adipose tissue blood flow (ATBF) was determined by (133)Xenon wash-out technique, and microvascular volume in the adipose tissue was studied by contrast-enhanced ultrasound imaging. Adipose tissue fluxes of glycerol, non-esterified fatty acids (NEFA), triacylglycerol and glucose were measured by Fick's principle after catherisation of a radial artery and a vein draining the abdominal, subcutaneous adipose tissue. RESULTS: ATBF increased similarly in both groups during the adrenaline infusion. One hour post adrenaline, ATBF was still increased in overweight T2DM subjects. Adrenaline increased microvascular volume in non-T2DM subjects while this response was impaired in overweight T2DM subjects. Adrenaline-induced increase in lipolysis was similar in both groups, but NEFA output from adipose tissue was delayed in overweight T2DM subjects. Glucose uptake in adipose tissue increased in non-T2DM subjects during adrenaline infusion but was unchanged in overweight T2DM subjects. This results in a delayed excess release of NEFA from the adipose tissue in overweight T2DM subjects after cessation of the adrenaline infusion. CONCLUSION: Capillaries in the adipose tissue are recruited by adrenaline in non-T2DM subjects; however, this response is impaired in overweight T2DM subjects. NEFA, released in adipose tissue during adrenaline stimulation, is insufficiently re-esterified in situ in overweight T2DM subjects, probably owing to increased ATBF after adrenaline infusion and inability to increase adipose tissue glucose uptake.
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spelling pubmed-34613552012-10-03 Vascular and metabolic effects of adrenaline in adipose tissue in type 2 diabetes Tobin, L Simonsen, L Galbo, H Bülow, J Nutr Diabetes Original Article OBJECTIVE: The aim was to investigate adipose tissue vascular and metabolic effects of an adrenaline infusion in vivo in subjects with and without type 2 diabetes mellitus (T2DM). DESIGN: Clinical intervention study with 1-h intravenous adrenaline infusion. SUBJECTS: Eight male overweight T2DM subjects and eight male weight-matched, non-T2DM subjects were studied before, during and after an 1-h intravenous adrenaline infusion. Adipose tissue blood flow (ATBF) was determined by (133)Xenon wash-out technique, and microvascular volume in the adipose tissue was studied by contrast-enhanced ultrasound imaging. Adipose tissue fluxes of glycerol, non-esterified fatty acids (NEFA), triacylglycerol and glucose were measured by Fick's principle after catherisation of a radial artery and a vein draining the abdominal, subcutaneous adipose tissue. RESULTS: ATBF increased similarly in both groups during the adrenaline infusion. One hour post adrenaline, ATBF was still increased in overweight T2DM subjects. Adrenaline increased microvascular volume in non-T2DM subjects while this response was impaired in overweight T2DM subjects. Adrenaline-induced increase in lipolysis was similar in both groups, but NEFA output from adipose tissue was delayed in overweight T2DM subjects. Glucose uptake in adipose tissue increased in non-T2DM subjects during adrenaline infusion but was unchanged in overweight T2DM subjects. This results in a delayed excess release of NEFA from the adipose tissue in overweight T2DM subjects after cessation of the adrenaline infusion. CONCLUSION: Capillaries in the adipose tissue are recruited by adrenaline in non-T2DM subjects; however, this response is impaired in overweight T2DM subjects. NEFA, released in adipose tissue during adrenaline stimulation, is insufficiently re-esterified in situ in overweight T2DM subjects, probably owing to increased ATBF after adrenaline infusion and inability to increase adipose tissue glucose uptake. Nature Publishing Group 2012-09 2012-09-17 /pmc/articles/PMC3461355/ /pubmed/23446661 http://dx.doi.org/10.1038/nutd.2012.19 Text en Copyright © 2012 Macmillan Publishers Limited http://creativecommons.org/licenses/by-nc-nd/3.0/ This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/
spellingShingle Original Article
Tobin, L
Simonsen, L
Galbo, H
Bülow, J
Vascular and metabolic effects of adrenaline in adipose tissue in type 2 diabetes
title Vascular and metabolic effects of adrenaline in adipose tissue in type 2 diabetes
title_full Vascular and metabolic effects of adrenaline in adipose tissue in type 2 diabetes
title_fullStr Vascular and metabolic effects of adrenaline in adipose tissue in type 2 diabetes
title_full_unstemmed Vascular and metabolic effects of adrenaline in adipose tissue in type 2 diabetes
title_short Vascular and metabolic effects of adrenaline in adipose tissue in type 2 diabetes
title_sort vascular and metabolic effects of adrenaline in adipose tissue in type 2 diabetes
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3461355/
https://www.ncbi.nlm.nih.gov/pubmed/23446661
http://dx.doi.org/10.1038/nutd.2012.19
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