Remodeling of Oxidative Energy Metabolism by Galactose Improves Glucose Handling and Metabolic Switching in Human Skeletal Muscle Cells
Cultured human myotubes have a low mitochondrial oxidative potential. This study aims to remodel energy metabolism in myotubes by replacing glucose with galactose during growth and differentiation to ultimately examine the consequences for fatty acid and glucose metabolism. Exposure to galactose sho...
Main Authors: | , , , , , , |
---|---|
Format: | Online |
Language: | English |
Published: |
Public Library of Science
2013
|
Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3613401/ |
id |
pubmed-3613401 |
---|---|
recordtype |
oai_dc |
spelling |
pubmed-36134012013-04-04 Remodeling of Oxidative Energy Metabolism by Galactose Improves Glucose Handling and Metabolic Switching in Human Skeletal Muscle Cells Kase, Eili Tranheim Nikolić, Nataša Bakke, Siril Skaret Bogen, Kaja Kamilla Aas, Vigdis Thoresen, G. Hege Rustan, Arild Christian Research Article Cultured human myotubes have a low mitochondrial oxidative potential. This study aims to remodel energy metabolism in myotubes by replacing glucose with galactose during growth and differentiation to ultimately examine the consequences for fatty acid and glucose metabolism. Exposure to galactose showed an increased [14C]oleic acid oxidation, whereas cellular uptake of oleic acid uptake was unchanged. On the other hand, both cellular uptake and oxidation of [14C]glucose increased in myotubes exposed to galactose. In the presence of the mitochondrial uncoupler carbonylcyanide p-trifluormethoxy-phenylhydrazone (FCCP) the reserve capacity for glucose oxidation was increased in cells grown with galactose. Staining and live imaging of the cells showed that myotubes exposed to galactose had a significant increase in mitochondrial and neutral lipid content. Suppressibility of fatty acid oxidation by acute addition of glucose was increased compared to cells grown in presence of glucose. In summary, we show that cells grown in galactose were more oxidative, had increased oxidative capacity and higher mitochondrial content, and showed an increased glucose handling. Interestingly, cells exposed to galactose showed an increased suppressibility of fatty acid metabolism. Thus, galactose improved glucose metabolism and metabolic switching of myotubes, representing a cell model that may be valuable for metabolic studies related to insulin resistance and disorders involving mitochondrial impairments. Public Library of Science 2013-04-01 /pmc/articles/PMC3613401/ /pubmed/23560061 http://dx.doi.org/10.1371/journal.pone.0059972 Text en © 2013 Kase et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Kase, Eili Tranheim Nikolić, Nataša Bakke, Siril Skaret Bogen, Kaja Kamilla Aas, Vigdis Thoresen, G. Hege Rustan, Arild Christian |
spellingShingle |
Kase, Eili Tranheim Nikolić, Nataša Bakke, Siril Skaret Bogen, Kaja Kamilla Aas, Vigdis Thoresen, G. Hege Rustan, Arild Christian Remodeling of Oxidative Energy Metabolism by Galactose Improves Glucose Handling and Metabolic Switching in Human Skeletal Muscle Cells |
author_facet |
Kase, Eili Tranheim Nikolić, Nataša Bakke, Siril Skaret Bogen, Kaja Kamilla Aas, Vigdis Thoresen, G. Hege Rustan, Arild Christian |
author_sort |
Kase, Eili Tranheim |
title |
Remodeling of Oxidative Energy Metabolism by Galactose Improves Glucose Handling and Metabolic Switching in Human Skeletal Muscle Cells |
title_short |
Remodeling of Oxidative Energy Metabolism by Galactose Improves Glucose Handling and Metabolic Switching in Human Skeletal Muscle Cells |
title_full |
Remodeling of Oxidative Energy Metabolism by Galactose Improves Glucose Handling and Metabolic Switching in Human Skeletal Muscle Cells |
title_fullStr |
Remodeling of Oxidative Energy Metabolism by Galactose Improves Glucose Handling and Metabolic Switching in Human Skeletal Muscle Cells |
title_full_unstemmed |
Remodeling of Oxidative Energy Metabolism by Galactose Improves Glucose Handling and Metabolic Switching in Human Skeletal Muscle Cells |
title_sort |
remodeling of oxidative energy metabolism by galactose improves glucose handling and metabolic switching in human skeletal muscle cells |
description |
Cultured human myotubes have a low mitochondrial oxidative potential. This study aims to remodel energy metabolism in myotubes by replacing glucose with galactose during growth and differentiation to ultimately examine the consequences for fatty acid and glucose metabolism. Exposure to galactose showed an increased [14C]oleic acid oxidation, whereas cellular uptake of oleic acid uptake was unchanged. On the other hand, both cellular uptake and oxidation of [14C]glucose increased in myotubes exposed to galactose. In the presence of the mitochondrial uncoupler carbonylcyanide p-trifluormethoxy-phenylhydrazone (FCCP) the reserve capacity for glucose oxidation was increased in cells grown with galactose. Staining and live imaging of the cells showed that myotubes exposed to galactose had a significant increase in mitochondrial and neutral lipid content. Suppressibility of fatty acid oxidation by acute addition of glucose was increased compared to cells grown in presence of glucose. In summary, we show that cells grown in galactose were more oxidative, had increased oxidative capacity and higher mitochondrial content, and showed an increased glucose handling. Interestingly, cells exposed to galactose showed an increased suppressibility of fatty acid metabolism. Thus, galactose improved glucose metabolism and metabolic switching of myotubes, representing a cell model that may be valuable for metabolic studies related to insulin resistance and disorders involving mitochondrial impairments. |
publisher |
Public Library of Science |
publishDate |
2013 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3613401/ |
_version_ |
1611966632333148160 |