NARA Discovery
Article Details
← Back to Search Results
Journal Article

Substrate oxidation in primary human skeletal muscle cells is influenced by donor age

Vigdis Aas; G. Hege Thoresen; Arild C. Rustan; Jenny Lund
Cell and Tissue Research · Vol. 382, Issue 3 · pp. 599-608 · 2020

Abstract

Primary human myotubes represent an alternative system to intact skeletal muscle for the study of human diseases related to changes in muscle energy metabolism. This work aimed to study if fatty acid and glucose metabolism in human myotubes in vitro were related to muscle of origin, donor gender, age, or body mass index (BMI). Myotubes from a total of 82 donors were established from three different skeletal muscles, i.e., musculus vastus lateralis , musculus obliquus internus abdominis , and musculi interspinales , and cellular energy metabolism was evaluated. Multiple linear regression analyses showed that donor age had a significant effect on glucose and oleic acid oxidation after correcting for gender, BMI, and muscle of origin. Donor BMI was the only significant contributor to cellular oleic acid uptake, whereas cellular glucose uptake did not rely on any of the variables examined. Despite the effect of age on substrate oxidation, cellular mRNA expression of pyruvate dehydrogenase kinase 4 ( PDK4 ) and peroxisome proliferator–activated receptor gamma coactivator 1 alpha ( PPARGC1A ) did not correlate with donor age. In conclusion, donor age significantly impacts substrate oxidation in cultured human myotubes, whereas donor BMI affects cellular oleic acid uptake.

Bibliographic Information

JournalCell and Tissue Research
PublisherSpringer
Publication Date2020-12-01
Publication Year2020
Volume382
Issue3
Pages599-608
Document TypeJournal Article
Print ISSN0302-766X
eISSN1432-0878
DOI10.1007/s00441-020-03275-w

Access Information

NARA Access Coverage1924-01-01~Current
Journal Homepagehttps://www.springer.com/journal/441
Publisher PageOpen Publisher Page
Full-text access depends on NARA's subscribed coverage and institutional access.