α-Hydroxyisocaproic Acid Decreases Protein Synthesis but Attenuates TNFα/IFNγ Co-Exposure-Induced Protein Degradation and Myotube Atrophy via Suppression of iNOS and IL-6 in Murine C2C12 Myotube

Autor: Koichiro Sumi, Misato Sakuda, Ashida Kinya, Kentaro Nakamura, Kinuyo Munakata
Jazyk: angličtina
Rok vydání: 2021
Předmět:
0301 basic medicine
MAPK/ERK pathway
AMPK
Cachexia
protein synthesis
Muscle Fibers
Skeletal

Nitric Oxide Synthase Type II
AMP-Activated Protein Kinases
Mice
0302 clinical medicine
TNFα
TX341-641
Phosphorylation
Extracellular Signal-Regulated MAP Kinases
Nutrition and Dietetics
Myogenesis
Chemistry
Methylhistidines
iNOS
Muscular Atrophy
ERK
medicine.anatomical_structure
Tumor necrosis factor alpha
medicine.medical_specialty
Down-Regulation
Protein degradation
Article
Cell Line
Interferon-gamma
03 medical and health sciences
Atrophy
atrophy
Internal medicine
medicine
Animals
Caproates
IL-6
Nutrition. Foods and food supply
Interleukin-6
Tumor Necrosis Factor-alpha
Skeletal muscle
030229 sport sciences
medicine.disease
α-hydroxyisocaproic acid
030104 developmental biology
Endocrinology
Protein Biosynthesis
Proteolysis
myotube
Interferon-γ
Food Science
Zdroj: Nutrients
Volume 13
Issue 7
Nutrients, Vol 13, Iss 2391, p 2391 (2021)
ISSN: 2072-6643
Popis: There is ongoing debate as to whether or not α-hydroxyisocaproic acid (HICA) positively regulates skeletal muscle protein synthesis resulting in the gain or maintenance of skeletal muscle. We investigated the effects of HICA on mouse C2C12 myotubes under normal conditions and during cachexia induced by co-exposure to TNFα and IFNγ. The phosphorylation of AMPK or ERK1/2 was significantly altered 30 min after HICA treatment under normal conditions. The basal protein synthesis rates measured by a deuterium-labeling method were significantly lowered by the HICA treatment under normal and cachexic conditions. Conversely, myotube atrophy induced by TNFα/IFNγ co-exposure was significantly improved by the HICA pretreatment, and this improvement was accompanied by the inhibition of iNOS expression and IL-6 production. Moreover, HICA also suppressed the TNFα/IFNγ co-exposure-induced secretion of 3-methylhistidine. These results demonstrated that HICA decreases basal protein synthesis under normal or cachexic conditions
however, HICA might attenuate skeletal muscle atrophy via maintaining a low level of protein degradation under cachexic conditions.
Databáze: OpenAIRE