NDLI: Myostatin expression is increased by food deprivation in a muscle-specific manner and contributes to muscle atrophy during prolonged food deprivation in mice.

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Myostatin expression is increased by food deprivation in a muscle-specific manner and contributes to muscle atrophy during prolonged food deprivation in mice.

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Myostatin expression is increased by food deprivation in a muscle-specific manner and contributes to muscle atrophy during prolonged food deprivation in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Allen, David L. Cleary, Allison S. Lindsay, Sarah F. Loh, Amanda S. Reed, Jason M.
Description	Country affiliation: United States Author Affiliation: Allen DL ( Department of Integrative Physiology, University of Colorado, Boulder, Campus Box 354, Boulder, CO 80309, USA. allendl@colorado.edu)
Abstract	During food deprivation (FD), skeletal muscle protein is broken down to produce amino acids for hepatic gluconeogenesis to maintain blood glucose levels. However, it is unclear what role, if any, the secreted antigrowth factor myostatin (MSTN) plays in the muscle atrophy induced by FD. We therefore examined expression and function of MSTN in FD in mice. Two days of FD significantly decreased muscle mass and protein content and increased mRNA levels of ubiquitin ligases MuRF-1 and atrogin-1 in fast-twitch tibialis anterior (TA) muscle but not slow-twitch soleus (Sol) muscle, while 2 days of refeeding returned these to fed values in TA. MSTN mRNA levels were significantly increased approximately threefold by 2 days, but not 1 day, of FD and returned to fed levels with 2 days of refeeding in TA but were not significantly affected by FD or refeeding in Sol. TA mass decreased to a similar amount after 1 day of FD in wild-type mice and mice null for the MSTN gene but was decreased to a greater amount in wild-type than MSTN-null mice by 2 days of FD. In addition, blood glucose levels decreased and corticosterone levels increased to a greater extent in MSTN-null mice after 2 days of FD, but surprisingly muscle MuRF-1 and atrogin-1 mRNA levels were not affected by the lack of MSTN during FD. Similarly, changes in hepatic enzyme expression in response to FD were identical between wild-type and MSTN-null mice. Our data are consistent with the hypothesis that MSTN is dispensable for the initial atrophy occurring in response to FD but attenuates the decrease in fast-twitch muscle mass during prolonged FD.
File Format	HTM / HTML
ISSN	87507587
e-ISSN	15221601
Journal	Journal of Applied Physiology
Issue Number	3
Volume Number	109
Language	English
Publisher	American Physiological Society
Publisher Date	2010-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Food Deprivation Muscle, Skeletal Metabolism Muscular Atrophy Etiology Myostatin Animals Blood Glucose Corticosterone Blood Glucokinase Genetics Gluconeogenesis Mice Mice, Inbred C57bl Mice, Knockout Muscle Fibers, Fast-twitch Pathology Muscle Fibers, Slow-twitch Muscle Proteins Deficiency Organ Size Phosphoenolpyruvate Carboxykinase (gtp) Rna, Messenger Skp Cullin F-box Protein Ligases Time Factors Ubiquitin-protein Ligases Up-regulation Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Sports Science

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