Title: Reduced skeletal muscle AMPK and mitochondrial markers do not promote age-induced insulin resistance
Authors: Bujak, AL
Blumer, RME
Marcinko, K
Fullerton, MD
Kemp, BE
Steinberg, GR
Issue Year: 2014
Publisher AMER PHYSIOLOGICAL SOC
Series JOURNAL OF APPLIED PHYSIOLOGY: 117(2): 171-179
Abstract In both rodents and humans, aging-associated reductions in skeletal muscle AMP-activated protein kinase (AMPK) activity and mitochondrial function have been linked to the development of skeletal muscle insulin resistance. However, whether reductions in skeletal muscle AMPK and mitochondrial capacity actually precipitate the development of aging-induced insulin resistance is not known. Mice lacking both isoforms of the AMPK beta-subunit in skeletal muscle (AMPK-MKO) have no detectable AMPK activity and are characterized by large reductions in exercise capacity, mitochondrial content, and contraction-stimulated glucose uptake making them an ideal model to determine whether reductions in AMPK and mitochondrial content promote the development of aging-induced insulin resistance. In the current study we find that a lack of skeletal muscle AMPK results in a life-long reduction in mitochondrial activity but does not affect body mass, body composition, glucose tolerance, or insulin sensitivity as measured by hyperinsulinemic- euglycemic clamp in mice of old age (18 mo). These data demonstrate that reductions in skeletal muscle AMPK and mitochondrial activity do not cause the development of age-induced insulin resistance.
URI: https://publications.svi.edu.au/publications/1801
Other Identifiers 10.1152/japplphysiol.01101.2013
Publication type Article
Find it online http://jap.physiology.org/content/117/2/171.long