Abstract
The purpose of the present study was to investigate how the effects of high-fat diet feeding on the skeletal muscle persisted during aging using mice. Post-weaned male mice were fed a high-fat diet between 1- and 3-mo-old followed by return to supply a normal diet until 13-mo-old. Monthly physical tests demonstrated that age-related glucose intolerance that was generally developed after 10-mo-old in the control mice was significantly improved in mice fed a high-fat diet. Interestingly, mRNA expressions of Pdk4, Ucp3, and Zmynd17 were up-regulated by high-fat feeding and persisted in the tibialis anterior muscle until 13-mo-old. At Pdk4 and Ucp3 loci, enhanced distributions of active histone modifications were noted in the high-fat-fed mice at 13-mo-old. In contrast, age-related accumulation of histone variant H3.3 at these loci was suppressed. These results indicated that epigenetic modifications caused by early nutrition mediated the changes in skeletal muscle gene expression during aging.
Highlights
IntroductionThe decline in skeletal muscle mass as a result of aging, is a primary contributor to the decline in physical performance (e.g., daily activities)
For all individuals, the decline in skeletal muscle mass as a result of aging, is a primary contributor to the decline in physical performance
Choi et al [10] reported that UCP3 overexpression in skeletal muscle protected mice from insulin resistance induced by high fat diet feeding. These results indicate that uncoupling protein 3 (Ucp3) and zinc finger MYND domain-containing protein 17 (Zmynd17) functioned to counteract the developing abnormal glucose tolerance
Summary
The decline in skeletal muscle mass as a result of aging, is a primary contributor to the decline in physical performance (e.g., daily activities). The progression of age-related diseases largely differs between individuals. The Dunedin study was based on aging in a population-representative 1972–1973 birth cohort of 1037 young adults followed from birth to age 38 y with 95% retention. When subjects were 38 y old, their physiologies were examined to test whether this young population would show evidence of individual variation in aging despite remaining free of age-related disease. Belsky et al [1] recently reported that the Dunedin Study contained longitudinal data on 18 biomarkers established as risk factors or correlates of chronic disease. Individual differences have been reported in response to exercise training and the pathogenesis of lifestyle-related diseases. Resistance training-induced muscle hypertrophy was highly variable between individuals, who could be classified into high and low responders [2, 3]. In an experiment using rodents, Nakamura et al [6] reported that disuse atrophy was not induced in fast-
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
