The impact of acute caloric restriction on the metabolic phenotype in male C57BL/6 and DBA/2 mice

Hempenstall, Sarah; Picchio, Lucie; Mitchell, Sharon E.; Speakman, John R.; Selman, Colin

doi:10.1016/j.mad.2009.12.008

Cited by 55 publications

(71 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Consequently both strains responded to CR in similar ways suggesting the reduction in RMR is not causally linked to the lifespan extension. Similar data were observed in response to acute 30% CR for 6 weeks (Hempenstall et al, 2010) -DBA/2 mice had higher metabolic rates than C57BL/6 mice when fed AL. Both strains reduced their whole body RMR when restricted but these effects disappeared when the effects of body mass were taken in to account.…”

Section: Resting Metabolic Rate (Rmr)supporting

confidence: 78%

Caloric restriction

Speakman

Mitchell

2011

Molecular Aspects of Medicine

Self Cite

671

675

View full text Add to dashboard Cite

Section: Resting Metabolic Rate (Rmr)supporting

confidence: 78%

Caloric restriction

Speakman

Mitchell

2011

Molecular Aspects of Medicine

Self Cite

671

675

View full text Add to dashboard Cite

“…1 A and B). CR is associated with a robust improvement in glucose homeostasis, which can be assessed using a glucose tolerance test (24). Again, both MKO and FLOX CR mice demonstrated striking improvement in glucose tolerance compared with control diet counterparts ( Fig.…”

Section: Improvements In Metabolic Homeostasis During Cr Do Not Requirementioning

confidence: 94%

Skeletal muscle transcriptional coactivator PGC-1α mediates mitochondrial, but not metabolic, changes during calorie restriction

Finley

Lee

Souza

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Calorie restriction (CR) is a dietary intervention that extends lifespan and healthspan in a variety of organisms. CR improves mitochondrial energy production, fuel oxidation, and reactive oxygen species (ROS) scavenging in skeletal muscle and other tissues, and these processes are thought to be critical to the benefits of CR. PGC-1α is a transcriptional coactivator that regulates mitochondrial function and is induced by CR. Consequently, many of the mitochondrial and metabolic benefits of CR are attributed to increased PGC-1α activity. To test this model, we examined the metabolic and mitochondrial response to CR in mice lacking skeletal muscle . Surprisingly, MKO mice demonstrated a normal improvement in glucose homeostasis in response to CR, indicating that skeletal muscle PGC-1α is dispensable for the wholebody benefits of CR. In contrast, gene expression profiling and electron microscopy (EM) demonstrated that PGC-1α is required for the full CR-induced increases in mitochondrial gene expression and mitochondrial density in skeletal muscle. These results demonstrate that PGC-1α is a major regulator of the mitochondrial response to CR in skeletal muscle, but surprisingly show that neither PGC-1α nor mitochondrial biogenesis in skeletal muscle are required for the whole-body metabolic benefits of CR.

show abstract

“…Acetylcarnitine fed to old rats increased cardiolipin levels to that of young rats and also restored protein synthesis in the inner mitochondrial membrane, as well as cellular oxidant/antioxidant balance, suggesting that administration of this compounds may improve cellular bioenergetics in aged rats [59]. Interestingly, caloric restriction, a dietary regimen that extends life-span in rodents, maintains the levels of 18:2 acyl side chains and inhibits the cardiolipin composition changes [60] In addition, caloric restriction showed to retards the aging associated changes in oxidative damage, mitochondrial oxidant generation and antioxidant defenses observed during aging [2,61].…”

Section: The Mitochondrial Theory Of Agingmentioning

confidence: 98%

Cellular Stress Responses, Mitostress and Carnitine Insufficiencies as Critical Determinants in Aging and Neurodegenerative Disorders: Role of Hormesis and Vitagenes

et al. 2010

View full text Add to dashboard Cite

The widely accepted oxidative stress theory of aging postulates that aging results from accumulation of oxidative damage. A prediction of this theory is that, among species, differential rates of aging may be apparent on the basis of intrinsic differences in oxidative damage accrual. Although widely accepted, there is a growing number of exceptions to this theory, most contingently related to genetic model organism investigations. Proteins are one of the prime targets for oxidative damage and cysteine residues are particularly sensitive to reversible and irreversible oxidation. The adaptation and survival of cells and organisms requires the ability to sense proteotoxic insults and to coordinate protective cellular stress response pathways and chaperone networks related to protein quality control and stability. The toxic effects that stem from the misassembly or aggregation of proteins or peptides, in any cell type, are collectively termed proteotoxicity. Despite the abundance and apparent capacity of chaperones and other components of homeostasis to restore folding equilibrium, the cell appears poorly adapted for chronic proteotoxic stress which increases in cancer, metabolic and neurodegenerative diseases. Pharmacological modulation of cellular stress response pathways has emerging implications for the treatment of human diseases, including neurodegenerative disorders, cardiovascular disease, and cancer. A critical key to successful medical intervention is getting the dose right. Achieving this goal can be extremely challenging due to human inter-individual variation as affected by age, gender, diet, exercise, genetic factors and health status. The nature of the dose response in and adjacent to the therapeutic zones, over the past decade has received considerable advances. The hormetic dose-response, challenging long-standing beliefs about the nature of the dose-response in a lowdose zone, has the potential to affect significantly the design of pre-clinical studies and clinical trials as well as strategies for optimal patient dosing in the treatment of numerous diseases. Given the broad cytoprotective properties of the heat shock response there is now strong interest in discovering and developing pharmacological agents capable of inducing stress responses, including carnitines. This paper describes in mechanistic detail how hormetic dose responses are mediated for endogenous cellular defense pathways, including the possible signaling mechanisms by which the carnitine system, by interplaying metabolism, mitochondrial energetics and activation of critical vitagenes, modulates signal transduction cascades that confer cytoprotection against chronic degenerative damage associated to aging and neurodegenerative disorders.

show abstract

The impact of acute caloric restriction on the metabolic phenotype in male C57BL/6 and DBA/2 mice

Cited by 55 publications

References 58 publications

Caloric restriction

Caloric restriction

Skeletal muscle transcriptional coactivator PGC-1α mediates mitochondrial, but not metabolic, changes during calorie restriction

Cellular Stress Responses, Mitostress and Carnitine Insufficiencies as Critical Determinants in Aging and Neurodegenerative Disorders: Role of Hormesis and Vitagenes

Contact Info

Product

Resources

About