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Gene expression profile of aging and its retardation by caloric restriction

C K Lee1, R G Klopp, R Weindruch

  • 1Environmental Toxicology Center, Institute on Aging, Department of Genetics, University of Wisconsin, Madison, WI 53706, USA.

Science (New York, N.Y.)
|August 28, 1999
PubMed

Insights

Aging in mouse skeletal muscle shows a stress response and reduced metabolic gene expression. Caloric restriction reverses these changes, suggesting it slows aging by shifting metabolism to increase protein turnover and reduce damage.

Area of Science:

  • Gerontology
  • Molecular Biology
  • Skeletal Muscle Physiology

Background:

  • Aging is associated with significant molecular and physiological changes in skeletal muscle.
  • Understanding the gene expression profile of aging is crucial for developing interventions.
  • Caloric restriction is a known intervention that retards aging in mammals.

Purpose of the Study:

  • To analyze the gene expression profile of aging in mouse skeletal muscle.
  • To investigate the effects of caloric restriction on age-related gene expression changes.

Main Methods:

  • High-density oligonucleotide arrays were used to analyze the expression of 6347 genes.
  • Gene expression patterns were compared between aging and young mice.
  • The impact of caloric restriction on these patterns was assessed.

Main Results:

  • Aging induced a differential gene expression pattern characterized by a stress response and decreased expression of metabolic and biosynthetic genes.
  • Caloric restriction largely prevented or reversed these age-related gene expression alterations.
  • Transcriptional patterns in calorie-restricted mice indicated a metabolic shift.

Conclusions:

  • Aging in skeletal muscle involves a distinct stress response and reduced metabolic activity at the gene expression level.
  • Caloric restriction effectively counteracts age-related gene expression changes in skeletal muscle.
  • Caloric restriction may retard aging by promoting protein turnover and reducing macromolecular damage through metabolic shifts.

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