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Power-boosting signal in muscle declines with age

ted to chronic activation of the AMPK pathway.

"In regards to insulin resistance and type 2 diabetes, having more AMPK activity in our skeletal muscle is probably a good thing because AMPK activation stimulates glucose uptake, increases fat oxidation, and promotes mitochondrial biogenesis," he said.

In the current study, the researchers set out to determine whether the declining mitochondrial function and increased intracellular fat content seen with aging could be traced back to deficiencies of AMPK. They compared AMPK activity in young and old rats following three "perturbations" that normally stimulate the enzyme and, in turn, mitochondria production. The treatments included acute exposure to an AMPK-stimulating chemical, chronic exposure through feeding of another chemical that induces AMPK by mimicking an energy shortage, and exercise.

In every case, older rats showed a decline in AMPK activity compared to younger animals. Young rats infused with a stimulatory chemical showed an increase in muscular AMPK activity not seen in old rats, they found. Similarly, the muscle of exercise-trained young rats showed more than a doubling in AMPK activity. In older rats, that AMPK hike with exercise was "severely blunted." The muscles of young rats fed the AMPK-stimulating chemical also showed an increase in AMPK and a 38% increase in mitochondrial density, they reported. In contrast, older animals' AMPK activity and mitochondrial numbers held steady.

"These results suggest that aging-associated reductions in AMPK-stimulated activity may be an important contributing factor in the reduced mitochondrial function and dysregulated intracellular fat metabolism associated with aging-induced insulin resistance and type 2 diabetes," the researchers concluded.
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Source:Cell Press


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