期刊
CELL METABOLISM
卷 5, 期 2, 页码 151-156出版社
CELL PRESS
DOI: 10.1016/j.cmet.2007.01.008
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资金
- NHLBI NIH HHS [R01 HL-63811, R01 HL063811] Funding Source: Medline
- NIDDK NIH HHS [R01 DK040936, P30 DK-45735, U24 DK059635, P30 DK045735, R01 DK-40936, U24 DK-59635] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007499, T32 GM-07499] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
Recent studies have demonstrated a strong relationship between aging-associated reductions in mitochondrial function, dysregulated intracellular lipid metabolism, and insulin resistance. Given the important role of the AMP-activated protein kinase (AMPK) in the regulation of fat oxidation and mitochondrial biogenesis, we examined AMPK activity in young and old rats and found that acute stimulation of AMPK-alpha 2 activity by 5'-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) and exercise was blunted in skeletal muscle of old rats. Furthermore, mitochondrial biogenesis in response to chronic activation of AMPK with D-guanidinopropionic acid (beta-GPA) feeding was also diminished in old rats. These results suggest that aging-associated reductions in AMPK activity may be an important contributing factor in the reduced mitochondrial function and dysregulated intracellular lipid metabolism associated with aging.
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