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Alternative splice ...
Alternative splice variant PGC-1α-b is strongly induced by exercise in human skeletal muscle
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- Norrbom, J (författare)
- Karolinska Institutet
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Sallstedt, EK (författare)
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- Fischer, H (författare)
- Karolinska Institutet
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- Sundberg, CJ (författare)
- Karolinska Institutet
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- Rundqvist, H (författare)
- Karolinska Institutet
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- Gustafsson, T (författare)
- Karolinska Institutet
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(creator_code:org_t)
- American Physiological Society, 2011
- 2011
- Engelska.
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Ingår i: American journal of physiology. Endocrinology and metabolism. - : American Physiological Society. - 1522-1555 .- 0193-1849. ; 301:6, s. E1092-E1098
- Relaterad länk:
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http://kipublication...
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https://doi.org/10.1...
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Abstract
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- The present study investigated whether exercise induces the expression of PGC-1α splice variants in human skeletal muscle and the possible influence of metabolic perturbation on this response. The subjects exercised one leg for 45 min with restricted blood flow (R-leg), followed by 45 min of exercise using the other leg at the same absolute workload but with normal blood flow (NR-leg). This ischemic model (R-leg) has been shown previously to induce a greater metabolic perturbation and enhance the expression of PGC-1α beyond that observed in the NR-leg. Cultured human myotubes were used to test suggested exercise-induced regulatory stimuli of PGC-1α. We showed, for the first time, that transcripts from both the canonical promoter (PGC-1α-a) and the proposed upstream-located promoter (PGC-1α-b) are present in human skeletal muscle. Both transcripts were upregulated after exercise in the R-leg, but the fold change increase of PGC-1α-b was much greater than that of PGC-1α-a. No differences were observed between the two conditions regarding the marker for calcineurin activation, MCIP1, or p38 phosphorylation. AMPK phosphorylation increased to a greater extent in the R-leg, and AICAR stimulation of cultured human myotubes induced the expression of PGC-1α-a and PGC-1α-b. AICAR combined with norepinephrine yielded an additive effect on the PGC-1α-b expression only. Our results indicate clearly that exercise can activate an upstream promoter in humans and support AMPK as a major regulator of transcripts from the canonical PGC-1α promoter and the involvement of β-adrenergic stimulation in combination with AMPK in the regulation of PGC-1α-b.
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