# |
PMID |
Sentence |
1 |
11259402
|
We investigated in the adult rodent heart 1) whether changes in workload, substrate supply, or cytokine (TNF-alpha) administration affect UCP-2 and UCP-3 expression, and 2) whether peroxisome proliferator-activated receptor alpha (PPARalpha) regulates the expression of either UCP-2 or UCP-3.
|
2 |
11259402
|
However, when fatty acid (the natural ligand for PPARalpha) supply was increased (high-fat feeding, fasting, and STZ-induced diabetes), cardiac UCP-3 but not UCP-2 expression increased.
|
3 |
11259402
|
The level of cardiac UCP-3 but not UCP-2 expression was severely reduced (20-fold) in PPARalpha-/- mice compared to wild-type mice.
|
4 |
11259402
|
These results suggest that in the adult rodent heart, UCP-3 expression is regulated by PPARalpha.
|
5 |
15292030
|
On the assumption that UCP3 and MTE1 act in partnership to increase FAO, we hypothesized that mte1 is also a PPAR alpha-regulated gene in cardiac and skeletal muscle.
|
6 |
16306367
|
Treatment with the PPARalpha-specific agonist, WY-14,643, increased cardiac UCP2 and UCP3 levels in wild-type mice but did not alter UCP levels in PPARalpha-/- mice.
|
7 |
16306367
|
Inhibition of beta-oxidation with etomoxir increased cardiac UCP2 and UCP3 levels in wild-type mice and UCP2 levels in PPARalpha-/- mice but did not alter UCP3 levels in PPARalpha-/- mice.
|
8 |
16306367
|
Streptozotocin treatment, which increased circulating FFAs by 91%, did not alter cardiac UCP2 levels in wild-type or PPARalpha-/- mice but increased UCP3 levels in wild-type, and not in PPARalpha-/-, mice.
|
9 |
16306367
|
We conclude that high plasma FFAs activated PPARalpha to increase cardiac UCP3 levels, but cardiac UCP2 levels changed via PPARalpha-dependent and -independent mechanisms.
|