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PMID |
Sentence |
1 |
3033176
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Control of -PGC with ACE inhibitor is also protective even when therapy is delayed until systemic hypertension and glomerular injury are established.
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2 |
10894153
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Bcl-x and Bax regulate mouse primordial germ cell survival and apoptosis during embryogenesis.
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3 |
10894153
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Primordial germ cells (PGCs) in bcl-x hypomorph mice migrated to the genital ridge by E12.5 but were depleted by E15.5, a time when Bcl-x and Bax were present.
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4 |
10894153
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Bax was detected by immunohistochemistry in germ cells from bcl-x hypomorph and control testes at E12.5 and E13.5.
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5 |
10894153
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These findings demonstrate that the balance of Bcl-x and Bax control PGC survival and apoptosis.
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6 |
15294042
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Such adaptations are largely the result of a coordinated genetic response that increases mitochondrial proteins, fatty acid oxidation enzymes and the exercise- and insulin-stimulated glucose transporter GLUT4, and shifts the contractile and regulatory proteins to their more efficient isoforms.
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7 |
15294042
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The PPAR gamma co-activator (PGC) family of proteins have been identified as the central family of transcriptional co-activators for induction of mitochondrial biogenesis.
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8 |
15294042
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PGC-1 alpha is activated by exercise, and is sufficient to produce the endurance phenotype through direct interactions with NRF-1 and PPAR alpha, and potentially NRF-2.
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9 |
16513826
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Thiazolidinediones and rexinoids induce peroxisome proliferator-activated receptor-coactivator (PGC)-1alpha gene transcription: an autoregulatory loop controls PGC-1alpha expression in adipocytes via peroxisome proliferator-activated receptor-gamma coactivation.
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16513826
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They are activators of peroxisome proliferator-activated receptor (PPAR)-gamma, and adipose tissue constitutes a major site for their biological effects.
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11 |
16513826
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PPAR coactivator (PGC)-1alpha is a transcriptional coactivator of PPARgamma and other transcription factors.
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12 |
16513826
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Here we report that PGC-1alpha gene expression in brown and white adipocytes is a direct target of TZDs via PPARgamma activation.
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13 |
16513826
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Activators of the retinoid X receptor also induce PGC-1alpha gene expression.
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14 |
16513826
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This is due to the presence of a PPARgamma-responsive element in the distal region of the PGC-1alpha gene promoter that binds PPARgamma/retinoid X receptor heterodimers.
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15 |
16513826
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Moreover, there is a positive autoregulatory loop of control of the PGC-1alpha gene through coactivation of PPARgamma responsiveness to TZDs by PGC-1alpha itself.
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16 |
16644684
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Insulin increased phosphorylation of Akt and Akt substrate of 160 kDa (AS160) in a dose-dependent manner, with comparable responses between groups.
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17 |
16644684
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Skeletal muscle mRNA expression of peroxisome proliferator-activated receptor (PPAR) gamma coactivator (PGC)-1alpha, PGC-1beta, PPARdelta, nuclear respiratory factor-1, and uncoupling protein-3 was comparable between first-degree relatives and control subjects.
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18 |
16644684
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In conclusion, the uncoupling of insulin action on Akt/AS160 signaling and glucose transport implicates defective GLUT4 trafficking as an early event in the pathogenesis of type 2 diabetes.
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19 |
17456854
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The objective of this study was to further establish and confirm the relationship of adipose mitochondrial biogenesis in diabetes/obesity and the effects of rosiglitazone (RSG), a peroxisome proliferator-activated receptor (PPAR) gamma agonist, by systematically analyzing mitochondrial gene expression and function in two mouse models of obesity and type 2 diabetes.
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20 |
17456854
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Transcription factors, including PPAR coactivator (PGC)-1beta, PGC-1alpha, estrogen-related receptor alpha, and PPARalpha, were suppressed in both models and induced by RSG.
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21 |
19448711
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Estrogen-related receptor-alpha transcription factor is a key regulator of Mfn2 transcription and recruits peroxisome proliferator-activated receptor gamma coactivator (PGC)-1beta and PGC-1alpha.
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22 |
19448711
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These 2 nuclear coactivators are potent, positive regulators of Mfn2 expression in muscle cells, and ablation of PGC-1beta causes Mfn2 downregulation in skeletal muscle and in the heart.
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23 |
19448711
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We propose that PGC-1beta is a regulator of normal expression of Mfn2 in muscle, whereas PGC-1alpha participates in the stimulation of Mfn2 expression under a variety of conditions characterized by enhanced energy expenditure.
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24 |
20032281
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In particular, the regulatory pathway peroxisome proliferator-activated receptor gamma coactivator (PGC)-1alpha/mitofusin-2 (Mfn2) was analyzed.
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25 |
20032281
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CONCLUSIONS Our results demonstrate alterations in the regulatory pathway that controls PGC-1alpha expression and induction of Mfn2 in muscle from patients with early-onset type 2 diabetes.
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26 |
20032281
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Patients with early-onset type 2 diabetes display abnormalities in the exercise-dependent pathway that regulates the expression of PGC-1alpha and Mfn2.
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27 |
20929977
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Accordingly, the deacetylase SIRT1 and the kinase AMPK increase PGC-1α activity.
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28 |
20929977
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RESEARCH DESIGN AND METHODS We tested whether chronic treadmill exercise or a single exercise session modifies PGC-1α activation and mitochondrial biogenesis differentially in obese ob/ob mice with dysregulated adiponectin/leptin-mediated AMPK activation compared with C57BL/6J wild-type mice.
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29 |
20929977
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RESULTS Exercise training (12 weeks) induced adiponectin and lowered plasma insulin and glucose, suggesting improved insulin sensitivity in wild-type mice.
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30 |
20929977
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Parallel to this, we observed AMPK activation, PGC-1α deacetylation, and SIRT1 induction in trained wild-type mice.
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31 |
20929977
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Treatment of C2C12 myoblasts with leptin or adiponectin resulted in increased AMPK phosphorylation and PGC-1α deacetylation.
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32 |
20929977
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CONCLUSIONS Chronic exercise induces mitochondrial biogenesis in wild-type mice, which may require intact AMPK activation by adipocytokines and involve SIRT1-dependent PGC-1α deacetylation.
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33 |
20929977
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Trained ob/ob mice appear to have partially adapted to reduced mitochondrial biogenesis by AMPK/SIRT1/PGC-1α-independent mechanisms without mtDNA replication.
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34 |
22216325
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Increased renal methylglyoxal formation with down-regulation of PGC-1α-FBPase pathway in cystathionine γ-lyase knockout mice.
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35 |
22216325
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Recently, H(2)S was shown to up-regulate peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α, a key gluconeogenic regulator that enhances the gene expression of the rate-limiting gluconeogenic enzyme, fructose-1,6-bisphosphatase (FBPase).
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36 |
22216325
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Q-PCR was used to measure mRNA levels of PGC-1α and FBPase-1 and -2.
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37 |
22216325
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Administration of NaHS, a H(2)S donor, increased the gene expression of PGC-1α and FBPase-1 and -2 in cultured rat A-10 cells.
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38 |
22216325
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In conclusion, overproduction of MG in CSE(-/-) mice is due to a H(2)S-mediated down-regulation of the PGC-1α-FBPase pathway, further suggesting the important role of H(2)S in the regulation of glucose metabolism and MG generation.
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39 |
23624629
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Deletion of mTOR reduced mTORC1 and mTORC2 signaling after in vivo insulin stimulation.
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40 |
23624629
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Consistent with reduced palmitate oxidation, expression of fatty acid metabolism genes fatty acid-binding protein 3, medium-chain acyl-CoA dehydrogenase, and hydroxyacyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase/enoyl-CoA hydratase (trifunctional protein)-α and -β was reduced, and carnitine palmitoyl transferase-1 and -2 enzymatic activity was decreased.
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41 |
23624629
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However, mRNA for peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α and -1β, protein levels of PGC-1α, and electron transport chain subunits, mitochondrial DNA, and morphology were unchanged.
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