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Peng Xu, John J Gildea, Chi Zhang, Prasad Konkalmatt, Santiago Cuevas, Dora Bigler Wang, Hanh T Tran, Pedro A Jose, and Robin A Felder

cells is not known. Ciprofibrate, a peroxisome proliferator-activated receptor α (PPAR-α) agonist, given by oral gavage, increases gastrin secretion, associated with a doubling of G cell density in the stomach antrum of Sprague–Dawley rats ( Martinsen

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M J Watt, R J Southgate, A G Holmes, and M A Febbraio

Fatty acids are an important ligand for peroxisome proliferator-activated receptor (PPAR) activation and transcriptional regulation of metabolic genes. To examine whether reduced plasma free fatty acid (FFA) availability affects the mRNA content of proteins involved in fuel metabolism in vivo, the skeletal muscle mRNA content of various transcription factors, transcriptional coactivators and genes encoding for lipid regulatory proteins were examined before and after 3 h of cycle exercise with (NA) and without (CON) pre-exercise ingestion of nicotinic acid (NA). NA resulted in a marked (3- to 6-fold) increase (P<0.05) in PPARα, PPARδ and PPAR coactivator 1α (PGC1α) mRNA, but was without effect on nuclear respiratory factor-1 and Forkhead transcription factor, fatty acid transcolase/CD36, carnitine palmitoyl transferase 1, hormone sensitive lipase (HSL) and pyruvate dehydrogenase kinase 4. Exercise in CON was associated with increased (P<0.05) PPARα, PPARδ and PGC1α mRNA, which was similar in magnitude to levels observed with NA at rest. Exercise was generally without effect on the mRNA content of lipid regulatory proteins in CON and did not affect the mRNA content of the measured subset of transcription factors, transcriptional co-activators and lipid regulatory proteins during NA. To determine the possible mechanisms by which NA might affect PGC1α expression, we measured p38 MAP kinase (MAPK) and plasma epinephrine. Phosphorylation of p38 MAPK was increased (P<0.05) by NA treatment at rest, and this correlated (r 2=0.84, P<0.01) with increased PGC1α. Despite this close relationship, increasing p38 MAPK in human primary myotubes was without effect on PGC1α mRNA content. Plasma epinephrine was elevated (P<0.05) by NA at rest (CON: 0.27±0.06, NA: 0.72±0.11 nM) and throughout exercise. Incubating human primary myotubes with epinephrine increased PGC1α independently of changes in p38 MAPK phosphorylation. Hence, despite the fact that NA ingestion decreased FFA availability, it promoted the induction of PPARα/δ and PGC1α gene expression to a similar degree as prolonged exercise. We suggest that the increase in PGC1α may be due to the elevated plasma epinephrine levels. Despite these changes in transcription factors/coactivators, the mRNA content of lipid regulatory proteins was generally unaffected by plasma FFA availability.

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Anke Gutgesell, Robert Ringseis, Eileen Schmidt, Corinna Brandsch, Gabriele I Stangl, and Klaus Eder

fatty acid uptake and oxidation are transcriptionally regulated by peroxisome proliferator-activated receptor α ( Ppar α ; Bruns et al . 1999 , Barbera et al . 2000 , Young et al . 2001 , Mandard et al . 2004 ). Ppar α is a ligand

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Qi Zhang, Qin Zhu, Ruyuan Deng, Feiye Zhou, Linlin Zhang, Shushu Wang, Kecheng Zhu, Xiao Wang, Libin Zhou, and Qing Su

′ 5′-GCCTCAGTTCCGAAAACCA-3′ FGF21 5′-GGGGTCATTCAAATCCTGGGTGTCA-3′ 5′-ACACATTGTAACCGTCCTCCAGCAG-3′ PPAR-α 5′-AGAGGCAGAGGTCCGATTCT-3′ 5′-ACTCGCGTGTGATAAAGCCA-3′ PPAR-γ 5′-ATTGAGTGCCGAGTCTGTGG-3′ 5′-GGCATTGTGAGACATCCCCA-3

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Weiwei Fan, Annette R Atkins, Ruth T Yu, Michael Downes, and Ronald M Evans

appears to be necessary for the maintenance of oxidative fibers and their oxidative functions in skeletal muscle. However, it remains to be demonstrated whether Ppar δ is required for exercise-induced muscle remodeling. Ppar α ( Ppara ) is abundantly

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Sofia A Rahman, Azizun Nessa, and Khalid Hussain

fatty acids causes a rise in the level of transcription factors such as PPAR-α. It has been suggested that PPAR-α directs fatty acids to the β-oxidation pathway and promotes an elevation of insulin secretion during hypoglycaemia ( Sugden & Holness 2004

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Bo Li, Zhiguo Zhang, Huizhi Zhang, Kai Quan, Yan Lu, Dongsheng Cai, and Guang Ning

was comprehensively upregulated in hepatic steatosis, and could be regulated by FFA. Notably we found that OA/PA could further decrease miR199a-5p-suppressed CAV1 / PPAR α expression and ATP activity, indicating that FFA may regulate CAV1 / PPAR α

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Sachie Nakamichi, Yoko Senga, Hiroshi Inoue, Aki Emi, Yasushi Matsuki, Eijiro Watanabe, Ryuji Hiramatsu, Wataru Ogawa, and Masato Kasuga

S Kulkarni R Evans RM Olefsky J Montminy M 2004 PGC-1 promotes insulin resistance in liver through PPAR-α-dependent induction of TRB-3 . Nature Medicine 10 530 – 534 . Koo SH Flechner L Qi L Zhang X Screaton RA Jeffries S

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Rodolfo Gomez, Francisca Lago, Juan Gomez-Reino, Carlos Dieguez, and Oreste Gualillo

activation of AMP-activated protein kinase peroxisome proliferator activated receptors (PPARs; α and γ) and seemingly other signal molecules. To note, targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and all its metabolic

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You-Hong Cheng, Hiroki Utsunomiya, Mary Ellen Pavone, Ping Yin, and Serdar E Bulun

in vivo effects of the PPAR-α agonists fenofibrate and retinoic acid in endometrial cancer . Molecular Cancer 5 13 doi:10.1186/1476-4598-5-13 . Schulman IG Li C Schwabe JW Evans RM 1997 The phantom ligand effect: allosteric control