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Author(s): Sparks LM; Xie H; Koza RA; Mynatt R; Hulver MW; Bray GA; Smith SR
Title: A high-fat diet coordinately downregulates genes required for mitochondrial oxidative phosphorylation in skeletal muscle
Source: DIABETES 54 (7): 1926-1933
Date: 2005 JUL
Document Type: Journal : Article
DOI:
Language: English
Comment:
Address: Pennington Biomed Res Ctr, Baton Rouge, LA 70808 USA.
Reprint: Smith, SR, Pennington Biomed Res Ctr, 6400 Perkins Rd, Baton Rouge, LA
70808 USA. E-mail: smithsr@pbre.edu
Author Keywords:
KeyWords Plus: MICROARRAY DATA; INSULIN-RESISTANCE; PHYSICAL-ACTIVITY; CLUSTER-
ANALYSIS; ANIMAL-CELLS; EXPRESSION; COACTIVATOR; METABOLISM; GAMMA;
QUANTIFICATION
Abstract: Obesity and type 2 diabetes have been associated with a high-fat diet (HFD) and reduced mitochondrial mass and function. We hypothesized a HFD may affect expression of genes involved in mitochondrial function and biogenesis. To test this hypothesis, we fed 10 insulin-sensitive males an isoenergetic HFD for 3 days with muscle biopsies before and after intervention. Oligonucleotide microarray analysis revealed 297 genes were differentially regulated by the HFD (Bonferonni adjusted P < 0.001). Six genes involved in oxidative phosphorylation (OXPHOS) decreased. Four were members of mitochondrial complex I: NDUFB3, NDUFB5, NDUFS1, and NDUFV1; one was SDHB in complex II and a mitochondrial carrier protein SLC25A12. Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC1) a and PGC1 beta mRNA were decreased by -20%, P < 0.01, and -25%, P < 0.01, respectively. In a separate experiment, we fed C57Bl/6J mice a HFD for 3 weeks and found that the same OXPHOS and PGC1 mRNAs were downregulated by similar to 90%, cytochrome C and PGC1 alpha protein by similar to 40%. Combined, these results suggest a mechanism whereby HFD downregulates genes necessary for OXPHOS and mitochondrial biogenesis. These changes mimic those observed in diabetes and insulin resistance and, if sustained, may result in mitochondrial dysfunction in the prediabetic/insulin-resistant state.
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