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Chronic AMP-activated protein kinase activation and a high-fat diet have an additive effect on mitochondria in rat skeletal muscle.
J Appl Physiol (1985). 2010 Aug; 109(2):511-20.JA

Abstract

Factors that stimulate mitochondrial biogenesis in skeletal muscle include AMP-activated protein kinase (AMPK), calcium, and circulating free fatty acids (FFAs). Chronic treatment with either 5-aminoimidazole-4-carboxamide riboside (AICAR), a chemical activator of AMPK, or increasing circulating FFAs with a high-fat diet increases mitochondria in rat skeletal muscle. The purpose of this study was to determine whether the combination of chronic chemical activation of AMPK and high-fat feeding would have an additive effect on skeletal muscle mitochondria levels. We treated Wistar male rats with a high-fat diet (HF), AICAR injections (AICAR), or a high-fat diet and AICAR injections (HF + AICAR) for 6 wk. At the end of the treatment period, markers of mitochondrial content were examined in white quadriceps, red quadriceps, and soleus muscles, predominantly composed of unique muscle-fiber types. In white quadriceps, there was a cumulative effect of treatments on long-chain acyl-CoA dehydrogenase, cytochrome c, and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) protein, as well as on citrate synthase and beta-hydroxyacyl-CoA dehydrogenase (beta-HAD) activity. In contrast, no additive effect was noted in the soleus, and in the red quadriceps only beta-HAD activity increased additively. The additive increase of mitochondrial markers observed in the white quadriceps may be explained by a combined effect of two separate mechanisms: high-fat diet-induced posttranscriptional increase in PGC-1alpha protein and AMPK-mediated increase in PGC-1alpha protein via a transcriptional mechanism. These data show that chronic chemical activation of AMPK and a high-fat diet have a muscle type specific additive effect on markers of fatty acid oxidation, the citric acid cycle, the electron transport chain, and transcriptional regulation.

Authors+Show Affiliations

Department of Physiology and Developmental Biology, Birgham Young University, Provo, UT 84602, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

20522731

Citation

Fillmore, Natasha, et al. "Chronic AMP-activated Protein Kinase Activation and a High-fat Diet Have an Additive Effect On Mitochondria in Rat Skeletal Muscle." Journal of Applied Physiology (Bethesda, Md. : 1985), vol. 109, no. 2, 2010, pp. 511-20.
Fillmore N, Jacobs DL, Mills DB, et al. Chronic AMP-activated protein kinase activation and a high-fat diet have an additive effect on mitochondria in rat skeletal muscle. J Appl Physiol. 2010;109(2):511-20.
Fillmore, N., Jacobs, D. L., Mills, D. B., Winder, W. W., & Hancock, C. R. (2010). Chronic AMP-activated protein kinase activation and a high-fat diet have an additive effect on mitochondria in rat skeletal muscle. Journal of Applied Physiology (Bethesda, Md. : 1985), 109(2), 511-20. https://doi.org/10.1152/japplphysiol.00126.2010
Fillmore N, et al. Chronic AMP-activated Protein Kinase Activation and a High-fat Diet Have an Additive Effect On Mitochondria in Rat Skeletal Muscle. J Appl Physiol. 2010;109(2):511-20. PubMed PMID: 20522731.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Chronic AMP-activated protein kinase activation and a high-fat diet have an additive effect on mitochondria in rat skeletal muscle. AU - Fillmore,Natasha, AU - Jacobs,Daniel L, AU - Mills,David B, AU - Winder,William W, AU - Hancock,Chad R, Y1 - 2010/06/03/ PY - 2010/6/5/entrez PY - 2010/6/5/pubmed PY - 2015/4/10/medline SP - 511 EP - 20 JF - Journal of applied physiology (Bethesda, Md. : 1985) JO - J. Appl. Physiol. VL - 109 IS - 2 N2 - Factors that stimulate mitochondrial biogenesis in skeletal muscle include AMP-activated protein kinase (AMPK), calcium, and circulating free fatty acids (FFAs). Chronic treatment with either 5-aminoimidazole-4-carboxamide riboside (AICAR), a chemical activator of AMPK, or increasing circulating FFAs with a high-fat diet increases mitochondria in rat skeletal muscle. The purpose of this study was to determine whether the combination of chronic chemical activation of AMPK and high-fat feeding would have an additive effect on skeletal muscle mitochondria levels. We treated Wistar male rats with a high-fat diet (HF), AICAR injections (AICAR), or a high-fat diet and AICAR injections (HF + AICAR) for 6 wk. At the end of the treatment period, markers of mitochondrial content were examined in white quadriceps, red quadriceps, and soleus muscles, predominantly composed of unique muscle-fiber types. In white quadriceps, there was a cumulative effect of treatments on long-chain acyl-CoA dehydrogenase, cytochrome c, and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) protein, as well as on citrate synthase and beta-hydroxyacyl-CoA dehydrogenase (beta-HAD) activity. In contrast, no additive effect was noted in the soleus, and in the red quadriceps only beta-HAD activity increased additively. The additive increase of mitochondrial markers observed in the white quadriceps may be explained by a combined effect of two separate mechanisms: high-fat diet-induced posttranscriptional increase in PGC-1alpha protein and AMPK-mediated increase in PGC-1alpha protein via a transcriptional mechanism. These data show that chronic chemical activation of AMPK and a high-fat diet have a muscle type specific additive effect on markers of fatty acid oxidation, the citric acid cycle, the electron transport chain, and transcriptional regulation. SN - 1522-1601 UR - https://www.unboundmedicine.com/medline/citation/20522731/Chronic_AMP_activated_protein_kinase_activation_and_a_high_fat_diet_have_an_additive_effect_on_mitochondria_in_rat_skeletal_muscle_ L2 - http://www.physiology.org/doi/full/10.1152/japplphysiol.00126.2010?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -