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Obesity (Silver Spring). 2008 Mar;16(3):572-7. doi: 10.1038/oby.2007.91. Epub 2008 Jan 17.

Impaired resting muscle energetics studied by (31)P-NMR in diet-induced obese rats.

Author information

1
INRA, UMR1019, Clermont-Ferrand, France.

Abstract

OBJECTIVE:

Mitochondrial activity is altered in skeletal muscle of obese, insulin-resistant or type 2 diabetic patients. We hypothesized that this situation was associated with profound adaptations in resting muscle energetics. For that purpose, we used in vivo (31)P-nuclear magnetic resonance ((31)P-NMR) in male sedentary Wistar rats fed with obesogenic diets known to induce alterations in muscle mitochondrial activity.

METHODS AND PROCEDURES:

Two experimental diets (high sucrose and high fat) were provided for 6 weeks at two levels of energy (standard, N and high, H) and compared to control diet. The rates of the adenosine triphosphate (ATP) exchange between phosphocreatine (PCr) and gamma-ATP (k(a)) and beta-adenosine diphosphate (beta-ADP) to beta-ATP (k(b)) were evaluated using (31)P-NMR in resting gastrocnemius muscle. Muscle contents in phosphorylated compounds as well as creatine, were assessed using (31)P-NMR and biochemical assays, respectively.

RESULTS:

ATP content increased by 6.7-8.5% in standard-energy high-sucrose (NSU), high-energy high-fat (HF) and high-energy high-sucrose (HSU) groups compared to control (P < 0.05), whereas PCr content decreased by 4.2-6.4% (P < 0.01). Consequently, PCr to ATP ratio decreased in NSU, HF, and HSU groups, compared to control (P < 0.01). Furthermore in high-energy groups (HF and HSU) compared to control, creatine contents were decreased by 14-19% (P < 0.001), whereas k(a) and k(b) fluxes were increased by 89-133% (P < 0.001) and 243-277% (P < 0.01), respectively.

DISCUSSION:

Our in vivo data showed adaptations of resting skeletal muscle energetics in response to high-energy diets. Increased activity of enzymes catalyzing ATP production may reflect a compensatory mechanism to face impaired mitochondrial ATP synthesis in order to preserve intracellular energy homeostasis.

PMID:
18239558
DOI:
10.1038/oby.2007.91
[Indexed for MEDLINE]
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