Body weight and food intake.

<p>Body weight and food intake.</p

Primers and program conditions for real-time PCR.

<p>Primers and program conditions for real-time PCR.</p

Concentrations of isobutyrate, isovalerate, and valerate in cecal contents.

<p>Concentrations of isobutyrate, isovalerate, and valerate in cecal contents.</p

An Alteration in the Cecal Microbiota Composition by Feeding of 1-Kestose Results in a Marked Increase in the Cecal Butyrate Content in Rats - Fig 1

<p><b>(a)-(e). Photographs of the cecum with cecal contents in rats.</b> The cecum from each group of rats: (a) control, (b) 0.5%, (c) 1%, (d) 2.5%, (e) 5%. Bars: 2 cm.</p

Measurement of SCFAs in cecal contents.

<p>Values represent the means ± SE (n = 8), * P <0.05 vs. control group.</p

Weights of the cecum and cecal contents.

<p>Weights of the cecum and cecal contents.</p

Experimental diets.

<p>Experimental diets.</p

Concentrations of total cholesterol, triglyceride, glucose, and insulin.

<p>Concentrations of total cholesterol, triglyceride, glucose, and insulin.</p

Levels of bacterial cell numbers (log₁₀ cells/g) in cecal contents.

<p>Levels of bacterial cell numbers (log₁₀ cells/g) in cecal contents.</p

Endurance performance and energy metabolism during exercise in mice with a muscle-specific defect in the control of branched-chain amino acid catabolism

<div><p>It is known that the catabolism of branched-chain amino acids (BCAAs) in skeletal muscle is suppressed under normal and sedentary conditions but is promoted by exercise. BCAA catabolism in muscle tissues is regulated by the branched-chain α-keto acid (BCKA) dehydrogenase complex, which is inactivated by phosphorylation by BCKA dehydrogenase kinase (BDK). In the present study, we used muscle-specific BDK deficient mice (BDK-mKO mice) to examine the effect of uncontrolled BCAA catabolism on endurance exercise performance and skeletal muscle energy metabolism. Untrained control and BDK-mKO mice showed the same performance; however, the endurance performance enhanced by 2 weeks of running training was somewhat, but significantly less in BDK-mKO mice than in control mice. Skeletal muscle of BDK-mKO mice had low levels of glycogen. Metabolome analysis showed that BCAA catabolism was greatly enhanced in the muscle of BDK-mKO mice and produced branched-chain acyl-carnitine, which induced perturbation of energy metabolism in the muscle. These results suggest that the tight regulation of BCAA catabolism in muscles is important for homeostasis of muscle energy metabolism and, at least in part, for adaptation to exercise training.</p></div