This study investigated the effect of 2 weeks of caloric restriction on whole body, liver and skeletal muscle energy handling. We measured whole body oxygen consumption, as well as mitochondrial protein mass, respiratory capacity and energetic coupling in liver and skeletal muscle from food-restricted rats, age- and weight-matched controls. We also assessed markers of oxidative damage and antioxidant defences. Our results show that, in response to caloric restriction, an adaptive decrease in whole body energy expenditure is coupled with structural and functional changes in mitochondrial compartment both in liver and skeletal muscle. In fact, liver mitochondrial mass/g liver significantly increased, while total hepatic mitochondrial oxidative capacity was lower in food restricted than in control rats, due to a significant decrease in liver contribution to total body weight. In skeletal muscle, subsarcolemmal mitochondrial respiratory capacity, as well as subsarcolemmal and intermyofibrillar mitochondrial protein mass/g tissue, was significantly lower in food restricted rats, compared to controls. Finally, a decrease in oxidative damage was found in liver but not in skeletal muscle mitochondria from food restricted rats, while an increase in antioxidant defence was found in both tissues. From the present results it appears that skeletal muscle is involved in the decrease in energy expenditure induced by caloric restriction. Energy sparing is achieved through changes in the activity (subsarcolemmal), mass (subsarcolemmal and intermyofibrillar) and efficiency (intermyofibrillar) of mitochondrial compartment.

Hepatic mitochondrial energetics during catch-up fat after caloric restriction / Crescenzo, Raffaella; Bianco, Francesca; Falcone, Italia; Prisco, Marina; Dulloo, A. G.; Liverini, Giovanna; Iossa, Susanna. - In: METABOLISM, CLINICAL AND EXPERIMENTAL. - ISSN 0026-0495. - STAMPA. - 59:(2010), pp. 1221-1230. [10.1016/j.metabol.2009.11.015]

Hepatic mitochondrial energetics during catch-up fat after caloric restriction.

CRESCENZO, RAFFAELLA;BIANCO, FRANCESCA;FALCONE, ITALIA;PRISCO, MARINA;LIVERINI, GIOVANNA;IOSSA, SUSANNA
2010

Abstract

This study investigated the effect of 2 weeks of caloric restriction on whole body, liver and skeletal muscle energy handling. We measured whole body oxygen consumption, as well as mitochondrial protein mass, respiratory capacity and energetic coupling in liver and skeletal muscle from food-restricted rats, age- and weight-matched controls. We also assessed markers of oxidative damage and antioxidant defences. Our results show that, in response to caloric restriction, an adaptive decrease in whole body energy expenditure is coupled with structural and functional changes in mitochondrial compartment both in liver and skeletal muscle. In fact, liver mitochondrial mass/g liver significantly increased, while total hepatic mitochondrial oxidative capacity was lower in food restricted than in control rats, due to a significant decrease in liver contribution to total body weight. In skeletal muscle, subsarcolemmal mitochondrial respiratory capacity, as well as subsarcolemmal and intermyofibrillar mitochondrial protein mass/g tissue, was significantly lower in food restricted rats, compared to controls. Finally, a decrease in oxidative damage was found in liver but not in skeletal muscle mitochondria from food restricted rats, while an increase in antioxidant defence was found in both tissues. From the present results it appears that skeletal muscle is involved in the decrease in energy expenditure induced by caloric restriction. Energy sparing is achieved through changes in the activity (subsarcolemmal), mass (subsarcolemmal and intermyofibrillar) and efficiency (intermyofibrillar) of mitochondrial compartment.
2010
Hepatic mitochondrial energetics during catch-up fat after caloric restriction / Crescenzo, Raffaella; Bianco, Francesca; Falcone, Italia; Prisco, Marina; Dulloo, A. G.; Liverini, Giovanna; Iossa, Susanna. - In: METABOLISM, CLINICAL AND EXPERIMENTAL. - ISSN 0026-0495. - STAMPA. - 59:(2010), pp. 1221-1230. [10.1016/j.metabol.2009.11.015]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/363607
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