Effects of 4 wk of hindlimb suspension on skeletal muscle mitochondrial respiration in rats

Yajid, Fatima; Mercier, Jacques; Mercier, B.; Dubouchaud, Hervé; Préfaut, Christian

doi:10.1152/jappl.1998.84.2.479

Cited by 55 publications

(56 citation statements)

References 28 publications

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“…These evidences clearly indicated the occurrence of mitochondria loss in GAS induced by unloading. Interestingly, in the isolated muscle mitochondria, mitochondrial respiration chain complexes activity did not compromise with the mitochondrial deficiency following unloading (data not shown), consistent with an earlier report (21). These results suggest that unloading preferentially affected GAS with muscle atrophy and mitochondria loss while TA showed resistance with little atrophy.…”

Section: Compared With Ta Gas Was Preferentially Affected To Atrophysupporting

confidence: 91%

“…), and members of the PGC-1 (peroxisome proliferator-activated receptor c coactivator 1) family (PGC-1a/b and PGC-1 related coactivator (PRC)) (9). PGC-1 can be transcriptionally regulated by the factors like cAMP response element-binding protein (CREB) and the type II multifunctional Ca 21 /calmodulin kinase (CaMK II). And, it can also be post-translationally modificated by silent mating type information regulation 2 homolog 1 (SIRT1) and AMP-activated protein kinase (AMPK) (10).…”

Section: Introductionmentioning

confidence: 99%

“…The fast-twitch muscles-EDL, GAS, and TA also respond to unloading in mouse or rat (19,20). Especially, GAS exhibited the specific dysfunction of mitochondrial respiration and TA showed distinct electromyogram following unloading (21,22). Thus, we hypothesized that diverse mitochondrial dynamics underlie the varied adaptations to unloading in TA and GAS.…”

Section: Introductionmentioning

confidence: 99%

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Depressed mitochondrial biogenesis and dynamic remodeling in mouse tibialis anterior and gastrocnemius induced by 4‐week hindlimb unloading

et al. 2012

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SummaryMitochondrial dynamics is highly involved in muscle atrophy, the slow twitch muscle as soleus, preferentially affected by hindlimb unloading (HU), was well characterized by mitochondrial dysfunction in biogenesis. However, the fast twitch muscles like tibialis anterior (TA) and gastrocnemius (GAS), which are the most massive parts of the hindlimb muscles, are less elucidated on mitochondrial adaptations responding to HU. To investigate the mitochondrial dynamic responses and the involved molecules mediating atrophy in TA and GAS, we studied a 4-week HU mouse model. We found GAS was preferentially affected to atrophy by unloading compared with TA. Furthermore, the depressed mitochondrial biogenesis occurred, accounting for mitochondrial loss in GAS by unloading. PGC-1a, as well as its transcriptional/post-translational modification regulators, such as p-CREB, SIRT1, and p-AMPK, were consistently reduced in response to unloading in GAS. Molecules relevant to autophagy, mitochondrial fusion, and fission, were compromised following unloading both in TA and GAS. These results suggested that TA exhibited resistance to unloading induced muscle atrophy while GAS presented significant mitochondrial loss, which might be due to the mitochondrial biogenesis suppressed by the inactivation of PGC-1a. However, both in TA and GAS muscles, a similar sedentary mitochondrial dynamics of mitochondrial fusion and fission was induced by unloading though TA exhibited little muscle atrophy. IUBMBIUBMB Life, 64(11): 901-910, 2012

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Section: Compared With Ta Gas Was Preferentially Affected To Atrophysupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Depressed mitochondrial biogenesis and dynamic remodeling in mouse tibialis anterior and gastrocnemius induced by 4‐week hindlimb unloading

et al. 2012

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“…In fact, we found an increase in lipid-supported respiration in both populations of mitochondria and an increase in NAD-linked respiration in intermyofibrillar mitochondria. Differential regulation of mitochondrial activity in the two subpopulations has been previously found in response to other environmental stimuli, 15,17,18 and could be due to differences in protein synthesis capacity, 15 rates of import of nuclear-coded mitochondrial proteins 29 and=or rates of protein degradation. 15,29 Our results also suggest that increased skeletal muscle lipid oxidative capacity is only due to an increase in mitochondrial specific activity.…”

Section: Discussionmentioning

confidence: 75%

“…In addition, it is well known that two distinct populations of mitochondria exist within muscle cells, 14 -16 and that these two populations adapt differently to experimental conditions (ie exercise, immobilization). 15,17,18 However, no studies so far have examined the effect of high-fat feeding on the activity of these two mitochondrial populations. We have therefore also measured oxidative capacity in isolated subsarcolemmal and intermyofibrillar organelles.…”

Section: Introductionmentioning

confidence: 99%

Skeletal muscle oxidative capacity in rats fed high-fat diet

et al. 2002

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OBJECTIVE: To investigate whether young rats respond to high-fat feeding through changes in energy efficiency and fuel partitioning at the level of skeletal muscle, to avoid obesity development. In addition, to establish whether the two mitochondrial subpopulations, which exist in skeletal muscle, ie subsarcolemmal and intermyofibrillar, are differently affected by high-fat feeding. DESIGN: Weaning rats were fed a low-fat or a high-fat diet for 15 days. MEASUREMENTS: Energy balance and lipid partitioning in the whole animal. State 3 and state 4 oxygen consumption rates in whole skeletal muscle homogenate. State 3 and state 4 oxygen consumption rates, membrane potential and uncoupling effect of palmitate in subsarcolemmal and intermyofibrillar mitochondria from skeletal muscle. RESULTS: Rats fed a high-fat diet showed an increased whole body lipid utilization. Skeletal muscle NAD-linked and lipid oxidative capacity significantly increased at the whole-tissue level, due to an increase in lipid oxidative capacity in subsarcolemmal and intermyofibrillar mitochondria and in NAD-linked activity only in intermyofibrillar ones. In addition, rats fed a highfat diet showed an increase in the uncoupling effect of palmitate in both the mitochondrial populations. CONCLUSIONS: In young rats fed a high-fat diet, skeletal muscle contributes to enhanced whole body lipid oxidation through an increased mitochondrial capacity to use lipids as metabolic fuels, associated with a decrease in energy coupling.

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