Effects of cold acclimation and palmitate on energy coupling in duckling skeletal muscle mitochondria

Roussel, Damien; Rouanet, Jean‐Louis; Duchamp, Claude; Barré, Hervé

doi:10.1016/s0014-5793(98)01382-9

Cited by 35 publications

(49 citation statements)

References 29 publications

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“…However, like the mammalian UCPs (Echtay et al, 2002), avUCP requires activation by superoxide before its proton conductance can be seen (Talbot et al, 2003), which suggests that avUCP would not be activated in phosphorylating mitochondria, when ATP is synthesized and superoxide production is largely decreased. This is in accordance with previous results showing an increased ATP production in fully phosphorylating active skeletal muscle mitochondria (in the presence of high concentration of adenine nucleotides) isolated from cold-acclimated ducklings (Roussel et al, 1998). Nonetheless, it is obvious that the proton leak reactions and the ATP synthase compete for the same driving force.…”

Section: Discussionsupporting

confidence: 93%

“…In the absence of both mammalian thermogenic brown adipose tissue and UCP1 (UCP, uncoupling protein) in birds (Johnston, 1971;Barré et al, 1986), there is some evidence that mitochondrial loose coupling might contribute to cold-induced heat production in skeletal muscle (Skulachev and Maslov, 1960;Duchamp et al, 1992;Roussel et al, 1998), i.e. the major tissue contributing to 70% of the observed NST in cold-acclimated ducklings (Duchamp and Barré, 1993).…”

Section: Introductionmentioning

confidence: 99%

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Cold-acclimation-induced non-shivering thermogenesis in birds is associated with upregulation of avian UCP but not with innate uncoupling or altered ATP efficiency

Teulier

Rouanet

Letexier

et al. 2010

Journal of Experimental Biology

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) were obtained from a commercial stockbreeder (Eclosion Grimaud-lacorbière, Roussay, France). Birds were fed ad libitum with commercial mash (Moulin Guenard, 645000MI, Vonnas, France) and had free access to water. From the age of 10 days, ducklings were caged for Accepted 7 April 2010 SUMMARY Despite their lack of brown adipose tissue, some bird species develop regulatory non-shivering thermogenesis (NST) of skeletal muscle origin in response to cold acclimation. Mechanisms involved in avian NST are still unclear but may involve reduced energetic coupling in skeletal muscle mitochondria through the expression of an avian homologue of mammalian uncoupling proteins. The aim of this work was to investigate whether the expression of avian uncoupling protein (avUCP) would correlate with the capacity for cold-induced muscle NST. Various levels of cold acclimation were obtained by rearing 1-week-old ducklings (Cairina moschata) for 4 weeks at three different ambient temperatures (25°C, 11°C or 4°C). Muscle NST was measured by simultaneous recordings of metabolic rate and electromyographic activity (gastrocnemius muscle) at ambient temperatures (T a ) ranging from 27°C to -5°C. The expression of avUCP gene and mitochondrial bioenergetics were also determined in gastrocnemius muscle. Results showed that muscle NST capacity depends on the T a at which ducklings were acclimated, i.e. the lower the rearing temperature, the higher the capacity for NST. This increased metabolic heat production occurred in parallel with an upregulation of avUCP, which was not associated with a change in mitochondrial membrane conductance. The intensity of mitochondrial oxidative phosphorylation also increased in proportion with the harshness of cold, while the efficiency of ATP generation was equally effective in all three acclimation temperatures. In the absence of mitochondrial uncoupling, these data indicate a clear link between avUCP expression and the capacity of ducklings to adjust their muscular aerobic activity to cold exposure.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Cold-acclimation-induced non-shivering thermogenesis in birds is associated with upregulation of avian UCP but not with innate uncoupling or altered ATP efficiency

Teulier

Rouanet

Letexier

et al. 2010

Journal of Experimental Biology

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“…Avian NST was also induced by chronic treatment of ducklings kept at thermoneutrality with glucagon, a thermogenic hormone in birds [6]. Avian NST mainly originates from skeletal muscle [7] and involves a loose coupling of mitochondrial oxidative phosphorylation under the control of fatty acids [8,9]. The molecular mechanisms of such uncoupling are not known.…”

Section: Introductionmentioning

confidence: 99%

An uncoupling protein homologue putatively involved in facultative muscle thermogenesis in birds

RAIMBAULT

Dridi²,

DENJEAN

et al. 2001

Biochemical Journal

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139

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The cDNA of an uncoupling protein (UCP) homologue was obtained by screening a chicken skeletal-muscle library. The predicted 307-amino-acid sequence of avian UCP (avUCP) is 55, 70, 70 and 46% identical with mammalian UCP1, UCP2 and UCP3 and plant UCP respectively. avUCP mRNA expression is restricted to skeletal muscle and its abundance was increased 1.3-fold in a chicken line showing diet-induced thermogenesis, and 3.6- and 2.6-fold in cold-acclimated and glucagon-treated ducklings developing muscle non-shivering thermogenesis respectively. The present data support the implication of avUCP in avian energy expenditure.

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“…Intermyofibrillar (IFM) and subsarcolemmal (SSM) mitochondria were isolated from gastrocnemius and heart muscles in a buffer containing 100 mM sucrose, 50 mM KCl, 5 mM EGTA and 50 mM Tris/HCl, pH 7.4 at 4°C as described previously (Roussel et al 1998).…”

Section: Mitochondrial Isolation and Activitymentioning

confidence: 99%

“…The rates of oxygen consumption were measured with a Clark oxygen electrode in a glass cell of 1.5 ml volume with constant stirring, as described previously (Roussel et al 1998(Roussel et al , 2000. Respiratory substrates were succinate (10 mM) in the presence of 5 µM rotenone, or 8 mM ascorbate plus 0.6 mM N,N,N', in the presence of 5 µM antimycin .…”

Section: Mitochondrial Isolation and Activitymentioning

confidence: 99%

Mitochondrial oxidative energy metabolism in guanethidine-induced sympathectomized ducklings

Filali-Zegzouti

Rouanet²,

Fechtali³

et al. 2014

gpb

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Abstract.Here we investigate the possible involvement of the sympathetic nervous system in the respiratory properties of intermyofibrillar and subsarcolemmal mitochondrial populations from heart and gastrocnemius muscles. Mitochondrial oxidative phosphorylation was assessed polarographically by using succinate (plus rotenone), and ascorbate plus N,N,N' ,N'-tetramethyl-p-phenyl-enediamine (plus antimycin) as respiratory substrates. We report that chronic chemical sympathectomy with guanethidine (150 mg/kg, daily for 3 weeks) induced a marked decrease in whole body metabolic and heart rates, in plasma metabolites (fatty acids and glucose) and norepinephrine levels. Guanethidine treatment decreased mainly the oxidative phosphorylation capacity of subsarcolemmal mitochondria in heart, irrespective of the substrate used. In contrast, both mitochondrial populations were affected by the treatment in skeletal muscle. This suggests that sympathetic nervous system activity can alter the energetic status of muscle cells, and to some extent play a thermogenic role in birds.

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Effects of cold acclimation and palmitate on energy coupling in duckling skeletal muscle mitochondria

Cited by 35 publications

References 29 publications

Cold-acclimation-induced non-shivering thermogenesis in birds is associated with upregulation of avian UCP but not with innate uncoupling or altered ATP efficiency

Cold-acclimation-induced non-shivering thermogenesis in birds is associated with upregulation of avian UCP but not with innate uncoupling or altered ATP efficiency

An uncoupling protein homologue putatively involved in facultative muscle thermogenesis in birds

Mitochondrial oxidative energy metabolism in guanethidine-induced sympathectomized ducklings

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