Increased oxidative capacity in skeletal muscles from cold-acclimated ducklings: a comparison with rats

Barré, Hervé; Bailly, Laurent; Rouanet, Jean‐Louis

doi:10.1016/0305-0491(87)90337-3

Cited by 66 publications

(54 citation statements)

References 13 publications

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“…Cytochrome oxidase (COX) specific activity was measured polarographically with a Clark-type electrode (Yellow Springs Instruments) at 30°C in a medium containing 30 mol/l cytochrome c, 4 mol/l rotenone, 0.5 mmol/l dinitrophenol, 10 mmol/l Na-malonate, and 75 mmol/l Hepes (pH 7.4) (25). Measurements of basal proton leak kinetics.…”

Section: Methodsmentioning

confidence: 99%

A Possible Link Between Skeletal Muscle Mitochondrial Efficiency and Age-Induced Insulin Resistance

et al. 2004

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The transition from young to adult age is associated with decreased insulin sensitivity. To investigate whether changes in skeletal muscle mitochondrial function could be involved in the development of insulin resistance, we measured the oxidative capacity and energetic efficiency of subsarcolemmal and intermyofibrillar mitochondria isolated from the skeletal muscle of 60-and 180-day-old rats. Mitochondrial efficiency was tested by measuring the degree of thermodynamic coupling and optimal thermodynamic efficiency, as well as mitochondrial proton leak, which was determined in both the absence (basal) and the presence (fatty acid induced) of palmitate. Serum glucose, insulin, and HOMA index were also measured. The results show that in adult rats, concomitant with increased HOMA index, skeletal muscle mitochondria display higher respiratory capacity and energy efficiency. In fact, thermodynamic coupling and optimal thermodynamic efficiency significantly increased and fatty acid-induced proton leak was significantly lower in the skeletal muscle mitochondria from adult than in younger rats. A deleterious consequence of increased mitochondrial efficiency would be a reduced utilization of energy substrates, especially fatty acids, leading to intracellular triglyceride accumulation and lipotoxicity, thus contributing to the onset of skeletal muscle insulin resistance. Diabetes 53: 2861-2866, 2004 I ncreasing age is associated with obesity and insulin resistance not only in humans but also in rodents (1-5). In fact, ad libitum-fed caged rats are a good animal model that simulates the situation (sedentary lifestyle and unrestricted diet) of people in the western world.It has been previously shown that age-induced insulin resistance in rats is already detectable at 4 months of age, concomitant to a rapid rise in fat mass, and does not further increase later in life (3). This early decrease in insulin sensitivity could in turn lead to the metabolic disturbance typical of old age.Our previous results also indicate that in the transition from postpubertal (60 days) to adult (180 days) age, rats display reduced sensitivity to the anorexic effect of leptin (6) and, at the cellular level, hepatic mitochondrial machinery shows some age-related biochemical impairment (7,8). From all the above findings, it can be deduced that adult rats can be considered a good experimental tool for studying the onset of the "aging" phenomenon.It has been postulated that defects in mitochondrial performance could contribute to the development of insulin resistance (9), and mitochondrial oxidative capacity has been considered a good predictor of insulin sensitivity (10). These suggestions are not surprising since control of mitochondrial respiration and oxidative phosphorylation is fundamental for the maintenance of cellular homeostasis. The above control is exerted at two levels, i.e., regulation of the rate of oxygen consumption and ATP production and regulation of oxidative phosphorylation efficiency (11). The main determinant of oxidative phosp...

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Section: Methodsmentioning

confidence: 99%

A Possible Link Between Skeletal Muscle Mitochondrial Efficiency and Age-Induced Insulin Resistance

et al. 2004

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“…Complex IV (cytochrome c oxidase) activity was determined by a polarographical procedure at 30° C (Barré et al, 1987) using a Gilson glass respirometer equipped with a Clark oxygen electrode (Yellow Springs Instruments Ohio USA).…”

Section: Activity Of Complexes Of Respiratory Chainmentioning

confidence: 99%

Involvement of PGC-1, NRF-1, and NRF-2 in metabolic response by rat liver to hormonal and environmental signals

Venditti

Bari

Stefano

et al. 2009

Molecular and Cellular Endocrinology

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Page 1 AbstractWe studied liver oxidative capacity and O 2 consumption in hypothyroid rats treated for 10 days with T 4 , or T 3 , or treated for 10 days with T 3 and exposed to cold for the last two days. The metabolic response of homogenates and mitochondria indicated that all treatments increased the synthesis of respiratory chain components, whereas only the cold induced mitochondrial proliferation. Determination of mRNA and protein expression of transcription factor activators, such as NRF-1 and NRF-2, and coactivators, such as PGC-1, showed that mRNA levels, except PGC-1 ones, were not related to aerobic capacities. Conversely, a strong correlation was found was between cytochrome oxidase activity and PGC-1 or NRF-2 protein levels.Such a correlation was not found for NRF-1. Our results strongly support the view that in rat liver PGC-1 and NRFs are responsible for the iodothyronine-induced increases in respiratory chain components, whereas their role in cold-induced mitochondrial proliferation needs to be further on clarified.

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“…NST is achieved by the uncoupling of oxidative metabolism from ATP production, primarily in brown adipose tissue (Jansky, 1966;Foster and Frydman, 1979). In contrast to the clear role of skeletal muscle in shivering thermogenesis, the extent of NST in this tissue remains controversial, with some reports demonstrating NST in the skeletal muscle of pigeons (Skulachev and Maslov, 1960), ducklings (Barre et al, 1987) and rats (Mollica et al, 2005), whilst others found no NST in this tissue (Golozoubova et al, 2001). However, skeletal muscle, which represents a large percentage of body mass, significantly contributes to the intensification of metabolic activity of the whole organism during thermogenesis (Rolfe and Brand, 1996) due to its huge capacity for ␤-oxidation and the oxidative capacity of mitochondria (Hoppeler and Fluck, 2003).…”

Section: Introductionmentioning

confidence: 99%

Antioxidative defence alterations in skeletal muscle during prolonged acclimation to cold: role ofl-arginine/NO-producing pathway

Petrović

Buzadžić

Korać

et al. 2008

Journal of Experimental Biology

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SUMMARYEarly in cold acclimation (1-7·days), heat is produced by shivering, while late in cold acclimation (12-45·days), skeletal muscle contributes to thermogenesis by tissue metabolism other than contractions. Given that both thermogenic phases augment skeletal muscle aerobic power and reactive species production, we aimed in this study to examine possible changes in skeletal muscle antioxidative defence (AD) during early and late cold acclimation with special emphasis on the influence of the Larginine/nitric oxide (NO)-producing pathway on the modulation of AD in this tissue. Adult Mill Hill hybrid hooded rat males were divided into two main groups: a control group, which was kept at room temperature (22±1°C), and a group maintained at 4±1°C for 45·days. The cold-acclimated group was divided into three subgroups: untreated, L-arginine treated and N -nitro-L-arginine methyl ester (L-NAME) treated. The AD parameters were determined in the gastrocnemius muscle on day 1, 3, 7, 12, 21 and 45 of cold acclimation. The results showed an improvement of skeletal muscle AD in both early and late cold acclimation. Clear phasedependent changes were seen only in copper, zinc superoxide dismutase activity, which was increased in early cold acclimation but returned to the control level in late acclimation. In contrast, there were no phase-dependent changes in manganese superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione S-transferase, the activities of which were increased during the whole cold exposure, indicating their engagement in both thermogenic phases. L-Arginine in early cold acclimation accelerated the cold-induced AD response, while in the late phase it sustained increases achieved in the early period. L-NAME affected both early and late acclimation through attenuation and a decrease in the AD response. These data strongly suggest the involvement of the L-arginine/NO pathway in the modulation of skeletal muscle AD.

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Increased oxidative capacity in skeletal muscles from cold-acclimated ducklings: a comparison with rats

Cited by 66 publications

References 13 publications

A Possible Link Between Skeletal Muscle Mitochondrial Efficiency and Age-Induced Insulin Resistance

A Possible Link Between Skeletal Muscle Mitochondrial Efficiency and Age-Induced Insulin Resistance

Involvement of PGC-1, NRF-1, and NRF-2 in metabolic response by rat liver to hormonal and environmental signals

Antioxidative defence alterations in skeletal muscle during prolonged acclimation to cold: role ofl-arginine/NO-producing pathway

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