Stimulatory effects of cold exposure and cold acclimation on glucose uptake in rat peripheral tissues

Vallerand, A. L.; Perusse, F.; Bukowiecki, L. J.

doi:10.1152/ajpregu.1990.259.5.r1043

Cited by 75 publications

(86 citation statements)

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“…It is known that maximal utilization of glucose by skeletal muscle is associated with acute cold exposure, while in long-term cold acclimation a marked increase in the utilization of lipid substrates occurs (Vallerand et al, 1990). Accordingly, a conspicuous increase of CAT and GSH-Px activities recorded here from day·7 of cold acclimation could be attributed to increased ␤-oxidation of fatty acids and, connected to that, increased H 2 O 2 production.…”

Section: Discussionmentioning

confidence: 51%

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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Section: Discussionmentioning

confidence: 51%

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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“…Cold exposure stimulates glucose uptake in brown adipose tissue (BAT) of normal rats (41). Because cold exposure activates UCP1 expression in BAT via the sympathetic nervous system, the effect on glucose transport may involve increased UCP1 activity, but this needs to be tested.…”

Section: Discussionmentioning

confidence: 99%

Uncoupling Protein 3 (UCP3) Stimulates Glucose Uptake in Muscle Cells through a Phosphoinositide 3-Kinase-dependent Mechanism

Huppertz¹,

Fischer²,

Kim³

et al. 2001

Journal of Biological Chemistry

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UCP3 is a mitochondrial membrane protein expressed in humans selectively in skeletal muscle. To determine the mechanisms by which UCP3 plays a role in regulating glucose metabolism, we expressed human UCP3 in L6 myotubes by adenovirus-mediated gene transfer and in H 9 C 2 cardiomyoblasts by stable transfection with a tetracycline-repressible UCP3 construct. Expression of UCP3 in L6 myotubes increased 2-deoxyglucose uptake 2-fold and cell surface GLUT4 2.3-fold, thereby reaching maximally insulin-stimulated levels in control myotubes. Wortmannin, LY 294002, or the tyrosine kinase inhibitor genistein abolished the effect of UCP3 on glucose uptake, and wortmannin inhibited UCP3-induced GLUT4 cell surface recruitment. UCP3 overexpression increased phosphotyrosine-associated phosphoinositide 3-kinase (PI3K) activity 2.2-fold compared with control cells (p < 0.05). UCP3 overexpression increased lactate release 1.5-to 2-fold above control cells, indicating increased glucose metabolism. In H 9 C 2 cardiomyoblasts stably transfected with UCP3 under control of a tetracycline-repressible promotor, removal of doxycycline resulted in detectable levels of UCP3 at 12 h and 2.2-fold induction at 7 days compared with 12 h. In parallel, glucose transport increased 1.3-and 2-fold at 12 h and 7 days, respectively, and the stimulation was inhibited by wortmannin or genistein. p85 association with membranes was increased 5.5-fold and phosphotyrosine-associated PI3K activity 3.8-fold. In contrast, overexpression of UCP3 in 3T3-L1 adipocytes did not alter glucose uptake, suggesting tissue-specific effects of human UCP3. Thus, UCP3 stimulates glucose transport and GLUT4 translocation to the cell surface in cardiac and skeletal muscle cells by activating a PI3K dependent pathway.Uncoupling proteins (UCPs) 1 are mitochondrial inner membrane proteins proposed to be central to the regulation of energy expenditure. Energy expenditure is composed of the resting metabolic rate, physical activity, and thermogenesis and can be increased by energy dissipation due to futile metabolic processes. Uncoupling protein 1 (UCP1), the first uncoupling protein to be identified, is selectively expressed in brown adipose tissue (BAT), a major site of thermogenesis in rodents. UCP1 uncouples mitochondrial respiration from ATP synthesis by dissipating the transmembrane proton gradient, releasing energy as heat (1). The importance of UCP1 in energy expenditure in adult humans is less clear, because little BAT is present. Recently UCP2 and UCP3 were identified with 59 and 57% amino acid identity to UCP1, respectively (2-4). UCP3, unlike UCP1 and UCP2, exists as short and long form transcripts (5). The long form of UCP3 was shown to be an uncoupling protein, because it increases O 2 consumption and decreases the mitochondrial electrochemical potential when expressed in yeast or C 2 C 12 myoblasts (2, 4, 6, 7). Reconstitution of UCPs into liposomes showed that UCP2 and UCP3, like UCP1, mediate electrophoretic proton flux across lipid bilayers (8), providing furthe...

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“…In mice and rats, cold exposure leads to an immediate decrease in blood sugar levels (e.g., at 1 and 3 h) due to increased glucose uptake by the muscles and adipose tissues for use in β-oxidation and lipogenesis [15,24,31,34,44,48]. Therefore, the tendency of reduced blood sugar in suncus after 1 h (Fig.…”

Section: General Resultsmentioning

confidence: 99%

Changes in Ucp1, D2 (Dio2) and Glut4 (Slc2a4) mRNA Expression in Response to Short-Term Cold Exposure in the House Musk Shrew (Suncus murinus)

2007

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Stimulatory effects of cold exposure and cold acclimation on glucose uptake in rat peripheral tissues

Cited by 75 publications

References 0 publications

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

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

Uncoupling Protein 3 (UCP3) Stimulates Glucose Uptake in Muscle Cells through a Phosphoinositide 3-Kinase-dependent Mechanism

Changes in Ucp1, D2 (Dio2) and Glut4 (Slc2a4) mRNA Expression in Response to Short-Term Cold Exposure in the House Musk Shrew (Suncus murinus)

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