Changes in the Adenyl Cyclase System of Skeletal Muscle of Cold-Acclimated Rats

1974 ◽  
Vol 52 (3) ◽  
pp. 176-180 ◽  
Author(s):  
Michelle Muirhead ◽  
Jean Himms-Hagen
Keyword(s):  
Skeletal Muscle ◽  
Plasma Membrane ◽  
Cold Acclimation ◽  
Metabolic Response ◽  
Adenyl Cyclase ◽  
Nonshivering Thermogenesis ◽  
Receptor System ◽  
Adenyl Cyclase System ◽  
Shivering Thermogenesis ◽  
Stimulation Of

No change could be detected in the adenyl cylase system (basal activity, noradrenaline-stimulated activity, adrenaline-stimulated activity, fluoride-stimulated activity) of skeletal muscle of cold-acclimated rats. It is concluded that the enhancement of metabolic response to noradrenaline during cold-acclimation, which occurs principally in skeletal muscle, can not be attributed to an alteration in this component of the receptor system for noradrenaline.An increase in the activity of the catecholamine-stimulated and fluoride-stimulated adenyl cyclase of skeletal muscle occurs during the 1st week of exposure to cold and has disappeared by the time the rats are fully acclimated. This increase coincides with the period of shivering thermogenesis rather than with the development of nonshivering thermogenesis; it may be related to the intense and repeated stimulation of plasma membrane associated with shivering.

Urinary Excretion of Cyclic AMP by Cold-Acclimated Rats

1974 ◽  
Vol 52 (5) ◽  
pp. 414-417 ◽  
Author(s):  
Michelle Muirhead ◽  
Aileen Inglis ◽  
Jean Himms-Hagen
Keyword(s):  
Cyclic Amp ◽  
Metabolic Rate ◽  
Room Temperature ◽  
Metabolic Response ◽  
Adenyl Cyclase ◽  
Nonshivering Thermogenesis ◽  
Brown Adipose ◽  
Adenyl Cyclase System ◽  
First Time ◽  
Noradrenaline And Adrenaline

Cold-acclimated rats living in the cold (4°) excrete more cyclic AMP in their urine than do control warm-acclimated rats living at room temperature (26°–28°). However, cold-acclimated rats, returned to the cold after a few days at room temperature and presumably raising their metabolic rate by nonshivering thermogenesis in response to the noradrenaline and adrenaline secreted by the sympathetic nervous system, excrete the same amount of cyclic AMP in their urine as do warm-acclimated rats of the same age put into the cold for the first time and presumably raising their metabolic rate by shivering. Thus, no evidence could be found for an altered utilization of the adenyl cyclase system in the cold-acclimated rat. This, together with previous findings of unaltered levels and properties of noradrenaline-stimulated adenyl cyclase in brown adipose tissue and skeletal muscle of cold-acclimated rats, leads us to the conclusion that the enhancement of the metabolic response to noradrenaline in cold-acclimated rats is not due to any alteration in the adenyl cyclase system.

CHANGES IN THE RESTING POTENTIAL OF SKELETAL MUSCLE IN RATS WITH COLD ACCLIMATION

1966 ◽  
Vol 44 (5) ◽  
pp. 791-802 ◽  
Author(s):  
M. H. Sherebrin ◽  
A. C. Burton
Keyword(s):  
Skeletal Muscle ◽  
Electrical Properties ◽  
Cold Acclimation ◽  
White Muscle ◽  
Single Cells ◽  
Temperature Gradients ◽  
Resting Potential ◽  
The Mean ◽  
Shivering Thermogenesis ◽  
Main Factor

The resting potential of single cells in the flexor thigh muscles of rats was measured in an attempt to find a change in the electrical properties of the cell membrane with cold acclimation, in order to identify and relate metabolic changes occurring with non-shivering thermogenesis. The mean resting potential of cells in cold-acclimated rats was found to be slightly but significantly higher than in the controls. A larger temperature gradient with depth was measured in the cold-acclimated animals than in the controls. If the Q10 of resting potential with temperature is as great as 1.16, the higher potential in the cold-acclimated rats may be accounted for by this temperature difference. The resting potential was also found to vary with depth in both groups of rats. This could not be attributed to temperature gradients, and change from red to white muscle cells with depth is thought to be the main factor for the increase of potential with depth.

Stimulation of glucose transport in skeletal muscle by hypoxia

1991 ◽  
Vol 70 (4) ◽  
pp. 1593-1600 ◽  
Author(s):  
G. D. Cartee ◽  
A. G. Douen ◽  
T. Ramlal ◽  
A. Klip ◽  
J. O. Holloszy
Keyword(s):  
Skeletal Muscle ◽  
Plasma Membrane ◽  
Muscle Contraction ◽  
Glucose Transport ◽  
Glucose Transporter ◽  
Cytochalasin B ◽  
Sugar Transport ◽  
Transport Activity ◽  
Hindlimb Muscles ◽  
Stimulation Of

Hypoxia caused a progressive cytochalasin B-inhibitable increase in the rate of 3-O-methylglucose transport in rat epitrochlearis muscles to a level approximately six-fold above basal. Muscle ATP concentration was well maintained during hypoxia, and increased glucose transport activity was still present after 15 min of reoxygenation despite repletion of phosphocreatine. However, the increase in glucose transport activity completely reversed during a 180-min-long recovery in oxygenated medium. In perfused rat hindlimb muscles, hypoxia caused an increase in glucose transporters in the plasma membrane, suggesting that glucose transporter translocation plays a role in the stimulation of glucose transport by hypoxia. The maximal effects of hypoxia and insulin on glucose transport activity were additive, whereas the effects of exercise and hypoxia were not, providing evidence suggesting that hypoxia and exercise stimulate glucose transport by the same mechanism. Caffeine, at a concentration too low to cause muscle contraction or an increase in glucose transport by itself, markedly potentiated the effect of a submaximal hypoxic stimulus on sugar transport. Dantrolene significantly inhibited the hypoxia-induced increase in 3-O-methylglucose transport. These effects of caffeine and dantrolene suggest that Ca2+ plays a role in the stimulation of glucose transport by hypoxia.

The molecular and biochemical basis of nonshivering thermogenesis in an African endemic mammal, Elephantulus myurus

2007 ◽  
Vol 293 (5) ◽  
pp. R2120-R2127 ◽  
Author(s):  
Nomakwezi Mzilikazi ◽  
Martin Jastroch ◽  
Carola W. Meyer ◽  
Martin Klingenspor
Keyword(s):  
Cold Acclimation ◽  
Metabolic Response ◽  
Uncoupling Protein ◽  
Mammalian Species ◽  
Liver Mitochondria ◽  
Nonshivering Thermogenesis ◽  
Vertebrate Lineage ◽  
Biochemical Basis ◽  
Fat Deposits ◽  
Brown Adipose

Uncoupling protein 1 (UCP1) mediated nonshivering thermogenesis (NST) in brown adipose tissue (BAT) is an important avenue of thermoregulatory heat production in many mammalian species. Until recently, UCP1 was thought to occur exclusively in eutherians. In the light of the recent finding that UCP1 is already present in fish, it is of interest to investigate when UCP1 gained a thermogenic function in the vertebrate lineage. We elucidated the basis of NST in the rock elephant shrew, Elephantulus myurus (Afrotheria: Macroscelidea). We sequenced Ucp1 and detected Ucp1 mRNA and protein restricted to brown fat deposits. We found that cytochrome c oxidase activity was highest in these deposits when compared with liver and skeletal muscle. Consistent with a thermogenic function of UCP1 isolated BAT mitochondria showed increased state 4 respiration in the cold, as well as palmitate-induced, GDP-sensitive proton conductance, which was absent in liver mitochondria. On the whole animal level, evidence of thermogenic function was further corroborated by an increased metabolic response to norepinephrine (NE) injection. Cold acclimation (18°C) led to an increased basal metabolic rate relative to warm acclimation (28°C) in E. myurus, but there was no evidence of additional recruitment of NE-induced NST capacity in response to cold acclimation. In summary, we showed that BAT and functional UCP1 are already present in a member of the Afrotheria, but the seasonal regulation and adaptive value of NST in Afrotherians remain to be elucidated.

Type 2 iodothyronine deiodinase is upregulated in rat slow- and fast-twitch skeletal muscle during cold exposure

2014 ◽  
Vol 307 (11) ◽  
pp. E1020-E1029 ◽  
Author(s):  
Ruy A. Louzada ◽  
Maria C. S. Santos ◽  
João Paulo A. Cavalcanti-de-Albuquerque ◽  
Igor F. Rangel ◽  
Andrea C. F. Ferreira ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Acclimation ◽  
Soleus Muscle ◽  
Cold Exposure ◽  
Skeletal Muscles ◽  
Nonshivering Thermogenesis ◽  
Brown Adipose

During cold acclimation, shivering is progressively replaced by nonshivering thermogenesis. Brown adipose tissue (BAT) and skeletal muscle are relevant for nonshivering thermogenesis, which depends largely on thyroid hormone. Since the skeletal muscle fibers progressively adapt to cold exposure through poorly defined mechanisms, our intent was to determine whether skeletal muscle type 2 deiodinase (D2) induction could be implicated in the long-term skeletal muscle cold acclimation. We demonstrate that in the red oxidative soleus muscle, D2 activity increased 2.3-fold after 3 days at 4°C together with the brown adipose tissue D2 activity, which increased 10-fold. Soleus muscle and BAT D2 activities returned to the control levels after 10 days of cold exposure, when an increase of 2.8-fold in D2 activity was detected in white glycolytic gastrocnemius but not in red oxidative gastrocnemius fibers. Propranolol did not prevent muscle D2 induction, but it impaired the decrease of D2 in BAT and soleus after 10 days at 4°C. Cold exposure is accompanied by increased oxygen consumption, UCP3, and PGC-1α genes expression in skeletal muscles, which were partialy prevented by propranolol in soleus and gastrocnemius. Serum total and free T3 is increased during cold exposure in rats, even after 10 days, when BAT D2 is already normalized, suggesting that skeletal muscle D2 activity contributes significantly to circulating T3 under this adaptive condition. In conclusion, cold exposure is accompanied by concerted changes in the metabolism of BAT and oxidative and glycolytic skeletal muscles that are paralleled by type 2 deiodinase activation.

Creatine metabolism in skeletal muscle of cold-acclimated rats

1978 ◽  
Vol 44 (1) ◽  
pp. 12-16 ◽  
Author(s):  
M. Kurahashi ◽  
A. Kuroshima
Keyword(s):  
Skeletal Muscle ◽  
Cold Acclimation ◽  
Turnover Rate ◽  
Early Stage ◽  
Control Level ◽  
Nonshivering Thermogenesis ◽  
Creatine Uptake ◽  
Total Creatine ◽  
Muscle Creatine ◽  
Creatine Metabolism

Creatine metabolism in skeletal muscle of cold-acclimated rats was studied with the aid of [14C]creatine as a tracer. Creatine contents of all muscles studied were significantly lower in cold-acclimated rats than in controls. Radioactive creatine uptake by soleus of cold-acclimated rats was significantly lower than that of controls, while radioactive creatine uptakes by heart, diaphragm, and gastrocnemius of cold-acclimated rats were not different from those of controls. Urinary creatine dervied from muscle creatine plus urinary creatinine, which corresponds to total creatine release from muscle, increased in the early stage of cold exposure and was restored to control level after completion of cold acclimation. Creatine turnover rate in skeletal muscle was not different between control and cold-acclimated rats. These findings indicate that cold acclimation results in reduced creatine content and uptake of skeletal muscle, and could be interpreted as reflecting enhanced ability of nonshivering thermogenesis in skeletal muscle.

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

1990 ◽  
Vol 259 (5) ◽  
pp. R1043-R1049 ◽  
Author(s):  
A. L. Vallerand ◽  
F. Perusse ◽  
L. J. Bukowiecki
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Cold Acclimation ◽  
Cold Exposure ◽  
Skeletal Muscles ◽  
Contractile Activity ◽  
Peripheral Tissues ◽  
Brown Adipose ◽  
Shivering Thermogenesis ◽  
Stimulation Of

The effects of cold exposure on the net rates of 2-[3H]deoxy-D-glucose uptake (Ki) in rat peripheral tissues were investigated comparatively in warm- and cold-acclimated animals to determine whether cold acclimation induces regulatory alterations in glucose metabolism. Acute exposure of warm-acclimated (25 degrees C) rats to cold (48 h at 5 degrees C) markedly increased the Ki values in red and white skeletal muscles (2-5 times), in the heart (8 times), in several white adipose tissue (WAT) depots (4-20 times), and in brown adipose tissue (BAT) (110 times). After cold acclimation (3 wk at 5 degrees C), the Ki values further increased in the heart (15 times) and WAT (up to 29 times) but decreased in BAT (36 times). Remarkably, glucose uptake was still increased in muscles of cold-exposed/cold-acclimated animals (that do not shiver), demonstrating that enhanced glucose uptake may occur in muscles in the absence of shivering thermogenesis (or contractile activity). When cold-acclimated rats were returned to the warm for 18 h, the Ki values of all tissues, except WAT, returned to control levels. Cold exposure synergistically potentiated the stimulation of tissue glucose uptake induced by a maximal effective dose of insulin (0.5 U/kg iv) in warm- as well as in cold-acclimated animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document