Increased insulin sensitivity in soleus muscle from cold‐exposed rats: reversal by an adenosine‐receptor agonist

Abstract

The effect of 0.5,2,7 and 14 days cold exposure at 4°C on insulin sensitivity was investigated in the stripped soleus muscle preparation incubated in vitro. Cold-exposure for 2 or 7 days increased the sensitivity of glycolysis, but did not affect the sensitivity of glycogen synthesis to insulin. Cold-exposure for 0.5 or 14 days had no effect on the sensitivity of either process to insulin. The increased sensitivity to insulin after exposure of animals to the cold for 2 days was completely reversed by addition of the adenosine receptor agonist, 2_chloroadenosine, to the incubation medium. This suggests that cold exposure may increase insulin sensitivity in the muscle, either by a decrease in the concentration of adenosine in the muscle, or by a decrease in the number or affinity of the adenosine receptors.Cold-exposure Cold-acclimation Insulin sensitivity bChloroadenosine Muscle

Adenosine Deaminase Activity in the Serum of Type 2 Diabetic Patients

“…Insulin acts on peripheral tissues to stimulate glucose transport, glycogen storage, and glycolysis (11,17,25,27) and stimulates hepatic glucose oxidation and decreases gluconeogenesis. Previous works have demonstrated that ubiquitous purine nucleoside adenosine differentially modulates the action of insulin in various tissues, i.e., potentiation in adipose tissue (18,31,33) and myocardium (23) and inhibition in skeletal muscle (4,5,9,28). Some adenosinereseptor-mediated activity is required for insulin to stimulate myocardial glucose uptake (22).…”

“…Adenosine has been shown to increase gluconeogenesis (22) and glycogenolysis (9,10,28). In vivo (5,9,28) and in vitro studies have shown that adenosine can stimulate glucose formation (10,22). In contrast, adenosine has been shown to decrease (12,21) or have no effect on (5) gluconeogenesis, and have no effect on glycogenolysis (2).…”

Alteration of the counterregulatory hormones in the conscious rat after protein-energy restriction

“…There are studies in the literature which demonstrate that chronic elevation of norepinephrine [34] or epinephrine [35] improved the whole body glucose disposal as well as the insulin-stimulated glucose uptake in skeletal muscle. Despite the lack of knowledge concerning the mechanism by which chronic high catecholamine levels potentiate whole body glucose disposal, it is recognized that they play a crucial role in the improvement of glucose uptake by rat peripheral tissues after physical training [36], cold exposure [37] or ventromedial hypothalamic stimulation [38].…”

Adenosine receptors mediate synergistic stimulation of glucose uptake and transport by insulin and by contractions in rat skeletal muscle.

“…Therefore, we studied the effect of A1 receptor agonism on glucose uptake in hindquarters perfused with insulin in the perfusion mix. As shown in Table I ( 19,20,(40)(41)(42), which have demonstrated Al receptor stimulation to inhibit insulin action. The reason for this discrepancy is unclear.…”