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      Resistencia a la insulina y efecto sobre la excitabilidad y contracción del músculo esquelético en rata Translated title: Insulin resistance and its effect on excitability and contraction of the skeletal muscle in rats

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          Abstract

          Introducción: la resistencia a la insulina es una condición metabólica que afecta múltiples tejidos entre ellos al músculo esquelético. El propósito del presente trabajo es analizar si la resistencia a la insulina inducida experimentalmente en ratas, modifica la excitabilidad y las propiedades contráctiles del músculo esquelético. Métodos: se incluyeron 22 ratas Sprague Dawley sanas para formar 2 grupos: Al grupo experimental (n=10) se le indujo resistencia a la insulina mediante la administración oral de prednisona (45mg/Kg.) durante 7 días. Al grupo control (n=12) se le administró solo agua. En ambos grupos se compararon principalmente los parámetros de la contractura muscular: tensión al pico, tensión total, activación contráctil y grado de excitabilidad muscular mediante una curva de umbrales así como su respuesta a una infusión continua de insulina intravenosa. Los experimentos fueron realizados en músculo gastrocnemio utilizando registros de tensión isométrica y estimulación eléctrica. Se analizaron las varianzas entre grupos para utilizar prueba t de Students o U de Mann Whitney, determinándose diferencias significativas entre ambos grupos cuando p<0.05. Resultados: (Control vs. Experimental): 1) Excitabilidad muscular: Reobase: 0.59± 0.12 V vs. 0.27 ± 0.03V (p = 0.19); Cronaxia: 0.07 ms vs. 0.08 ms. 2) Parámetros de la contractura muscular: Tensión al pico: 58.5±5.1 g vs. 48.3±4.3 g (p =0.19). Tensión total: 0.55±0.13 V/ms vs. 0.44±0.05 V/ms (p=0.45). Activación contráctil: 9.13±1.3 ms vs. 10.5±1.6 ms (p=0.19). Conclusiones: los resultados del presente estudio sugieren que la resistencia a la insulina al parecer modifica parcialmente la excitabilidad de la fibra muscular además de favorecer el desarrollo de contracciones musculares de menor intensidad y mas lentas, lo que sugiere una posible afección del acople excitación-contracción del músculo esquelético.

          Translated abstract

          Introduction: Insulin resistance is a metabolic condition that affects many tissues including skeletal muscle tissue. The objective of the present study was to analyze whether or not experimentally induced insulin resistance modifies skeletal muscle excitability and contraction in the rat. Methods : Twenty-two healthy Sprague-Dawley rats were used to form two groups. In the experimental group (n=10) insulin resistance was induced by means of oral prednisone administration (45mg/Kg) over a period of 7 days. The control group (n=12) received only water. The following muscle contraction parameters were compared between groups: peak tension, contractile activation, total tension, degree of muscle excitability during threshold curve and response to continuous intravenous insulin infusion. Experiments were carried out in gastrocnemius muscle, utilizing isometric tension registers and electrical stimulation. Variance between groups was analyzed to determine use of Student t test or Mann Whitney U test. Difference between groups was considered statistically significant when P<0.05. Results : (Control group vs Experimental group): 1) Muscle excitability: Rheobase: 0.59± 0.12 V vs 0.27 ± 0.03V (P = 0.19); Chronaxie: 0.07 ms vs 0.08 ms. 2) Muscle contraction parameters: Peak tension: 58.5±5.1 g vs 48.3±4.3 g (P =0.19). Total tension: 0.55±0.13 V/ms vs 0.44±0.05 V/ms ( P=0.45). Contractile activation: 9.13±1.3 ms vs 10.5±1.6 ms (P=0.19). Conclusions: In the results of the present study insulin resistance appears to partially modify muscle fiber excitability in addition to favoring the development of slow, low intensity muscle contractions, suggesting a possible affectation of excitation-contraction coupling in skeletal muscle.

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          Most cited references 34

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          Exercise and insulin sensitivity: a review.

          Physical activity has a beneficial effect on insulin sensitivity in normal as well as insulin resistant populations. A distinction should be made between the acute effects of exercise and genuine training effects. Up to two hours after exercise, glucose uptake is in part elevated due to insulin independent mechanisms, probably involving a contraction-induced increase in the amount of GLUT4 associated with the plasma membrane and T-tubules. However, a single bout of exercise can increase insulin sensitivity for at least 16 h post exercise in healthy as well as NIDDM subjects. Recent studies have accordingly shown that acute exercise also enhances insulin stimulated GLUT4 translocation. Increases in muscle GLUT4 protein content contribute to this effect, and in addition it has been hypothesized that the depletion of muscle glycogen stores with exercise plays a role herein. Physical training potentiates the effect of exercise on insulin sensitivity through multiple adaptations in glucose transport and metabolism. In addition, training may elicit favourable changes in lipid metabolism and can bring about improvements in the regulation of hepatic glucose output, which is especially relevant to NIDDM. It is concluded that physical training can be considered to play an important, if not essential role in the treatment and prevention of insulin insensitivity.
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            Invited review: Effects of acute exercise and exercise training on insulin resistance.

             E Henriksen (2002)
            Insulin resistance of skeletal muscle glucose transport is a key defect in the development of impaired glucose tolerance and Type 2 diabetes. It is well established that both an acute bout of exercise and chronic endurance exercise training can have beneficial effects on insulin action in insulin-resistant states. This review summarizes the present state of knowledge regarding these effects in the obese Zucker rat, a widely used rodent model of obesity-associated insulin resistance, and in insulin-resistant humans with impaired glucose tolerance or Type 2 diabetes. A single bout of prolonged aerobic exercise (30-60 min at approximately 60-70% of maximal oxygen consumption) can significantly lower plasma glucose levels, owing to normal contraction-induced stimulation of GLUT-4 glucose transporter translocation and glucose transport activity in insulin-resistant skeletal muscle. However, little is currently known about the effects of acute exercise on muscle insulin signaling in the postexercise state in insulin-resistant individuals. A well-established adaptive response to exercise training in conditions of insulin resistance is improved glucose tolerance and enhanced skeletal muscle insulin sensitivity of glucose transport. This training-induced enhancement of insulin action is associated with upregulation of specific components of the glucose transport system in insulin-resistant muscle and includes increased protein expression of GLUT-4 and insulin receptor substrate-1. It is clear that further investigations are needed to further elucidate the specific molecular mechanisms underlying the beneficial effects of acute exercise and exercise training on the glucose transport system in insulin-resistant mammalian skeletal muscle.
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              Decreased sarcoplasmic reticulum activity and contractility in diabetic db/db mouse heart.

              Although it is known that insulin-dependent (type 1) diabetes results in depressed contractile performance associated with diminished sarcoendoplasmic reticular Ca2+-ATPase (SERCA2a) activity, findings in insulin-resistant (type 2) diabetes suggest a less clear association. The db/db insulin-resistant mouse model exhibits decreased cardiac performance both in situ and in isolated ex vivo working hearts. In this study, contractile performance and calcium transients were measured in Langendorff-perfused hearts and isolated cardiac myocytes. Diabetic (db/db) mouse hearts demonstrated decreased rates of contraction, relaxation, and pressure development. Calcium transients from isolated myocytes revealed significantly lower diastolic and systolic levels of calcium in diabetic hearts. Furthermore, the decay rate of the calcium transient was significantly reduced in diabetic myocytes, suggesting a diminished capacity for cytosolic calcium removal not associated with a change in sodium-calcium exchanger activity. Calcium leakage from the sarcoplasmic reticulum (SR) measured using tetracaine was significantly increased in diabetic myocytes. Western blot analysis indicated only a small decrease in SERCA2a expression in diabetic mice, but a large increase in phospholamban expression. Expression of the ryanodine receptor did not differ between groups. In conclusion, the decreased contractile function observed in the db/db diabetic mouse model appears to be related to decreased calcium handling by the SR.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                ibi
                Revista Cubana de Investigaciones Biomédicas
                Rev Cubana Invest Bioméd
                ECIMED (Ciudad de la Habana )
                1561-3011
                June 2014
                : 33
                : 2
                : 241-252
                Affiliations
                [1 ] Universidad de Colima
                [2 ] Universidad de Colima
                [3 ] Universidad de Colima
                Article
                S0864-03002014000200013
                Product
                Product Information: website
                Categories
                MEDICINE, RESEARCH & EXPERIMENTAL

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