Mediation of ?-endorphin in exercise-induced improvement in insulin resistance in obese Zucker rats

Su, Chin-Hui; Chang, Yen‐Hsiang; Pai, Hui-Ching; Liu, I. M.; Lo, Chia-Ying; Cheng, Juei‐Tang

doi:10.1002/dmrr.496

Cited by 35 publications

(31 citation statements)

References 30 publications

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“…It could be that the attenuated effect of exercise on hyperglycemia observed with the DHT inhibitor led to a compensatory adaptation to elevate insulin secretion. It has been well documented that exercise training induced the improvement of insulin sensitivity, which is measured by the hyperinsulinemic-euglycemic clamp technique [23,24]. In the present study, exercise training improved fasting blood glucose and insulin levels through the activation of Akt and PKCζ/λ-GLUT-4 signaling pathway in our Zucker fatty obese rats.…”

Section: Discussionsupporting

confidence: 62%

The Exercise-Induced Improvement in hyperglycemia is Mediated by DHT Produced in the Skeletal Muscle of Zucker Diabetic Fatty Rats

Sato¹

2012

J Diabetes Metab

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The ability of exercise to improve hyperglycemia by enhancing glucose metabolism in the skeletal muscle of type 2 diabetic patients is well established. We reported sex steroid hormones can be locally synthesized in skeletal muscle and decrease fasting blood glucose levels in obese rats. Here, we determined whether exercise-induced production of sex steroid hormones in skeletal muscle could directly reverse hyperglycemia in the Zucker diabetic fatty rat model using osmotic mini pump.Thirty Zucker diabetic fatty rats were randomly assigned to the following groups: control, exercise, or exercise with continuous infusion of 5α-reductase inhibitor.The results indicated 6 weeks of exercise significantly reduced serum insulin and fasting glucose levels compared to control group. Dehydroepiandrosterone, 5α-dehydrotestosterone, and 5α-reductase levels were all significantly higher in skeletal muscle of the exercise group. Moreover, exercise increased glucose transporter-4 translocation with a concomitant upregulation of phosphorylated phosphoinositide 3-kinase, protein kinase B and C-ζ/λ. Furthermore, significant correlations were observed between fasting glucose and muscular DHT levels. Interestingly, the observed exercise-induced improvements in serum insulin and fasting glucose levels were all suppressed by administration of 5α-reductase inhibitor.These results indicated the exercise-induced improvements in glucose metabolism signaling and glucose levels may be directly attributed to the increased levels of sex steroid hormones within skeletal muscles.

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Section: Discussionsupporting

confidence: 62%

The Exercise-Induced Improvement in hyperglycemia is Mediated by DHT Produced in the Skeletal Muscle of Zucker Diabetic Fatty Rats

Sato¹

2012

J Diabetes Metab

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“…Chemical agents such as loperamide or tramadol increased glucose utilization via activation of opioid -receptors to lower plasma glucose in STZ-induced diabetic rats (14,15). In obese Zucker rats, mediation of ␤-endorphin in exercise-induced improvement of insulin resistance has also been observed (16). These findings support a beneficial effect of opioid -receptor activation on plasma glucose regulation.…”

mentioning

confidence: 62%

Novel Mechanism for Plasma Glucose–Lowering Action of Metformin in Streptozotocin-Induced Diabetic Rats

et al. 2006

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To better understand the insulin-independent plasma glucose-lowering action of metformin, we used streptozotocin (STZ)-induced diabetic rats to investigate the possible mechanisms. Oral intake of metformin decreased the plasma glucose of STZ-induced diabetic rats with a parallel increase of plasma ␤-endorphin-like immunoreactivity (BER). Mediation of opioid -receptors in the action of metformin was identified by the blockade of receptors with antagonist in STZ-induced diabetic rats and the failure of action in opioid -receptor knockout diabetic mice. Release of BER from adrenal glands by metformin was characterized, using bilateral adrenalectomy and the release of BER from isolated adrenal medulla of STZ-induced diabetic rats. Repeated treatment with metformin in STZ-induced diabetic rats increased the mRNA and protein levels of GLUT-4 in soleus muscle that was blocked by naloxonazine. Reduction of the mRNA or protein levels of hepatic PEPCK was also impeded in the same group of STZ-induced diabetic rats. In conclusion, our results provide novel mechanisms for the plasma glucose-lowering action of metformin, via an increase of ␤-endorphin secretion from adrenal glands to stimulate opioid -receptor linkage, leading to an increase of GLUT-4 gene expression and an attenuation of hepatic PEPCK gene expression in STZinduced diabetic rats. Diabetes 55:819 -825, 2006

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“…These symptoms are similar to those observed in people with type 2 diabetes, making this rat a useful model for the study of this disease (Tofovic and Jackson 2003). Skeletal muscle is the principal site of insulin-mediated glucose uptake, and long-term aerobic exercise training has been shown to improve insulin resistance in obese Zucker rats (Saengsirisuwan et al 2002;Su et al 2005). These exerciserelated improvements in muscle response to insulin are specific to exercise intensity and to muscle fiber type (affecting mostly fast-twitch fibers), and they appear to occur only in muscles that are substantially recruited during exercise (Brozinick et al 1993).…”

Section: Introductionmentioning

confidence: 71%

Increase of adiponectin receptor gene expression by physical exercise in soleus muscle of obese Zucker rats

et al. 2006

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Aerobic exercise, including treadmill running has been widely used to treat insulin resistance and type 2 diabetes. We studied the effects of endurance training on gene expression of adiponectin receptor 1 (AdipoR1) in skeletal muscle of obese Zucker rats: the 8-week moderate exercise program consisted of treadmill running at 20 m/min and 0 degrees gradient for 1 h/day, 7 days/week. After 8 weeks, insulin action on glucose disposal rate was measured by glucose-insulin index, the product of the areas under the curve of glucose and insulin during intraperitoneal glucose tolerance testing. In contrast to results for sedentary obese rats, exercise training decreased plasma levels of insulin and glucose as well as the glucose-insulin index in obese rats, indicating the merit of regular moderate exercise for improvement of insulin sensitivity in this insulin-resistant animal model. Also, diabetes-related reductions in mRNA and protein content of AdipoR1 in soleus muscle were observed in obese rats at baseline; they were markedly reversed after the 8-week exercise program. However, such exercise training did not alter plasma levels of insulin and glucose in lean Zucker rats. Also, AdipoR1 gene expression in soleus muscle was not changed by exercise in lean Zucker rats compared with the sedentary, lean littermates. These results suggest that long-term exercise training may reverse reduced AdipoR1 gene expression in soleus muscle and improve insulin sensitivity in the obese Zucker rats. Thus, an endurance exercise training is probably helpful clinically for obese individuals with insulin resistance.

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Mediation of ?-endorphin in exercise-induced improvement in insulin resistance in obese Zucker rats

Cited by 35 publications

References 30 publications

The Exercise-Induced Improvement in hyperglycemia is Mediated by DHT Produced in the Skeletal Muscle of Zucker Diabetic Fatty Rats

The Exercise-Induced Improvement in hyperglycemia is Mediated by DHT Produced in the Skeletal Muscle of Zucker Diabetic Fatty Rats

Novel Mechanism for Plasma Glucose–Lowering Action of Metformin in Streptozotocin-Induced Diabetic Rats

Increase of adiponectin receptor gene expression by physical exercise in soleus muscle of obese Zucker rats

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