Thyroid hormones mediated effect of insulin on alloxan diabetic rat atria

Karasu, Çi̇men; Öztürk, Yusuf; Altan, Nilgün; Arı, Nuray; C, Ikizler; Altan, V.Melih

doi:10.1016/0306-3623(90)91026-n

Cited by 32 publications

(20 citation statements)

References 38 publications

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“…In addition to that in our previous study, we demonstrated that thyroid hormones were needed for insulin effect to reverse diabetes induced alterations in heart tissue [27], in a different study with experimental diabetic rats, decreased levels of thyroid hormones were maintained by insulin treatment [28], and different treatment protocols also reduced the 8-OHdG levels in various tissues [29,30]. In our study, DNA damage was not able to be controlled with insulin treatment, but in surgically thyroidectomized rats with diabetes treated with both with insulin and appropriate thyroid hormone doses were succeeded.…”

Section: Discussionmentioning

confidence: 68%

Oxidative DNA damage: the thyroid hormone-mediated effects of insulin on liver tissue

Altan

Sepici-Dinçel

Şahin

et al. 2010

Endocr

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Thyroid hormone affects glucose homeostasis with its actions between the skeletal muscle and liver and the altered oxidative and non-oxidative glucose metabolism. In our study three chemicals are considered biomarkers associated with oxidative stress for protein modifications were measured; 8-hydroxy-2-deoxyyguanosine (8-OHdG), a major lesion that can be generated by reactive oxygen species for DNA damage, protein carbonyl content (PCO), products of protein oxidation and advanced oxidation protein products (AOPPs) a dithyrosine containing cross-linked protein products. The purpose of the recent study was to determine the effects of insulin and T4 or their combination in diabetic, thyroidectomized, or diabetic-thyroidectomized rats and possible relations with oxidative DNA and protein damages. For this purpose, rats were assigned to eight groups: Group 1; control, Group 2; diabetes, Group 3; diabetes+insulin, Group 4; surgically thyroidectomized control, Group 5; thyroidectomized+diabetes, Group 6; thyroidectomized+diabetes+insulin, Group 7; thyroidectomized+diabetes+insulin+thyroid hormone, levothyroxin sodium, 2.5 μg/kg and Group 8; thyroidectomized+diabetes+insulin+thyroid hormone, levothyroxin sodium, 5.0 μg/kg for 5 weeks. After the genomic DNA of liver tissues was extracted, the ratio of 8-OHdG to deoxyguanosine and liver tissue protein oxidation markers was determined. The main findings of our recent study were the increased 8-OHdG levels during the diabetes, hypothyroidism, and hypothyroidism with diabetes, which can be regulated in different percentages with the treatment of 2.5 and 5.0 μg/kg doses of thyroid hormone and the altered protein carbonyl and AOPP levels of liver tissue. Consequently, it was observed that the DNA and protein damage induced by oxidative stress in diabetes could be regulated by dose-dependent thyroid hormone-mediated effects to insulin treatment.

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Section: Discussionmentioning

confidence: 68%

Oxidative DNA damage: the thyroid hormone-mediated effects of insulin on liver tissue

Altan

Sepici-Dinçel

Şahin

et al. 2010

Endocr

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“…Similarly, increased cardiac sympathetic drive may contribute to the development and progression of diabetic cardiomyopathy [60,62]. One of the typical features observed in hearts from diabetic rats is the decreased inotropic and chronotropic responses to b-adrenoceptor stimulation [11][12][13][14]. In accordance with the decreased functional responses, a decreased expression of cardiac b 1 -adrenoceptors from diabetic rats has been demonstrated [28,67].…”

Section: Resultsmentioning

confidence: 88%

“…In these models of rats, biochemical and functional myocardial abnormalities usually develop 4-6 weeks after untreated diabetes [10]. Among the prominent defects observed in chemically induced diabetic rats is the reduced responsiveness of cardiac preparations to the inotropic and chronotropic effects of b-adrenoceptor agonists stimulation [11][12][13][14]. Indeed, the defective cardiac responses to catecholamines may be associated with the high frequency of cardiac pump failure in diabetes.…”

Section: Introductionmentioning

confidence: 99%

The influence of diabetes on cardiac β-adrenoceptor subtypes

et al. 2007

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Despite the significant developments in the treatment of diabetes mellitus, diabetic patients still continue to suffer from cardiac complications. The increase of cardiac adrenergic drive may ultimately contribute to the development and progression of diabetic cardiomyopathy. beta-Adrenoceptors play an important role in the regulation of heart function. However, responsiveness of diabetic heart to beta-adrenoceptor agonist stimulation is diminished. The chronotropic responses mediated by beta(1)-subtype, which is mainly responsible for cardiac effects of catecholamines are decreased in the atria of diabetic rats. The expression of cardiac beta(1)-subtype is significantly decreased in diabetic rats as well. beta(2)-Adrenoceptors also increase cardiac function. Although the expression of this subtype is slightly decreased in diabetic rat hearts, beta(2)-mediated chronotropic responses are preserved. On the other hand, functional beta(3)-adrenoceptor subtype was characterized in human heart. Interestingly, stimulation of cardiac beta(3)-adrenoceptors, on the contrary of beta(1)- and beta(2)-subtypes, mediates negative inotropic effect in human ventricular muscle. Cardiac beta(3)-adrenoceptors are upregulated in experimental diabetes as well as in human heart failure. These findings suggest that each beta-adrenoceptor subtype may play an important role in the pathophysiology of diabetes-induced heart disease. However, it is still not known whether the changes in the expression and/or responsiveness of beta-adrenoceptors are adaptive or maladaptive. Therefore, this review outlines the potential roles of these receptor subtypes in cardiac pathologies of diabetes.

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“…Diabetes is also frequently associated with the development of heart failure, even in the absence of coronary artery complications or hypertension (20). The mechanisms involved in diabetes-induced cardiac problems are not clearly understood, but bradycardia (2,21) and decreased chronotropic and inotropic responses to ␤-AR-agonist stimulation (1-3) have been demonstrated. Thus a reduction in the number of cardiac ␤-ARs has been questioned as one of the causative factors for diabetic cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

“…Alloxan and streptozotocin (STZ) are two drugs that are commonly used to experimentally reproduce this pathology in animals, including rats. Among the prominent defects observed in these models are the decreased responsiveness of cardiac preparations to the inotropic and chronotropic effects of ␤-adrenoreceptor (␤-AR) agonist stimulation (1)(2)(3). Although the mechanisms underlying depressed cardiac responses to stimulation of ␤-AR agonists are poorly understood, of interest are studies demonstrating that the density of cardiac ␤-ARs decreases in diabetic rats (4)(5)(6)(7).…”

mentioning

confidence: 99%

The Effect of Diabetes on Expression of β1-,β2-, and β3-Adrenoreceptors in Rat Hearts

et al. 2001

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Diabetic hearts exhibit decreased responsiveness to stimulation by ␤-adrenoreceptor (␤-AR) agonists. This decrease in activity may be due to changes in expression and/or signaling of ␤-AR. Recently we showed that right atrial strips from 14-week streptozotocin (STZ)-induced diabetic rat hearts exhibit decreased responsiveness to ␤ 1 -AR agonist stimulation, but not to ␤ 2 -AR agonist. In the present study, we investigated the effects of long-term diabetes on the expression of cardiac ␤ 1 -, ␤ 2 -, and ␤ 3 -ARs and looked at whether these changes could be restored with insulin treatment. Using reverse transcription-polymerase chain reaction (RT-PCR), PAGE, and Western blot analysis, we found that ␤ 1 -AR mRNA and protein levels decreased by 34.9 ± 5.8 and 44.4 ± 5.8%, respectively, in 14 week-STZtreated diabetic rat hearts when compared with agematched controls. On the other hand, mRNA levels encoding ␤ 2 -and ␤ 3 -ARs increased by 72.5 ± 16.6 and 97.3 ± 26.1%, respectively. Although the latter translated into a proportional increase in ␤ 3 -AR protein levels (100.0 ± 17.0%), ␤ 2 -AR protein levels decreased to 82.6 ± 1.1% of control. Insulin treatment for 2 weeks, after 12 weeks of untreated diabetes, partially restored ␤ 1 -AR mRNA and protein levels to 60.1 ± 8.4 and 83.2 ± 5.0%, respectively, of control. Although insulin treatment minimally attenuated the rise in mRNA levels encoding ␤ 2 -and ␤ 3 -ARs, the steady-state levels of these proteins returned to near control values. These data suggest that the decreased responsiveness of diabetic hearts to stimulation of ␤-AR agonists may be due to a decrease in ␤ 1 -AR and an increase ␤ 3 -AR expression. Diabetes 50: [455][456][457][458][459][460][461] 2001

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Thyroid hormones mediated effect of insulin on alloxan diabetic rat atria

Cited by 32 publications

References 38 publications

Oxidative DNA damage: the thyroid hormone-mediated effects of insulin on liver tissue

Oxidative DNA damage: the thyroid hormone-mediated effects of insulin on liver tissue

The influence of diabetes on cardiac β-adrenoceptor subtypes

The Effect of Diabetes on Expression of β1-,β2-, and β3-Adrenoreceptors in Rat Hearts

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