Thyroid hormones-mediated effects of insulin on antioxidant enzymes from diabetic rat hearts

Kosova, Funda; Altan, Nilgün; Sepici, Aylin; Engin, Ayşe Başak; N, Kocamanoglu

doi:10.4149/bll_2013_039

Cited by 1 publication

(1 citation statement)

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“…Because the etiology of T2DM differs substantially from that of T1DM, studies of T1DM were not included here. Furthermore, studies and reviews on TH actions and glucose metabolism in T1DM already exist (Yuan et al, 2021;Liu & Severson, 1994;Biondi et al, 2019;Kosova et al, 2013), which include studies using streptozotocin (STZ)-induced diabetic rodents, a model of T1DM, therefore, these studies were excluded from this review.…”

Section: Search Methodologymentioning

confidence: 99%

Thyroid hormones and the potential for regulating glucose metabolism in cardiomyocytes during insulin resistance and T2DM

Mendez

Ortiz

2021

Physiol Rep

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In order for the heart to maintain its continuous mechanical work and provide the systolic movement to uphold coronary blood flow, substantial synthesis of adenosine triphosphate (ATP) is required. Under normal conditions cardiac tissue utilizes roughly 70% fatty acids (FA), and 30% glucose for the production of ATP; however, during impaired metabolic conditions like insulin resistance and diabetes glucose metabolism is dysregulated and FA account for 99% of energy production. One of the major consequences of a shift in FA metabolism in cardiac tissue is an increase in reactive oxygen species (ROS) and lipotoxicity, which ultimately lead to mitochondrial dysfunction. Thyroid hormones (TH) have direct effects on cardiac function and glucose metabolism during impaired metabolic conditions suggesting that TH may improve glucose metabolism in an insulin resistant condition. None-classical TH signaling in the heart has shown to phosphorylate protein kinase B (Akt) and increase activity of phosphoinositide-3-kinase (PI3K), which are critical mediators in the insulin-stimulated glucose uptake pathway. Studies on peripheral tissues such as skeletal muscle and adipocytes have demonstrated TH treatment improved glucose intolerance in a diabetic model and increased insulin-regulated glucose transporter (GLUT4) mRNA levels. GLUT4 is a downstream target of thyroid response element (TRE), which demonstrates that THs regulate glucose via GLUT4. Elevated 3,5,3′-triiodothyronine (T3) increased glucose oxidation rate and decreased the glycolytic intermediate, fructose 6-phosphate (F6P) in cardiomyocytes, in addition to increasing mitochondrial biogenesis and pyruvate transport across the mitochondrial membrane. These findings along with a few other studies on T3 treatment in cardiac tissue suggest TH may improve glucose metabolism in an insulin resistant model and ameliorate the effects of diabetes and metabolic syndrome. This review highlights the potential benefits of exogenous TH on ameliorating metabolic dysfunction in the heart.

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Section: Search Methodologymentioning

confidence: 99%