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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Attenuation of Ca2+ homeostasis, oxidative stress, and mitochondrial dysfunctions in diabetic rat heart: insulin therapy or aerobic exercise?

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Author(s):
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da Silva, Marcia F. [1] ; Natali, Antonio J. [2] ; da Silva, Edson [1, 3] ; Gomes, Gilton J. [2] ; Teodoro, Bruno G. [4] ; Cunha, Daise N. Q. [2] ; Drummond, Lucas R. [2] ; Drummond, Filipe R. [2] ; Moura, Anselmo G. [2] ; Belfort, Felipe G. [2] ; de Oliveira, Alessandro [2] ; Maldonado, Izabel R. S. C. [1] ; Alberici, Luciane C. [4]
Total Authors: 13
Affiliation:
[1] Univ Fed Vicosa, Dept Gen Biol, Vicosa, MG - Brazil
[2] Univ Fed Vicosa, Dept Phys Educ, Vicosa, MG - Brazil
[3] Univ Fed Vales Jequitinhonha & Mucuri, Dept Basic Sci, Diamantina, MG - Brazil
[4] Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Dept Phys & Chem, BR-14040903 Ribeirao Preto, SP - Brazil
Total Affiliations: 4
Document type: Journal article
Source: Journal of Applied Physiology; v. 119, n. 2, p. 148-156, JUL 15 2015.
Web of Science Citations: 4
Abstract

We tested the effects of swimming training and insulin therapy, either alone or in combination, on the intracellular calcium ({[}Ca2+](i)) homeostasis, oxidative stress, and mitochondrial functions in diabetic rat hearts. Male Wistar rats were separated into control, diabetic, or diabetic plus insulin groups. Type 1 diabetes mellitus was induced by streptozotocin (STZ). Insulin-treated groups received 1 to 4 UI of insulin daily for 8 wk. Each group was divided into sedentary or exercised rats. Trained groups were submitted to swimming (90 min/day, 5 days/wk, 8 wk). {[}Ca2+](i) transient in left ventricular myocytes (LVM), oxidative stress in LV tissue, and mitochondrial functions in the heart were assessed. Diabetes reduced the amplitude and prolonged the times to peak and to half decay of the {[}Ca2+](i) transient in LVM, increased NADPH oxidase-4 (Nox-4) expression, decreased superoxide dismutase (SOD), and increased carbonyl protein contents in LV tissue. In isolated mitochondria, diabetes increased Ca2+ uptake, susceptibility to permeability transition pore (MPTP) opening, uncoupling protein-2 (UCP-2) expression, and oxygen consumption but reduced H2O2 release. Swimming training corrected the time course of the {[}Ca2+](i) transient, UCP-2 expression, and mitochondrial Ca2+ uptake. Insulin replacement further normalized {[}Ca2+](i) transient amplitude, Nox-4 expression, and carbonyl content. Alongside these benefits, the combination of both therapies restored the LV tissue SOD and mitochondrial O-2 consumption, H2O2 release, and MPTP opening. In conclusion, the combination of swimming training with insulin replacement was more effective in attenuating intracellular Ca2+ disruptions, oxidative stress, and mitochondrial dysfunctions in STZ-induced diabetic rat hearts. (AU)

FAPESP's process: 10/17259-9 - Studies on mechanisms of mitochondrial uncoupling by non-esterified fatty acids as a strategy for prevention / treatment of obesity
Grantee:Luciane Carla Alberici
Support Opportunities: Research Grants - Young Investigators Grants