type 2 diabetes mellitus, cardiomyocytes, mitochondrial permeability transition pore, mitochondria functional state, sex differences


Type 2 diabetes is one of the main factors of the cardiovascular risk, which leads to a disproportionate
increase in cardiovascular events in women and men. All causes of increased cardiovascular risk in women with
type 2 diabetes mellitus are not established, one of the most likely causes of cardiac activity is considered to be
gender features of biogenesis and activity of myocardial mitochondria. A comparative analysis of changes in the
functional state of the heart mitochondria in males and females rats with experimental type 2 diabetes mellitus
was conducted. It was established that the activity of succinate dehydrogenase, the part of complex II of the
electron transport chain, reduced more significantly in diabetic males compared with diabetic females. Type 2
diabetes mellitus also caused a greater decrease in the activity of the energy metabolism enzyme — aconitase,
in heart mitochondria of male compared to female. One of the leading mechanisms of cardiomyocytes’ apoptotic
or necrotic death in conditions of mitochondrial dysfunction, in particular induced by diabetes, is the activation
of a nonspecific mitochondrial pore opening (mPTP, mitochondrial permeability transition pore). It was found
a more pronounced activation of mPTP and more significant decrease in thioredoxin reductase activity in
males with type 2 diabetes mellitus compared with diabetic females. The obtained data may indicate a greater
sensitivity of male cardiomyocytes to the damaging effects of proapoptotic factors


Preis SR, Hwang SJ, Coady S, et al. Circulation 2009; 119(13): 1728-1735. doi: 108.829176.

Murphy E, Amanakis G, Fillmore N, et al. Cardiovasc Res 2017; 113(4): 370-377. doi:

Salinero AE, Anderson BM, Zuloaga KL. Int J Obes (Lond) 2018; 2(5): 1088-1091. doi: 0023-3.

Coronado M, Fajardo G, Nguyen K, et al. Circ Res 2018; 122: 282-295. doi: 117.310725.

Klinge CM. J Cell Biochem 2008; 105(6): 1342-1351. doi:

Lin S, Yang J, Wu G, et al. J Biomed Sci 2010; 17(1): 46-56. doi:

Karuzina II, Archakov AI. Sovremennye metody v biohimii, Moskva, 1977; 1: 47-49.

Straus W. Biochem Biophys Acta 1956; 19(1): 58-65.

Talbot DA, Brand MD. Biochem Biophys Acta 2005; 1709(2): 150-156. doi:

Krivchenkova RS. Sovremennye metody v biohimii, Moskva, 1977; 1: 44-47.

Di Lisa F, Menabò R, Canton M, et al. J Biol Chem 2001; 276(4): 2571-2575. doi:

Glans S. Mediko-biologicheskaja statistika, Moskva, 1998: 459 p.

Toedebusch R, Belenchia A, Pulakat L. Front Physiol 2018; 9(453): 14 p. doi:

Martins AR, Nachbar RT, Gorjao R, et al. Lipids Health Dis 2012; 11(30): 11 p. doi:

Choudhary C, Kumar C, Gnad F, et al. Science 2009; 325(5942): 834-840. doi:

Riojas-Hernández A, Bernal-Ramírez J, Rodríguez-Mier D, et al. Life Sci 2015; 141(15): 32-43. doi: lfs.2015.09.018.

Korge P, John SA, Calmettes G, et al. J Biol Chem 2017; 292: 9896-9905. doi:

Yoshioka J. J Amer Heart Assoc 2015; 4(7): 3 p. doi:

Conrad M, Jakupoglu C, Moreno SG, et al. Molec Cell Biol 2004; 24(21): 9414-9423. doi: 9414-9423.2004.




How to Cite

Gorbenko, N., Borikov, O., Ivanova, O., Kozar, V. V., & Kiprych, T. (2019). THE IMPACT OF DIABETES MELLITUS ON THE FUNCTIONAL STATE OF THE MITOCHONDRIA IN THE HEART OF MALE AND FEMALE RATS. Problems of Endocrine Pathology, 70(4), 110-115.

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