Morphometric assessment of structural remodeling of the left ventricular myocardium in experimental type 1 diabetes mellitus and with amino acids supplementation
DOI:
https://doi.org/10.14739/2310-1210.2026.3.358153Keywords:
type 1 diabetes mellitus, remodeling, myocardium, left ventricle, morphometry, L-arginine, N-acetyl-L-cysteine, ratsAbstract
Aim. To evaluate left ventricular myocardial structural remodeling in experimental type 1 diabetes mellitus (T1DM) and to assess the effects of L-arginine and N-acetyl-L-cysteine.
Materials and methods. The study involved 47 male Wistar rats. Type 1 diabetes mellitus was induced by streptozotocin (45 mg/kg). From week 6, rats received L-arginine or N-acetyl-L-cysteine (1.5 g/kg). ImageJ software was used to analyze cardiomyocyte area, nucleo-cytoplasmic ratio, and cell density.
Results. T1DM was found to cause pathological cardiomyocyte hypertrophy (area +17 %) alongside decreased cell density (-26 %) and suppression of the nuclear apparatus (nucleo-cytoplasmic ratio -10 %). L-arginine administration reduced perivascular infiltration but further decreased the nucleo-cytoplasmic ratio (-17 % compared to type 1 diabetes mellitus). N-acetyl-L-cysteine promoted nuclear area recovery (+34 % compared to type 1 diabetes mellitus) and stabilized cell density to control levels.
Conclusions. Experimental type 1 diabetes mellitus leads to pathological left ventricular hypertrophy with significant cardiomyocyte loss and disturbance of morphometric characteristics of nuclei with a decrease in nuclear-cytoplasmic ratio. The use of L-arginine attenuates the severity of perivascular inflammatory infiltration and reduces the nuclear-cytoplasmic ratio but does not eliminate muscle fiber fragmentation and cellular heterogeneity. N-acetyl-L-cysteine reverses pathological hypertrophic changes and restores nuclear apparatus.
References
- Lorenzo-Almorós A, Cepeda-Rodrigo JM, Lorenzo Ó. Diabetic cardiomyopathy. Revista clinica espanola. 2022;222(2):100-11. doi: 10.1016/j.rceng.2019.10.012
|
|
- Han X, Zheng R, Zhang J, Liu Y, Li Z, Liu G, et al. Cardiomyocyte OTUD1 drives diabetic cardiomyopathy via directly deubiquitinating AMPKα2 and inducing mitochondrial dysfunction. Nat Commun. 2025;16(1):6668. doi: 10.1038/s41467-025-61901-z
|
|
- Thakur MR, Tupe RS. l-Arginine: A multifaceted regulator of diabetic cardiomyopathy. Biochem Biophys Res Commun. 2025;761:151720. doi: 10.1016/j.bbrc.2025.151720
|
|
- Levick SP, Widiapradja A. The Diabetic Cardiac Fibroblast: Mechanisms Underlying Phenotype and Function. Int J Mol Sci. 2020;21(3):970. doi: 10.3390/ijms21030970
|
|
- Kolesnyk YM, Isachenko MI. [Analysis of the body composition of rats with experimental diabetes mellitus type 1 and its correction]. Modern Medical Technology. 2024;16(4):247-54. Ukrainian. doi: 10.14739/mmt.2024.4.311425
|
- Ruifrok AC, Johnston DA. Quantification of histochemical staining by color deconvolution. Anal Quant Cytol Histol. 2001;23(4):291-9.
- Rudokas MW, McKay M, Toksoy Z, Eisen JN, Bögner M, Young LH, et al. Mitochondrial network remodeling of the diabetic heart: implications to ischemia related cardiac dysfunction. Cardiovasc Diabetol. 2024;23(1):261. doi: 10.1186/s12933-024-02357-1
|
|
- Tan H, Yue T, Chen Z, Wu W, Xu S, Weng J. Targeting FGF21 in cardiovascular and metabolic diseases: from mechanism to medicine. Int J Biol Sci. 2023;19(1):66-88. doi: 10.7150/ijbs.73936
|
|
- Wei J, Zhao Y, Liang H, Du W, Wang L. Preliminary evidence for the presence of multiple forms of cell death in diabetes cardiomyopathy. Acta Pharm Sin B. 2022;12(1):1-17. doi: 10.1016/j.apsb.2021.08.026
|
|
- Wang H, Wang L, Hu F, Wang P, Xie Y, Li F, et al. Neuregulin-4 attenuates diabetic cardiomyopathy by regulating autophagy via the AMPK/mTOR signalling pathway. Cardiovasc Diabetol. 2022;21(1):205. doi: 10.1186/s12933-022-01643-0
|
|
- Rezaee A, Rahmanian P, Nemati A, Sohrabifard F, Karimi F, Elahinia A, et al. NF-ĸB axis in diabetic neuropathy, cardiomyopathy and nephropathy: A roadmap from molecular intervention to therapeutic strategies. Heliyon. 2024;10(9):e29871. doi: 10.1016/j.heliyon.2024.e29871
|
|
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