What question did this study set out to answer?

This research aims to evaluate how cobalamin supplementation affects cardiac health in rabbits lacking testosterone.

March 2, 2026Open Access

Physiological, molecular, and histological evaluation of the effects of cobalamin on cardiac function in castrated rabbits

Key Result

Cobalamin supplementation significantly reduced cardiac markers (cTnI, H-FABP, homocysteine) and improved histological heart damage in castrated rabbits (p<0.01).

Key Points

This research aims to evaluate how cobalamin supplementation affects cardiac health in rabbits lacking testosterone.
24 male rabbits were divided into control, castrated, and castrated with cobalamin groups.
Biochemical markers including cTnI and GSH were measured using ELISA.
Histological evaluation and gene expression analysis using qRT-PCR were conducted.
Castration increased cardiac markers and reduced GSH levels significantly.
Cobalamin supplementation restored these markers and improved heart health.
Histological analysis showed reduced inflammation and fibrosis with cobalamin supplementation.

Structured PICO

Does cobalamin supplementation improve cardiac function and mitigate adverse remodeling, oxidative stress, and inflammation in castrated rabbits?

Population

24 male rabbits (castrated model of testosterone deficiency)

Intervention

Cobalamin (vitamin B12) supplementation

Comparator

Castrated rabbits without supplementation and uncastrated controls

Outcome

Biochemical markers (cTnI, H-FABP, homocysteine, GSH, IL-3, Gal-3, TSPO, TSP-1), histological evaluation of myocardial tissue, and gene expression (GAPDH, ANP)surrogate

Cobalamin supplementation mitigates adverse cardiac remodeling, oxidative stress, and inflammation associated with testosterone deficiency in a preclinical rabbit model.

Main Result

Absolute Event Rate: 0% vs 0%

Abstract

Background: Testosterone deficiency is associated with adverse cardiac remodeling, oxidative stress, and inflammation. Aim: To investigate the physiological, biochemical, and histological effects of cobalamin (vitamin B12) supplementation on cardiac physiology in castrated rabbits. Methods: A total of 24 male rabbits were divided into three groups: control (C), castrated (CA), and castrated with cobalamin supplementation (CA + C). Biochemical markers, including cardiac troponin I (cTnI), heart-type fatty acid binding protein (H-FABP), homocysteine, glutathione (GSH), interleukin-3 (IL-3), galectin-3 (Gal-3), translocator protein (TSPO), and thrombospondin-1 (TSP-1), were measured using ELISA. Myocardial tissue was histologically evaluated alongside GAPDH and ANP gene expression analysis using quantitative real-time reverse-transcription PCR (qRT-PCR). Statistical significance was set at p value < 0.05. Results: Castration significantly increased the levels of cardiac markers, such as cTnI, H-FABP, homocysteine, IL-3, and Gal-3, while reducing GSH levels (p<0.001). Cobalamin supplementation significantly restored these biochemical parameters, with notable reductions in cTnI, H-FABP, homocysteine, IL-3, Gal-3, and GSH levels (p<0.01). Histological analysis revealed myocardial contraction failure, fibrosis, and inflammation in castrated rabbits, which were mitigated by cobalamin supplementation. Gene expression analysis showed GAPDH and ANP upregulation in the castrated group, which was partially restored after cobalamin treatment. Additionally, cobalamin supplementation significantly improved the expression of other markers, such as TSPO and TSP-1, its potential to modulate inflammatory and oxidative pathways in the heart. Conclusion: Cobalamin supplementation mitigates the harmful effects of testosterone deficiency on the heart by improving oxidative stress, inflammation, and cardiac remodeling. These findings the potential of this drug for correcting cardiovascular dysfunction associated with hormonal deficiencies.