Turkish journal of pharmaceutical sciences · 2024
Longitudinal Evaluation of Developmental Protein Malnutrition Resembling Marasmic-Kwashiorkor Condition in Wistar Rats.
СтатьяНазвание и аннотация: Перевод в очереди
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Augustin Varsha, Badanthadka Murali, R J Madhura, Dsouza Vinitha, Kumar B Mohana, Shetty A Veena
Аннотация
OBJECTIVES: Protein malnutrition (PMN) is a significant public health concern that can aggravate pathological states. The impact of early malnutrition on metabolism needs extensive evaluation. Current models employ short-term diet restriction and are neither ethically correct nor clinically relevant. This study aimed to develop a PMN rat model to evaluate the effects of a low-protein diet (LPD) on physiological, hematological, biochemical, and histological changes affected by malnourishment from postweaning to the 40th week.
MATERIALS AND METHODS: The PMN model was developed in Wistar rats (post-weaning) by assigning animals to patented LPD (10% protein) and a control group to a normal diet (18% protein). Developed model was confirmed by biometric, biochemcial parameters and Gomez classification of malnutrition.
RESULTS: LPD-induced PMN showed stunted growth, altered biochemical (albumin range, 1.9 - 2.4 g/dL, total protein range, 5.1 - 6.4 g/dL), and hematological markers mean corpuscular volume (52.03 ± 1.34, 47.45 ± 0.44, p≤0.01), mean corpuscular hemoglobin (17.67 ± 0.47, 15.37 ± 0.18, p≤0.001) and mean corpuscular haemoglobin concentration (33.87 ± 0.22, 32.37 ± 0.24, p≤0.001) and significantly affected hepatic histology. A long-term study was conducted to analyze the pattern of developmental PMN and its stabilization over time.
CONCLUSION: The developed PMN rat model imitates clinical conditions and is confirmed as a stable, reproducible, and reliable model for short- and long-term studies. The clinical relevance of this approach opens new avenues for research in treatment, drug development, molecular interactions, and disease model development.
MATERIALS AND METHODS: The PMN model was developed in Wistar rats (post-weaning) by assigning animals to patented LPD (10% protein) and a control group to a normal diet (18% protein). Developed model was confirmed by biometric, biochemcial parameters and Gomez classification of malnutrition.
RESULTS: LPD-induced PMN showed stunted growth, altered biochemical (albumin range, 1.9 - 2.4 g/dL, total protein range, 5.1 - 6.4 g/dL), and hematological markers mean corpuscular volume (52.03 ± 1.34, 47.45 ± 0.44, p≤0.01), mean corpuscular hemoglobin (17.67 ± 0.47, 15.37 ± 0.18, p≤0.001) and mean corpuscular haemoglobin concentration (33.87 ± 0.22, 32.37 ± 0.24, p≤0.001) and significantly affected hepatic histology. A long-term study was conducted to analyze the pattern of developmental PMN and its stabilization over time.
CONCLUSION: The developed PMN rat model imitates clinical conditions and is confirmed as a stable, reproducible, and reliable model for short- and long-term studies. The clinical relevance of this approach opens new avenues for research in treatment, drug development, molecular interactions, and disease model development.