Path Analysis in PLS for Assessing the Impact of Metabolic Syndrome on Pulmonary Fibrosis in a Rat Model
DOI:
https://doi.org/10.36497/jri.v45i3.889Keywords:
Male Sprague Dawley rats, Metabolic syndrome, PPARγ, lung fibrosis.Abstract
Background: Metabolic syndrome (MetS) is characterized by obesity, dyslipidemia, hyperglycemia, and insulin resistance, which are associated with increased risk for pulmonary fibrosis. This study investigates the impact of MetS on pulmonary fibrosis in a rat model using Partial Least Squares (PLS) path analysis.
Methods: Sprague Dawley rats were fed a high-fat, high-fructose diet for 37 weeks to induce MetS. Key metabolic parameters, including body weight, lipid profiles, fasting blood glucose, fibrosis markers and Aschroft scores, were assessed. PLS path analysis was conducted to explore the relationships between these variables and their influence on pulmonary fibrosis.
Results: PLS path analysis identified a strong correlation between increased body weight and MetS development (path coefficient 0.977). Dyslipidemia, with elevated triglycerides and reduced HDL cholesterol, was also linked to MetS. A novel association was found between glucose dysregulation and pulmonary fibrosis (R-square 0.908, path coefficient 0.947), suggesting that hyperglycemia contributes to lung fibrosis. Reduced PPARγ expression was associated with insulin resistance and inflammation, implicating it in fibrotic processes.
Conclusion: This study highlights the role of metabolic disturbances in promoting pulmonary fibrosis in MetS. PLS path analysis effectively identified key metabolic pathways, suggesting potential targets for therapeutic intervention to mitigate MetS effects and prevent fibrosis. Further research is warranted to explore these pathways and develop targeted therapies.
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References
Chomsy IN, Rohman MS, Khotimah H, Bramantyo BB, Auzan A, Lukitasari M, et al. Effect of the ethanolic extract of green tea and green coffee on cardiac fibrosis attenuation by suppressing activin-a and collagen-1 gene expression. AIP Conf Proc. 2022;2513(November).
Tsai MJ, Chang WA, Liao SH, Chang KF, Sheu CC, Kuo PL. The effects of epigallocatechin gallate (EGCG) on pulmonary fibroblasts of idiopathic pulmonary fibrosis (Ipf)—a next-generation sequencing and bioinformatic approach. Int J Mol Sci. 2019;20(8):1958.
Yang J. Pulmonary fibrosis : a possible diabetic complication. 2011;(August 2010):311–7.
Baffi CW, Wood L, Winnica D, Strollo PJ, Gladwin MT, Que LG, et al. Metabolic Syndrome and the Lung. Chest [Internet]. 2016; Available from: http://dx.doi.org/10.1016/j.chest.2015.12.034
Honda K, Marquillies P, Capron M, Dombrowicz D. Peroxisome proliferator–activated receptor γ is expressed in airways and inhibits features of airway remodeling in a mouse asthma model. J Allergy Clin Immunol. 2004;113(5):882–8.
Saifur Rohman M, Lukitasari M, Nugroho DA, Ramadhiani R, Widodo N, Kusumastuty I, et al. Decaffeinated light-roasted green coffee and green tea extract combination improved metabolic parameters and modulated inflammatory genes in metabolic syndrome rats. F1000Research. 2021;10.
Wang YC, Dong J, Nie J, Zhu JX, Wang H, Chen Q, et al. Amelioration of bleomycin-induced pulmonary fibrosis by chlorogenic acid through endoplasmic reticulum stress inhibition. Apoptosis. 2017;22(9):1147–56.
Lefterova MI, Steger DJ, Zhuo D, Qatanani M, Mullican SE, Tuteja G, et al. Cell-specific determinants of peroxisome proliferator-activated receptor γ function in adipocytes and macrophages. Mol Cell Biol. 2010;30(9):2078–89.
Lestari IP, Chozin IN, Sartono TR, Sasiarini L, Yudhanto HS. Effect of a high-calorie diet on pro-to anti-inflammatory macrophage ratio through fat accumulation in rat lung tissue. Med J Indones. 2023;32(4):212–6.
Tudela J, Martínez M, Valdivia R, Romo J, Portillo M, Rangel R. Enhanced Reader.pdf. Vol. 388, Nature. 2010. p. 539–47.
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