Chronic sleep deprivation, noise and high fat diet markedly induce C-reactive protein level in mice model
Abstract
Background: C-reactive protein (CRP) is a circulating sign of systemic chronic inflammation that your liver produces if your body is inflamed. Stressful events over a long period of time are linked to inflammatory disorders. Stress pathways are triggered by noise and sleep deprivation, as well as unhealthy habits like fatty meals. Several studies have connected higher CRP levels with plasma levels. The current study aims to explore the potential association’s relationship between chronic sleep deprivation, noise, high fat diet, and CRP disorders.
Methods: Three studies were carried out in our study to evaluate C-reactive protein levels in male Swiss albino mice groups after exposure to three different physical stressors for four weeks. The first study mice group were exposed to chronic sleep deprivation; second group was exposed to electrostatic speaker noise stressors; and the third group was fed a high fat diet. Quantitative estimation of C – reactive protein level in plasma using an ELISA kit.
Results: Significant changes in inflammatory CRP levels in the examined plasma were detected in the sleep deprivation group. CRP levels were found to be steadily increasing after two weeks, reaching a significant peak in the fourth week (p < 0.001). Moreover, in the fourth week, there were substantial increases in CRP plasma level with independent evidence, in the experimental noise group (p < 0.001). As well, the biomarker of inflammation level increased across the dietary high density fat diet, reaching the highest level at the end of the study (p < 0.05).
Conclusion: Our findings contribute to the body of evidence indicating a link between external stress and subclinical inflammatory markers. Furthermore, CRP concentrations are triggered by chronic sleep deprivation and noise exposure, and their concentrations rise with prolonged dietary fatty acid consumption.
Keywords: Sleep deprivation; Noise; High fat diet; Inflammation; CRP
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DOI: http://dx.doi.org/10.62940/als.v11i3.2770
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