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Heliyon. 2019 Dec 12;5(12):e03004. doi: 10.1016/j.heliyon.2019.e03004. eCollection 2019 Dec.

Adverse effects of noise stress on glucose homeostasis and insulin resistance in Sprague-Dawley rats.

Author information

1
Department of Physiology, College of Medicine of the University of Lagos, Idi-Araba, Lagos, Nigeria.
2
Department of Biochemistry, College of Medicine of the University of Lagos, Idi-Araba, Lagos, Nigeria.
3
Department of Physiology, Benjamin S. Carson (Snr.) School of Medicine, Babcock University Ilishan-Remo, Nigeria.

Abstract

Noise pollution remains a pervasive health hazard that people encounter especially in large commercial metropolis and has been implicated in many adverse non-auditory health conditions such as hypertension, atherosclerosis, vascular (endothelial) dysfunction and metabolic disorders. There is a growing body of evidence showing that chronic noise exposure is associated with an increased risk of hypercholesterol, adiposity and development of type 2 diabetes. The present study investigated the effect of noise stress on parameters of glucose homeostasis in male rats and possible recovery after noise cessation. Twenty-four (24) adult male Sprague-Dawley rats were designated into four groups (n = 6 per group). All rats except the control group were exposed to 95dB noise using a noise generator for 28 consecutive days. A group of rats was investigated immediately after 28 days of noise exposure (NE28), while others were left to recover from noise stress for 7 days (NER7) or 14 days (NER14). OGTT and ITT were performed using standard methods. Plasma levels of triglyceride (TRIG), total cholesterol (CHOL), low density lipoprotein (LDL) and high-density lipoprotein (HDL) were determined. Serum level of insulin, corticosterone (CORT) and corticosterone-releasing-factor (CRF) were determined using ELISA. Homeostasis model assessment-insulin resistance (HOMA-IR) and glycogen content in liver as well as gastrocnemius muscle were also determined. Although glucose tolerance remained unchanged in the noise-exposed groups, insulin sensitivity was however significantly reduced compared with control. There was significant increase (P < 0.05) in the level of CHOL, LDL and HDL. Noise also increased (P < 0.05) both insulin and CORT levels; and elicited a higher HOMA-IR index in NE28 rats. Hepatic and myocytic glycogen content were lower (P < 0.05) in NE28 rats relative to control. The reported changes above were reversed following a 14-day noise withdrawal period. Noise-induced insulin resistance may result from dysregulation of the stress axis and appears to be reversible with noise cessation.

KEYWORDS:

Biochemistry; Corticosterone; Diabetes; Glucose; Glycogen; Insulin; Insulin sensitivity; Lipids; Metabolism; Noise; Oxidative stress; Physiology; Stress; Systems biology

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