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

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.