Noise, one of the most widespread sources of environmental pollution, is considered not only an environmental nuisance but also a threat to public health. Beyond the well-recognized problem of hearing impairment, increasing attention is being paid to the cumulative adverse effects of noise exposure on extra-auditory systems. Several studies have reported significant increases in plasma stress hormone levels during and after various noises. In a more than 10-year prospective epidemiological study conducted by Sorensen et al. in a Danish cohort, each 10-dB increase in average road traffic noise at the current residence was found to be associated with a statistically significant 11% increased risk of incident diabetes. This risk increased to 14% when road traffic noise was estimated for all the places in which an individual had lived during the previous 5 years. Their study raised concern about noise as a risk factor of diabetes, particularly given the global epidemic of this disease and the increasingly widespread pattern of noise pollution. A previous study (Liu L et al. 2016) indicated that noise exposure at a 95-dB sound pressure level (dB SPL) induces insulin resistance in mice.
More recently, another experimental study reported abnormalities in glucose regulation and insulin sensitivity in rats that were chronically exposed to noise at a 100-dB. Because insulin resistance is well known to be a key contributor to type 2 diabetes mellitus (T2DM) and a key pathological feature of T2DM, these experimental studies together suggested a contributory role of noise exposure to increasing the risk of T2DM. Considering the alarming global epidemic of T2DM and the global prevalence of noise pollution, it is imperative to explore the mechanisms underlying the impairment of insulin sensitivity after noise exposure. Persistently elevated cortisol levels have been proposed to be associated with the development of insulin resistance. Positive associations between excess stress hormones, oxidative stress, and insulin resistance have been widely reported. It is also well documented that the release of inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), which are often cited as crucial cytokines that mediate insulin resistance, can be induced by chronic stress.
The protein c-Jun N-terminal kinase (JNK) has been increasingly recognized as an important mediator of insulin resistance that is associated with inflammation and oxidative stress through the phosphorylation of a downstream insulin receptor target, IRS-1. One of the major organ sensitive to insulin resistance is skeletal muscle. To confirm that the JNK-IRS1 axis Is involved in insulin resistance induced by noise, a team from the Institute of Life Sciences, Southeast University, Nanjin (China), has conducted a battery of experiments, proving that exposure of rats to noise is able to activate the JNK stress kinase pathway in skeletal muscle. This kinase, in turn, phosphorylates IRS-1 making the insulin signaling pathway inefficient for glucose utilization, fatty acids processing and cellular ionic control. Overall, this would translate in the onset of oxidative stress, which would further impair glucose metabolism and blood glucose control. This for what concerns direct effects of stress signaling on insulin network. There is another mechanism of insulin resistance that has not been explored at all by the team: the involvement of cortisol hormone.
It is produced in humans by the adrenal cortex within the adrenal gland. It is released in response to stress and low blood-glucose concentration. Cortisol counteracts insulin, contributes to hyperglycemia-causing hepatic gluconeogenesis and inhibits the peripheral use of glucose (insulin resistance) by decreasing the translocation to the cell membrane of glucose transporters (especially GLUT4). Elevated levels of cortisol, if prolonged, can lead to proteolysis (breakdown of proteins) and muscle wasting. Cortisol can weaken the activity of the immune system and has a negative-feedback effect on interleukin-1 (IL-1) and other immunostimulating cytokines (IL-2, TNF-alpha, ecc.). All these effects appear under long-lasting psychological stress. Cortisol is elevated in prolonged emotional or psychological stress; there is, therefore, reason to believe that cortisol could be involved in some aspects of insulin resistance generated by noise pollution. The influence of noise exposure on the insulin sensitivity of liver and adipose tissue, the other two main types of insulin-sensitive tissues, will be the next target investigated by the team in future studies.
- edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.
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