The Role Of Cortisol In Diabetes Management – A case of elastography-assisted laparoscopic fertility preservation for severe deep endometriosis causing urethral stricture and subtype II adenomyosis
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Received: 25/06/2021 / Revised: 2/08/2021 / Received: 30/08/2021 / Published: 06/09/2021
The hypothalamic-pituitary-adrenal axis is a tightly regulated system that represents one of the body’s mechanisms for responding to acute and chronic stress. Prolonged stress and/or underregulation of the stress system can lead to chronic hypercortisol or, in some cases, a blunted cortisol response to stress, contributing to insulin resistance, increased adiposity, and type 2 diabetes mellitus. In addition, acute and chronic stress can aggravate or exacerbate metabolic states by supporting inflammatory states, and the close relationship between stress, inflammation, and adipose tissue has been reported and has received increasing attention in recent years. We reviewed and summarized the evidence supporting dysregulation of the hypothalamic-pituitary-adrenal axis as an important biological link between stress, obesity, inflammation and type 2 diabetes. Furthermore, we highlighted the potential role of stress associated with infections such as SarsCov2 infection in adrenal dysregulation, insulin resistance and diabetes in a bidirectional context. Understanding and identifying the link between stress and obesity or diabetes may contribute to defining the pathogenesis and management of stress-related complications in which HPA axis dysregulation plays an important role.
The hypothalamic-pituitary-adrenal axis (HPA) is one of the most important systems that, together with the sympathetic nervous system (SNS), is activated in acute stressful situations and is therefore defined as the stress axis .
When there is chronic or unregulated stimulation at the central or peripheral level, it can affect a person’s health. In fact, through actions on the neuroendocrine, metabolic and immune systems, chronic stress can contribute to the development of several diseases, including obesity (OB) and diabetes (DM), especially in vulnerable individuals [ 1 , 2 ].
Exposure to chronic stress and the continuous release of glucocorticoids (GC) can lead to changes in the expression of certain genes involved in cellular pathways important for the body’s metabolism. These changes are associated with the development of adiposity, insulin resistance, reduced fat mass, and coagulation disorders that cause hypercoagulation, dyslipidemia, hypertension, and increased release of inflammatory cytokines [ 1 , 2 ]. The Cushingoid phenotype, which summarizes these changes well, is commonly characteristic of subjects with abdominal OB, metabolic syndrome (MS) or type 2 DM (T2DM), and subjects suffering from depression and alcoholism, i.e. the so-called “pseudo”-Cushing’s” conditions [2, 3, 4]. It should be noted that the Cushingoid phenotype caused by chronic stress can be influenced not only by chronic hypercortisolism but also by changes in corticosteroid levels – binding globulin, GC sensitivity peripheral tissues and 11β-hydroxysteroid dehydrogenase type 1 (. 11β-HSD1), an important enzyme in peripheral GC metabolism [2, 3, 4], activity These changes are also associated with a kind of “genetic programming” of the HPA axis that occurs in the fetal and perinatal period , Effect on the activity of this axis in adults and contributes to the onset of OB and MS [6, 7].
Traditional factors linking OB to DM are also associated with a high-calorie diet, a sedentary lifestyle, and socioeconomic status (SES). Individuals with low SES have limited autonomy and more limited opportunities, which can increase stress and cause an increase in stress hormones in addition to cortisol and catecholamines such as glucagon and growth hormone. This condition may ultimately alter fat deposition, increase visceral fat, and increase the risk of developing DM [8, 9]. Reduced amount or quality of sleep, such as during shift work or conditions such as sleep apnea, can also be associated with weight gain and OB. This can lead to cravings for high-calorie foods due to an imbalance in appetite hormones. Other effects include increased reactivity of the HPA axis and decreased growth hormone, which in turn can increase visceral fat mass and lead to insulin resistance .
In this article, we highlight and review the latest information on the association of HPA axis activity during chronic stress and its role in the development of MS, OB and T2DM. We also highlighted the potential role of infection-related stress, such as SarsCov2 infection, in HPA axis dysregulation, insulin resistance and T2DM in a double inverse association.
We reviewed articles published in PubMed/Medline from the past three decades until July 2021. These include original articles, review articles, systematic review articles, meta-analyses, and book chapters. We have reported the most interesting and recent discoveries. This literature search was performed using the following search syntax: (“stress” or “stress axis” or “cortisol” or “glucocorticoid receptor”) and (“diabetes” or “metabolic syndrome” or “metabolism” or “obesity” or “fatness”) and (” COVID-19″ or “SarsCov2 infection”) and (“inflammation” or “cytokines”).
A person’s adaptive stress response is largely determined by the effect of cortisol. This hormone has a powerful effect on the whole body through several effects, which are mostly catabolic and directed to ensure the maximum amount of available energy for adaptation to stressful events [1, 2]. GCs stimulate hepatic gluconeogenesis by increasing plasma glucose concentration. They also induce lipolysis in some areas of the body while promoting the accumulation of adipose tissue in other locations (such as the abdomen, perivisceral, and dorso-cervical). In addition, they lead to protein catabolism in muscles, bones and skin by promoting the use of amino acids as substrates of the oxidative pathway. In addition to their known catabolic action, GCs also inhibit the anabolic effects of growth hormone, insulin, thyroid and sex hormones during stress [1, 2].
In general, the consequences of excessive cortisol exposure or excessive sensitivity to the effects of GC can be summed up in the activation of lipoprotein lipase, which involves the accumulation of triglycerides and lipids in fat cells and the inhibition of the activation of fatty acids together with insulin. . 11]. Therefore, the prolonged effect of cortisol is associated with an increase in abdominal adiposity, which is further determined by the concomitant endocrine changes associated with chronic hypercortisol, especially gonadal and somatotropic axis inhibition. In addition, the latter facilitates the emergence of metabolic changes and increases the cardiovascular risk of MS and T2DM [2, 3, 4, 11, 12].
OB has been considered to be a disease related to functional hypercortisol or pseudo-Cushing’s condition, although precise and confirmed data on HPA axis hyperactivity are not available and contrary data are available [11, 12]. In addition to OB, other endocrine diseases, including poorly controlled DM and polycystic ovary disease, as well as other diseases such as chronic alcoholism and mental disorders, may show beneficial hypercortisol and some clinical and metabolic symptoms, causing the so-called pseudo-Cushing’s syndrome. . . Subjects with visceral OB cortisol may have elevated 24-h urinary cortisol levels and an elevated urinary cortisone-to-cortisol ratio . Therefore, several studies show a positive association between postprandial salivary cortisol and body mass index (BMI), waist-hip ratio (WHR), blood glucose, serum insulin, and lipids in adult male patients with visceral adiposity [3, 11, 12, 14]. Cortisol clearance has been reported to be negatively correlated with insulin sensitivity. In addition, an increased response of the HPA axis to various stimuli such as food, low doses of ACTH and CRH has been reported in obese humans . Thus, a general observational pattern appears to be that increased abdominal fat is associated with higher cortisol levels and HPA axis sensitivity, as reflected in morning awakening and acute stress responses,
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