How Stress Affects The Body Science Project – Although we often associate the word ‘stress’ with anxiety, the term really encompasses any challenge that has the potential to disrupt homeostasis. These include physical stress such as infection or injury. Physiological requirements in response to these diverse challenges are all mediated – at least in part – by the glucocorticoid cortisol.

Glucocorticoids are cholesterol-derived steroid hormones synthesized and secreted by the adrenal glands. They are anti-inflammatory in all tissues and regulate muscle, fat, liver and bone metabolism. Glucocorticoids also affect vascular tone and affect mood, behavior, and sleep-wake cycles in the brain.

How Stress Affects The Body Science Project

Glucocorticoid excess (due to pathology such as Cushing’s syndrome or prescribed synthetic glucocorticoids) can cause immunosuppression, muscle atrophy, central adiposity, hepatosteatosis, osteoporosis, insulin resistance, hypertension, depression, and insomnia.

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Elevated glucocorticoids can therefore be harmful, and therefore their production is under tight control of the hypothalamic-pituitary-adrenal (HPA) axis (Figure 1). Activation of the hypothalamus initiates the release of corticotrophin-releasing hormone (CRH), which then signals the anterior pituitary to release adrenocorticotrophin (ACTH). This then signals the cortical layer of the adrenal gland to release glucocorticoids, which can act on peripheral tissues.

Over time, elevated circulating glucocorticoids inhibit further release of CRH and ACTH in the hypothalamus and pituitary, respectively, which inhibit glucocorticoid secretion. Consequently, glucocorticoids are secreted in a pulsatile manner and exhibit a diurnal rhythm with circulating hormone levels peaking at the onset of awakening.

In the context of maintaining normal homeostasis, the daily peak of glucocorticoids is very important. Transient peaks increase vascular tone and alertness, circulate energy, and have primary effects on the immune system. Essentially, your morning dose of cortisol prepares you to face the potential challenges of your day.

Experiencing stress throughout the day can cause additional pulses of glucocorticoid to be released from the adrenals, leading to sustained, elevated glucocorticoid levels. It produces the same physiological response but with a greater magnitude. For example, in a ‘fight or flight’ context, glucocorticoids increase vascular tone and alertness, mobilize energy (getting you ready to run) and prime the immune system (getting you ready for injury). These preparatory effects increase the likelihood of overcoming stress, so that normal homeostasis can be quickly restored.

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It seems paradoxical that a potent immunosuppressive hormone would prime the immune system, but the benefit of activation of immune cells is beneficial. It enhances the immune system’s ability to recognize pathogens/injuries and respond accordingly, and it facilitates resolution and repair to restore balance. In the context of chronic infection or disease, the role of glucocorticoids is altered, to prevent growth and limit damage.

Glucocorticoids act directly on cells within damaged tissue to inhibit the production of inflammatory signals (cytokines, chemokines) that attract immune cells. They act directly on immune cells to inhibit their ability to infiltrate tissue and cause their death in some cell types. Glucocorticoids also promote activation of scavenger immune cells that help remove cell debris, repair, and prevent chronic damage (such as fibrosis). At the cellular level, glucocorticoids are able to regulate metabolism, inflammation, adhesion, migration and survival in a cell-specific and context-specific manner.

Glucocorticoids mediate their cellular effects by binding to and activating the glucocorticoid receptor (GR), which is expressed in almost every tissue. Glucocorticoids are used in cells and bind and activate GR, which then translocates to the nucleus.

GR can directly bind DNA to specific glucocorticoid response elements (GREs) and then recruit coactivator or corepressor proteins to increase or decrease target gene expression. GR can bind or tether itself to other DNA-bound transcription factors and alter their ability to modulate gene expression (Figure 2).

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The specific genes that GR can regulate—and therefore the cellular processes that glucocorticoids can regulate—are critically determined by their ability to bind GR. This adds an additional layer of regulation, as gene accessibility and transcription factor expression and activity are cell-specific and dynamically regulated.

For example, liver-specific transcription factors such as HNF4 (hepatocyte nuclear factor 4) facilitate GR binding to (and regulation of) metabolic genes, whereas macrophage-specific transcription factors such as PU.1 recruit GR to genes important in immunity.

Glucocorticoid responses are therefore fine-tuned to take context into account. Thus glucocorticoids may regulate metabolism in the liver, activate macrophages, and promote T-cell death.

GR is also recruited by the proinflammatory transcription factor NFκB (nuclear factor-κB). Unlike HNF4 and PU.1, NFκB is expressed in every cell, but only binds DNA when activated in response to pathogens or tissue damage. Consequently, GR is recruited to (and inhibits) proinflammatory genes only when NFκB is activated. This explains why GR (and glucocorticoids) is a powerful inhibitor of inflammation only when needed: that is, when inflammation is already present.

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Glucocorticoids (via GR) are therefore perfectly adapted to integrate signals from other pathways to respond appropriately to each specific challenge. We still have a long way to go to fully understand the full spectrum of glucocorticoid action. However, we now have some insight into how, by adding a few additional points of regulation, glucocorticoids can coordinate different cellular effects to reach a common goal: restoration of balance after stress. From green technology to functional olive oil: evaluating the best combinations of olive tree-related extracts with complementary bioactivities

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By Rosa Vona 1, *, † , Lucia Pallotta 2, † , Martina Cappelletti 2, Carola Severi 2 and Paola Matares 1

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Received: 23 December 2020 / Revised: 22 January 2021 / Accepted: 26 January 2021 / Published: 30 January 2021

Accumulating evidence shows that oxidative stress plays an essential role in the pathogenesis and progression of many diseases. An imbalance between the production of reactive oxygen species (ROS) and the antioxidant system has been extensively studied in pulmonary, neurodegenerative cardiovascular disorders; However, its contribution to gastrointestinal disorders is still controversial. Evidence suggests that oxidative stress affects gastrointestinal motility in obesity and post-infectious disorders by favoring the smooth muscle phenotypic switch to a synthetic phenotype. The aim of this review is to gain insight into the role of oxidative stress in gastrointestinal pathologies (GIT) and the involvement of ROS in signaling underlying gastrointestinal tract (GIT) muscle changes. In addition, potential therapeutic strategies based on the use of antioxidants for the treatment of inflammatory gastrointestinal diseases are reviewed and discussed. Although considerable progress has been made in identifying new techniques capable of assessing the presence of oxidative stress in humans, the biochemical-molecular mechanisms underlying GIT mucosal disorders are still not well defined. Therefore, further studies are needed to elucidate the mechanisms by which oxidative stress-related signals may contribute to changes in the GIT mucosa in order to develop effective preventive and curative therapeutic strategies.

Oxidative stress in living organisms results from an imbalance between the production of reactive oxygen species (ROS) and the ability to neutralize them. The disparity between overreactive molecules and weak endogenous defenses leads to damage to cell structures and molecules such as lipids, proteins, and DNA, which ultimately contribute to the pathogenesis of a wide range of diseases. ROS, when found in appropriately low amounts, act as signal transduction molecules driving cell activity and confer cell protection [1]. On the other hand, when generated in excess, such as in inflammation, ROS can trigger the production of additional highly reactive species [2]. Important are oxidative modifications of key enzymes or regulatory sites, whose redox changes trigger altered cell signaling and programmed cell death. Oxidative stress and inflammation are closely related

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