Stress and glucocorticoid modulation of feeding and metabolism

Abstract

This perspective highlights research presented as part of the symposium entitled, “Stress and Glucocorticoid Modulation of Feeding and Metabolism” at the 2018 Neurobiology of Stress Workshop held in Banff, AB, Canada. The symposium comprised five researchers at different career stages who each study different aspects of the interaction between the stress response and metabolic control. Their collective results reveal the complexity of this relationship in terms of behavioural and physiological outcomes. Their work emphasizes the need to consider the level of interaction (cellular, tissue, systems) as well as the timing and context in which the interaction is studied. Rather than a comprehensive review on the work presented at the Symposium, here we discuss recurring themes that emerged at the biennial workshop, which address new avenues of research that will drive the field forward.

Does inflammation link stress to poor COVID‐19 outcome?

“…One assumption is that CB2 receptors are recruited in response to neuroinflammation, suppressing immune responses in a number of pathological conditions (Nagarkatti, Pandey, Rieder, Hegde, & Nagarkatti, 2009). This may include stress, which exerts an effect, at least partially, through the ECS (Balsevich, Abizaid, Chen, Karatsoreos, & Schmidt, 2019). Indeed, systemic injections of a CB2 receptor agonist in mice inhibit chronic stress‐induced hypersecretion of proinflammatory cytokines and protect against neuroinflammatory responses in the frontal cortex (Zoppi et al., 2014).…”

Title: “Labels Matter: Is it stress or is it Trauma?”

“…Cortisol's role as a metabolic hormone is emphasized in this context, because of its effects on increasing blood glucose levels and its capacity to eventually directly affect mitochondrial function [19][20][21][22]. Indeed, an important part of the stress response is metabolic control, as increases in glucocorticoid levels can lead to increases in glucose and modulate adiponectin levels [22][23][24][25][26]. Furthermore, stress and trauma-related psychopathologies, such as post-traumatic stress disorder (PTSD), or stress-induced mood disorders, are known to have high comorbidity with metabolic dysregulation and metabolic syndromes [19,27,28].…”

“…Therefore, the stress response emerges nowadays as a complex and integrative process that involves, among others, neuronal-neuroendocrine-immune interactions [19,23,27,[29][30][31][32][33][34] and these interactions are also influenced by an individual's genetic background [35][36][37][38][39].…”

High‐fat diet during adulthood interacts with prenatal stress, affecting both brain inflammatory and neuroendocrine markers in male rats

“…We specifically assessed in these brain regions levels of Bdnf, Stress powerfully affects both mood and energy homeostasis. Such effects are achieved not only through the interaction between GC hormones and their receptors (that regulate hypothalamic-pituitary-adrenal-HPA-axis function in addition to glucose metabolism) but also by triggering a multitude of signalling cascades reciprocally modulating one another in a regional-, temporal-and functional-dependent manner (Balsevich et al, 2019). Among these, ghrelin is a peptide hormone produced in the stomach and involved in the signalling of meal initiation.…”

“…Both ghrelin and Ghs‐R are modulated by stress (Patterson et al., 2010); there is evidence that ghrelin may decrease anxiety‐like and depressive‐like behaviours in mice (Lutter et al., 2008), moreover, it appears to be involved in food anticipatory activity and consumption (Blum et al., 2009; Verhagen et al., 2011) as well as in mood disorders (Zarouna, 2015). Interestingly, both genetic variants within ghrelin and GC signalling pathways have been associated with obesity, stress‐related mental disorders, or both (see Balsevich et al., 2019 and references therein). To this regard, we also investigated changes in the expression levels of Ghs‐R as well as of Nr3c1 (encoding for the glucocorticoid receptors—GR) and the GC co‐chaperon Fkbp5 (encoding for the FK506 binding protein 51) in all the above‐mentioned brain regions.…”