Stress, Glucocorticoids and Bone: A Review From Mammals and Fish

Abstract

Glucocorticoids (GCs) are the final effector products of a neuroendocrine HPA/HPI axis governing energy balance and stress response in vertebrates. From a physiological point of view, basal GC levels are essential for intermediary metabolism and participate in the development and homeostasis of a wide range of body tissues, including the skeleton. Numerous mammalian studies have demonstrated that GC hormones exert a positive role during bone modeling and remodeling as they promote osteoblastogenesis to maintain the bone architecture. Although the pharmacological effect of the so-called stress hormones has been widely reported, the role of endogenous GCs on bone mineral metabolism as result of the endocrine stress response has been largely overlooked across vertebrates. In addition, stress responses are variable depending on the stressor (e.g., starvation, predation, and environmental change), life cycle events (e.g., migration and aging), and differ among vertebrate lineages, which react differently according to their biological, social and cognitive complexity (e.g., mineral demands, physical, and psychological stress). This review intends to summarize the endogenous GCs action on bone metabolism of mammals and fish under a variety of challenging circumstances. Particular emphasis will be given to the regulatory loop between GCs and the parathyroid hormone (PTH) family peptides, and other key regulators of mineral homeostasis and bone remodeling in vertebrates.

Short-Chain Alcohols Upregulate GILZ Gene Expression and Attenuate LPS-Induced Septic Immune Response

“…Glucocorticoids (GCs) are steroid hormones produced by the adrenal cortex under control of the hypothalamic-pituitaryadrenal (HPA) axis in response to internal circadian clock and external stress challenge (53,54). GCs are the most prescribed anti-inflammatory drugs.…”

Evaluation of Three Formulations of Essential Oils in Broiler Chickens under Cyclic Heat Stress

“…Additionally, HS induces cellular osmotic and dehydration associated with increased plasma triglyceride and glucose, serum calcium (due to bone demineralization), and total serum protein. These alternations have significant implications in the water holding capacity of the chicken meat products [ 45 , 46 , 47 ].…”

Hormonal regulation in male androgenetic alopecia—Sex hormones and beyond: Evidence from recent genetic studies

“…Macrophages can secrete PRL and are crucial for the cyclic activation of HFs [107,108] , as well as the development of RA [105] and MS. [109] Similarly, mast cells are important in terms of hair cycling [86] and their activation has been implicated in both RA [104] and MS. [110] As a further example, genetic analyses have identified a correlation between AGA and bone mineral density. [12] Here, PTHLH signalling-a major regulator of bone mineral homoeostasis [111] may serve as a link between the effects on bone mineral density and hair loss. Similarly, shared genetic determinants have been reported for AGA and key aspects of metabolic syndrome, including insulin resistance, elevated HOMA-B-levels and hypertension.…”