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multiple homeostatic perturbations. These include regulation of fluid ( O'Carroll & Lolait 2003 ) and cardiovascular homeostasis ( Ishida et al . 2004 ), the stress response ( O'Carroll et al . 2003 ), food intake ( Taheri et al . 2002 ), gastric cell

inhibitory role in the regulation of the HPA axis ( Maffei et al . 1995 ). Leptin administration blunts the restraint stress-induced activation of the HPA axis in mice ( Heiman et al . 1997 ) and can directly inhibit ACTH-stimulated cortisol

, differentiation, apoptosis, immune regulation and cellular adaptation to stress ( Ray et al . 2012 , Sena & Chandel 2012 ). A critical balance in redox status needs to be maintained and this is achieved by numerous interacting antioxidant pathways. Oxidative

Introduction Stress experienced during pregnancy has detrimental effects on the offspring across the life course, beginning during fetal development, persisting through the postnatal period and into adulthood ( Glover et al. 2018 ). This

early diabetes onset in MODY4 mutation carriers ( Fajans et al. 2010 ). In this condition β-cells are stressed and forced to compensate the increased insulin demand ( Ferrannini et al. 2004 ). Thus, the occurrence of any additional β-cell stress

the summer period induce metabolic heat stress, which has adverse effects on milk production, reproductive performance and animal welfare issues, among others. Counterregulatory mechanisms generally include an increased sweating rate, increased water

excess glucocorticoids via maternal stress, inhibition of placental 11β-hydroxysteroid dehydrogenase type 2, the normal ‘barrier’ to maternal glucocorticoids, or its bypass with non-substrate synthetic glucocorticoids, such as dexamethasone (DEX

Introduction Response to neuroendocrine stress begins with the activation of the hypothalamic–pituitary–adrenal (HPA) axis leading to the increase in stress hormones glucocorticoids (GCs). These hormones mediate adaptation to stress and also

. 2009 ). In other words, insulin resistance/hyperinsulinemia is a precursor of T2DM. It is still highly debatable as to how nutrients cause insulin resistance/hyperinsulinemia and then T2DM. Inflammation, endoplasmic reticulum stress, and mitochondrion

Introduction Activation of the hypothalamic–pituitary–adrenal (HPA) axis is a vital component of the stress response, driving production of glucocorticoid hormones (cortisol in humans, corticosterone in rodents) that mediate essential adaptations of