Stress threatens the homeostasis and mobilizes a plethora of adaptive physiological and behavioral changes via the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system. The HPA axis influences pituitary gland, hypothalamus and adrenal gland via a complex set of positive and negative feedback system. The feedback system operates in a well regulated neuroendocrine manner to reestablish the threatened body equilibrium. The HPA axis secreted major product is glucocorticoid (cortisol) which is kept within a physiologically optimal range and serve to accomplish the various physiological functions crucial for survival. In chronically stressed individuals dishabituation of HPA axis is followed by increased release of glucocorticoids and catecholamines. Higher secretion of glucocorticoids influence glucose metabolism by promoting gluconeogenesis in liver, suppressing glucose uptake (adipocytes and skeletal muscles), promoting lipolysis in adipocytes, suppressing insulin secretion, inflicting insulin resistance and inflammation. These biological changes alter neuroendocrine mechanisms and lead to maladaptive congregation of events which form the underlying cause of development of Type 2 diabetes (T2D). The current reviewed evidences advocate that targeting stress mediated hypersecretion of glucocorticoids may be a viable approach for treatment of T2D and to reinstate glucose homeostasis.
Keywords: Chronic stress, Hypothalamic-pituitary-adrenal axis, Diabetes, Glucocorticoids; Insulin, Inflammation
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