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Prolonged stress has long been shown to have major effects on the
development of both type of diabetes mellitus, Type 1 and Type 2.
Type 1 diabetes is an autoimmune disease that is characterized by
the immune system attacking self-antigens. There is a failure or
breakdown in immunological tolerance to allow this to happen.
Prolonged physical or emotional stress can activate the
hypothalamus-pituitary-adrenal (HPA) axis to induce production of
the stress hormone glucocorticoid, causing abrupt thymus involution
and result in escape of autoreactive T- cells. Though regulatory
T-cells (Treg) are present in the circulation, they are unable to
suppress the autoreative T-cells from initiating the destruction of
-cells and the subsequent development of Type 1 diabetes. Stress
also causes metabolic disturbances, including altered hepatic
glucose metabolism, increased peripheral insulin resistance and
hyperglycemia. Glucocorticoid is the potential contributor to the
chronic hyperglycemia that results in insulin resistance and -cell
dysfunction via the generation of oxidative stress which ultimately
leads to the development of Type 2 diabetes."
Psychological stress has extreme adverse consequences on health.
However, the molecular mechanisms that mediate and accelerate the
process of aging due to stress hormone are not well defined. This
review has focused on diverse molecular paths that come out in
response to chronic psychological stress via releasing of excessive
glucocorticoids (GCs), involved in the aging process. GCs suppress
transcription of nuclear cell adhesion molecules which impair
synaptic plasticity, memory formation, and cognitive ability.
Again, GCs promote muscle atrophy by means of motivating ubiquitin
proteasome system and can repress muscle protein synthesis by
inhibition of PI3-kinase/Akt pathway. GCs also inhibit
interleukin-2 synthesis through suppressing T cell receptor signal
that leads to loss of T cell activation, proliferation, and B-cell
activation. Moreover, GCs increase the expression of collagenase-3,
RANK ligand, and colony stimulating factor-1 that induce bone
resorption. In general, stress-induced GCs can play causal role for
aging and age-related disorders.
Chronic Psychological stress has several adverse effects both on
HIV- people and on HIV+ patient. When the HIV- people are
concerned, stress makes them more susceptible to HIV infection.
T-cells have CXCR4 receptor and Macrophage have CCR5 receptor which
can bind with both glucocorticoid and catecholamine hormone. HIV
has GP120 protein which has to bind with both CD4 and CXCR4/CCR5
receptor for its entry into the host cells. Mental stress increases
glucocorticoid and catecholamine concentration in blood. When these
stress hormones, glucocorticoid and catecholamine, bind with the
CXCR4/CCR5 receptors, cAMP signaling pathway gets activated. This
signal transduction pathway leads to the synthesis of more CXCR4
and CCR5 receptors by those cells, which in turn become more
susceptible to HIV infection. Stress inhibits Th2 when the cell
produces INF- as a response to viral attacks. So that other cells
remain vulnerable to viral infection. When T-cell count is
decreased in the blood, the body cannot protect itself from other
opportunistic infectious pathogens. As a result progression of AIDS
is increased."
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