Metabolic response Metabolism of glucose In general,<unk>  stimulates gluconeogenesis (the synthesis of 'new' glucose from non-carbohydrate sources, which occurs mainly in the liver, but also in the kidneys and small intestine under<unk> ertain<unk> ircumstances). The net effect is an increase in the<unk> oncentration of glucose in the blood, further<unk> omplemented by a decrease in the sensitivity of peripheral tissue to insulin, thus preventing this tissue from taking the glucose from the blood.<unk>  has a permissive effect on the actions of hormones that increase glucose production, such as glucagon and adrenaline.<unk>  also plays an important, but indirect, role in liver and muscle glycogenolysis (the breaking down of glycogen to glucose-1-phosphate and glucose) which occurs as a result of the action of glucagon and adrenaline. Additionally,<unk>  facilitates the activation of glycogen phosphorylase, which is necessary for adrenaline to have an effect on glycogenolysis. Paradoxically,<unk>  promotes not only gluconeogenesis in the liver, but also glycogenesis.<unk>  is thus better thought of as stimulating glucose/glycogen turnover in the liver. This is in<unk> ontrast to<unk> 's effect in the skeletal muscle where glycogenolysis is promoted indirectly through<unk> atecholamines. Metabolism of proteins and lipids Elevated levels of<unk> , if prolonged,<unk> an lead to proteolysis (breakdown of proteins) and muscle wasting. The reason for proteolysis is to provide the relevant tissue with a feedstock for gluconeogenesis; see glucogenic amino acids. The effects of<unk>  on lipid metabolism are more<unk> omplicated since lipogenesis is observed in patients with<unk> hronic, raised<unk> irculating glucocorticoid (i.e.<unk>  levels, although an acute increase in<unk> irculating<unk>  promotes lipolysis. The usual explanation to account for this apparent discrepancy is that the raised blood glucose<unk> oncentration (through the action of<unk>  will stimulate insulin release. Insulin stimulates lipogenesis, so this is an indirect<unk> onsequence of the raised<unk> <unk> oncentration in the blood but it will only occur over a longer time scale. Immune response<unk>  prevents the release of substances in the body that<unk> ause inflammation. It is used to treat<unk> onditions resulting from overactivity of the B-cell-mediated antibody response. Examples include inflammatory and rheumatoid diseases, as well as allergies. Low-dose topical hydrocortisone, available as a nonprescription medicine in some<unk> ountries, is used to treat skin problems such as rashes and eczema.<unk>  inhibits production of interleukin 12 (IL-12), interferon gamma (IFN-gamma), IFN-alpha, and tumor necrosis factor alpha (TNF-alpha) by antigen-presenting<unk> ells (APCs) and T helper<unk> ells (Th1<unk> ells), but upregulates interleukin 4, interleukin 10, and interleukin 13 by Th2<unk> ells. This results in a shift toward a Th2 immune response rather than general immunosuppression. The activation of the stress system (and resulting increase in<unk>  and Th2 shift) seen during an infection is believed to be a protective mechanism which prevents an over-activation of the inflammatory response.<unk> <unk> an weaken the activity of the immune system. It prevents proliferation of T-cells by rendering the interleukin-2 producer T-cells unresponsive to interleukin-1, and unable to produce the T-cell growth factor IL-2.<unk>  downregulates the expression of the IL2 receptor IL-2R on the surface of the helper T-cell which is necessary to induce a Th1 'cellular' immune response, thus favoring a shift towards Th2 dominance and the release of the<unk> ytokines listed above which results in Th2 dominance and favors the 'humoral' B-cell mediated antibody immune response).<unk>  also has a negative-feedback effect on IL-1. Though IL-1 is useful in<unk> ombating some diseases, endotoxic bacteria have gained an advantage by forcing the hypothalamus to increase<unk>  levels (forcing the secretion of<unk> orticotropin-releasing hormone, thus antagonizing IL-1). The suppressor<unk> ells are not affected by glucosteroid response-modifying factor, so the effective setpoint for the immune<unk> ells may be even higher than the setpoint for physiological processes (reflecting leukocyte redistribution to lymph nodes, bone marrow, and skin). Rapid administration of<unk> orticosterone (the endogenous type I and type II receptor agonist) or RU28362 (a specific type II receptor agonist) to adrenalectomized animals induced<unk> hanges in leukocyte distribution. Natural killer<unk> ells are affected by<unk> .<unk>  stimulates many<unk> opper enzymes (often to 50% of their total potential), including lysyl oxidase, an enzyme that<unk> ross-links<unk> ollagen and elastin. Especially valuable for immune response is<unk> 's stimulation of the superoxide dismutase, since this<unk> opper enzyme is almost<unk> ertainly used by the body to permit superoxides to poison bacteria.
Cortisol
Adrenocortical hormone
Menotropin
Orexin
Parathyroid hormone
Adrenocorticotropic hormone 
Counterregulatory hormone
Gonadotropin