Steroidogenesis showing<unk> s in green ellipse at right with the primary example being cortisol. It is not a strictly bounded group, but a continuum of structures with increasing<unk>  effect.<unk>  effects may be broadly classified into two major categories: immunological and metabolic. In addition,<unk> s play important roles in fetal development and body fluid homeostasis. Immune<unk> s function via interaction with the<unk>  receptor (see details below): * up-regulate the expression of anti-inflammatory proteins. * down-regulate the expression of proinflammatory proteins.<unk> s are also shown to play a role in the development and homeostasis of T lymphocytes. This has been shown in transgenic mice with either increased or decreased sensitivity of T cell lineage to<unk> s. Metabolic The name<unk> " derives from early observations that these hormones were involved in glucose metabolism. In the fasted state, cortisol stimulates several processes that collectively serve to increase and maintain normal concentrations of glucose in the blood. Metabolic effects: * Stimulation of gluconeogenesis, in particular, in the liver: This pathway results in the synthesis of glucose from non-hexose substrates, such as amino acids and glycerol from triglyceride breakdown, and is particularly important in carnivores and certain herbivores. Enhancing the expression of enzymes involved in gluconeogenesis is probably the best-known metabolic function of<unk> s. * Mobilization of amino acids from extrahepatic tissues: These serve as substrates for gluconeogenesis. * Inhibition of glucose uptake in muscle and adipose tissue: A mechanism to conserve glucose * Stimulation of fat breakdown in adipose tissue: The fatty acids released by lipolysis are used for production of energy in tissues like muscle, and the released glycerol provide another substrate for gluconeogenesis. *Increase in sodium retention and potassium excretion leads to hypernatremia and hypokalemia *Increase in hemoglobin concentration, likely due to hindrance of the ingestion of red blood cell by macrophage or other phagocyte. *Increased urinary uric acid *Increased urinary calcium and hypocalcemia *Alkalosis *Leukocytosis Excessive<unk>  levels resulting from administration as a drug or hyperadrenocorticism have effects on many systems. Some examples include inhibition of bone formation, suppression of calcium absorption (both of which can lead to osteoporosis), delayed wound healing, muscle weakness, and increased risk of infection. These observations suggest a multitude of less-dramatic physiologic roles for<unk> s. Developmental<unk> s have multiple effects on fetal development. An important example is their role in promoting maturation of the lung and production of the surfactant necessary for extrauterine lung function. Mice with homozygous disruptions in the corticotropin-releasing hormone gene (see below) die at birth due to pulmonary immaturity. In addition,<unk> s are necessary for normal brain development, by initiating terminal maturation, remodeling axons and dendrites, and affecting cell survival and may also play a role in hippocampal development.<unk> s stimulate the maturation of the Na+/K+/ATPase, nutrient transporters, and digestion enzymes, promoting the development of a functioning gastro-intestinal system.<unk> s also support the development of the neonate's renal system by increasing glomerular filtration. Arousal and cognition alt=A graphical representation of the Yerkes- A graphical representation of the Yerkes-Dodson curve<unk> s act on the hippocampus, amygdala, and frontal lobes. Along with adrenaline, these enhance the formation of flashbulb memories of events associated with strong emotions, both positive and negative. This has been confirmed in studies, whereby blockade of either<unk> s or noradrenaline activity impaired the recall of emotionally relevant information. Additional sources have shown subjects whose fear learning was accompanied by high cortisol levels had better consolidation of this memory (this effect was more important in men). The effect that<unk> s have on memory may be due to damage specifically to the CA1 area of the hippocampal formation. In multiple animal studies, prolonged stress (causing prolonged increases in<unk>  levels) have shown destruction of the neurons in this area of the brain, which has been connected to lower memory performance.<unk> s have also been shown to have a significant impact on vigilance (attention deficit disorder) and cognition (memory). This appears to follow the Yerkes-Dodson curve, as studies have shown circulating levels of<unk> s vs. memory performance follow an upside-down U pattern, much like the Yerkes-Dodson curve. For example, long-term potentiation (LTP; the process of forming long-term memories) is optimal when<unk>  levels are mildly elevated, whereas significant decreases of LTP are observed after adrenalectomy (low-glucocorticoid state) or after exogenous<unk>  administration (high-glucocorticoid state). Elevated levels of<unk> s enhance memory for emotionally arousing events, but lead more often than not to poor memory for material unrelated to the source of stress/emotional arousal. In contrast to the dose-dependent enhancing effects of<unk> s on memory consolidation, these stress hormones have been shown to inhibit the retrieval of already stored information. Long-term exposure to<unk>  medications, such as asthma and anti-inflammatory medication, has been shown to create deficits in memory and attention both during and, to a lesser extent, after treatment, a condition known as "steroid dementia". Body fluid homeostasis<unk> s could act centrally, as well as peripherally, to assist in the normalization of extracellular fluid volume by regulating body's action to atrial natriuretic peptide (ANP). Centrally,<unk> s could inhibit dehydration induce water intake; peripherally,<unk> s could induce a potent diuresis.
Glucocorticoid
Adrenal steroid
Corticosteroid
Antiglucocorticoid
Xenohormone
Anticorticotropin
Phytosteroid
Neurohormone