Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is clear that the sympathoadrenal system has a role in the regulation of endocrine pancreatic function and that the sympathetic nerves of the pancreas can change pancreatic hormone secretion to increase the availability of metabolic fuels. It seems likely that the classical sympathetic neurotransmitter, NE, acts in concert with peptide co-transmitters, such as galanin and NPY. Each is released during the stimulation of pancreatic sympathetic nerves and each is capable of influencing either islet function or pancreatic blood flow. There is considerable indirect evidence that the sympathetic innervation of the pancreas is activated during acute stress and influences the endocrine pancreas. However, proving such a physiologic role is difficult because of redundant mechanisms that influence the secretion of the metabolically-crucial hormones, insulin and glucagon. Such definitive proof therefore awaits the development of new techniques to dissect and dissociate these mechanisms.
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PMID:Neural control of islet function by norepinephrine and sympathetic neuropeptides. 192 79

Of all the psychological complications that an individual is likely to present with when confronted with an exceptional event, the Post-Traumatic Stress Disorder is characterized by being progressive, frequent, invalidating, strongly associated with comorbidity, and having the tendency to become chronic if it is not detected clinically. By definition, it is threatening and produces an intense fear reaction. The traumatic event is a situation of extreme stress, not only capable of altering the physical and psychological homeostasis of the individual, but is also recognized as determinant in the aetiopathology of complications. The intensity of this distress can be identified clinically and physiologically, and is currently considered as an important risk factor for the development of PTSD later on, together with other pre-, peri- and post-traumatic factors. In fact, the most studied field is the therapeutic approach, in particular drug treatment, of the fully-constituted disorder, although this actually represents tertiary prevention. Even though primary prevention seems to concern Medicine very little, any prospect of performing secondary prevention should begin by rapid identification of the risk or vulnerability factors and should allow a population at risk from developing complications to be defined. Its potential therapeutic impact brings together psychotherapeutic and drug treatment, since it is only this combination that seems able to allow the most favourable clinical outcome to be achieved for an individual, who is confronted by an out-of-the-ordinary event. The aims of secondary prevention strategies are, for example, to reduce the incidence of acute PTSD in patients seen following the event. The benefits for the individual and for the society can easily be measured in terms of the consequences on his/her social, professional and family life, or in terms of cost. The usefulness of this prevention can also be measured by the possible ways that other conditions, comorbid to PTSD, are controlled, such as anxiety disorders, depression and substance abuse, for example. Secondary prevention strategies may also be aimed at determining the therapeutic impact, by preventing or moderating the appearance of an acute stress, or even by contributing in avoiding the onset of chronic PTSD. Psychopharmacology of the immediate and post-immediate disorders, however, remains a field which has been studied very little. Reduction or control of the high, prolonged level of hyperarousal phenomena or hypersensitization of the hypothalamo-pituitary axis, would contribute to the comfort of the individual, and would participate in the prevention of PTSD. Based on current knowledge of the neurobiology of trauma, we look into the existing and potential pharmacological possibilities. Even though benzodiazepines tend to have an important role, knowledge of other drugs and therapeutic groups is rapidly increasing. In this review, we will see that the efficacy of anti-adrenergic drugs and certain other anxiolytics is now well-documented, this opening the door to their use in the future. Other drug groups offer interesting, well-proven approaches, such as serotoninergic drugs, CRF or NPY antagonists, NMDA antagonists, anticonvulsants or other GABAergic agents. In view of this disorder, which represents a true public health problem, we consider that it is now possible to widen the horizons of our drug therapy, in combination with any necessary psychotherapeutic treatment, to reach the heart of the traumatic event, that often upsets the victims, both by the psychological suffering it induces, and the loss of his/her social, family and professional references and support structures.
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PMID:[From the biology of trauma to secondary preventive pharmalogical measures for post-traumatic stress disorders]. 1595 48

Acute mild stress induces an inhibition of food intake in rats. In most studies, the cumulative daily food intake is measured but this only provides a quantitative assessment of ingestive behavior. The present study was designed to analyze the reduction in food intake induced by acute stress and to understand which behavioral and central mechanisms are responsible for it. Two different stressors, restraint stress (RS) and forced swimming stress (FSS), were applied acutely to male Wistar rats. We first measured corticosterone and ACTH in plasma samples collected immediately after acute RS and FSS in order to validate our stress models. We measured food intake after RS and FSS and determined meal patterns and behavioral satiety sequences. The expressions of CRF, NPY and POMC in the hypothalamus were also determined immediately after acute RS and FSS. The rise in corticosterone and ACTH levels after both acute RS and FSS validated our models. Furthermore, we showed that acute stress induced a reduction in cumulative food intake which lasted the whole day for RS but only for the first hour after FSS. For both stressors, this stress-induced food intake inhibition was explained by a decrease in meal size and duration, but there was no difference in ingestion speed. The behavioral satiety sequence was preserved after RS and FSS but grooming was markedly increased, which thus competed with, and could reduce, other behaviors, including eating. Lastly, we showed that RS induced an increase in hypothalamic POMC expression. These results suggest that acute stress may affect ingestive behavior by increasing satiation and to some extent by enhancing grooming, and this may be due to stimulation of the hypothalamic POMC neurons.
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PMID:Inhibition of food intake induced by acute stress in rats is due to satiation effects. 2178 97

Although regulation of energy metabolism has been linked with multiple disorders, its role in depression and responsiveness to antidepressants is less known. We found that an epigenetic and energetic agent, acetyl-l-carnitine (LAC, oral administration), rapidly rescued the depressive- and central and systemic metabolic-like phenotype of LAC-deficient Flinders Sensitive Line rats (FSL). After acute stress during LAC treatment, a subset of FSL continued to respond to LAC (rFSL), whereas the other subset did not (nrFSL). RNA sequencing of the ventral dentate gyrus, a mood-regulatory region, identified metabolic factors as key markers predisposing to depression (insulin receptors Insr, glucose transporters Glut-4 and Glut-12, and the regulator of appetite Cartpt) and to LAC responsiveness (leptin receptors Lepr, metabotropic glutamate receptors-2 mGlu2, neuropeptide-Y NPY, and mineralocorticoid receptors MR). Furthermore, we found that stress-induced treatment resistance in nrFSL shows a new gene profile, including the metabolic regulator factors elongation of long chain fatty acids 7 (Elovl7) and cytochrome B5 reductase 2 (Cyb5r2) and the synaptic regulator NPAS4. Finally, while improving central energy regulation and exerting rapid antidepressant-like effects, LAC corrected a systemic hyperinsulinemia and hyperglicemia in rFSL and failed to do that in nrFSL. These findings establish CNS energy regulation as a factor to be considered for the development of better therapeutics. Agents such as LAC that regulate metabolic factors and reduce glutamate overflow could rapidly ameliorate depression and could also be considered for treatment of insulin resistance in depressed subjects. The approach here serves as a model for identifying markers and underlying mechanisms of predisposition to diseases and treatment responsiveness that may be useful in translation to human behavior and psychopathology.
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PMID:Epigenetics and energetics in ventral hippocampus mediate rapid antidepressant action: Implications for treatment resistance. 2762 30