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

There is growing recognition that the O-linked attachment of N-acetyl-glucosamine (O-GlcNAc) on serine and threonine residues of nuclear and cytoplasmic proteins is a highly dynamic post-translational modification that plays a key role in signal transduction pathways. Numerous proteins have been identified as targets of O-GlcNAc modifications including kinases, phosphatases, transcription factors, metabolic enzymes, chaperons, and cytoskeletal proteins. Modulation of O-GlcNAc levels has been shown to modify DNA binding, enzyme activity, protein-protein interactions, the half-life of proteins, and subcellular localization. The level of O-GlcNAc is regulated in part by the metabolism of glucose via the hexosamine biosynthesis pathway (HBP), and the metabolic abnormalities associated with insulin resistance and diabetes, such as hyperglycemia, hyperlipidemia, and hyperinsulinemia, are all associated with increased flux through the HBP and elevated O-GlcNAc levels. Increased HBP flux and O-GlcNAc levels have been implicated in the impaired relaxation of isolated cardiomyocytes, blunted response to angiotensin II and phenylephrine, hyperglycemia-induced cardiomyocyte apoptosis, and endothelial and vascular cell dysfunction. In contrast to these adverse effects, recent studies have also shown that O-GlcNAc levels increase in response to acute stress and that this is associated with increased cell survival. Thus, while the relationship between O-GlcNAc levels and cellular function is complex and not well-understood, it is clear that these pathways play a critical role in the regulation of cell function and survival in the cardiovascular system and may be implicated in the adverse effects of metabolic disease on the heart.
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PMID:Role of protein O-linked N-acetyl-glucosamine in mediating cell function and survival in the cardiovascular system. 1697 Sep 29

Glucose is a very important energy source for a wide variety of cells, and the ability of cells to respond to changes in glucose availability or other cell stresses is of critical importance. Many mammalian cells respond to acute stress by increasing the V(max) of transport through GLUT1; the most ubiquitously expressed glucose transporter isoform. This study investigated the acute response of glucose uptake to glucose deprivation in L929 fibroblast cells--a cell line that expresses only the GLUT1 transporter. Results indicated that glucose deprivation of only a minute activated glucose uptake 10-fold and reached a maximum of 20-fold within 10 min. The activation was dose dependent and only partially muted by addition of up to 20mM pyruvate as an alternate energy source. In contrast to the kinetics of acute metabolic stress, glucose deprivation decreased the K(m) of transport, but did not alter the V(max). Maximal activation of glucose transport by glucose deprivation was completely additive to activation of transport by methylene blue--a stimulant that increased the V(max) of transport without a change in the K(m). Glucose-deprived activation of glucose transport was not inhibited by wortmannin or herbimycin A, but was completely inhibited by phenylarsine oxide. Altogether, the data indicate that L929 fibroblast cells respond quickly and robustly to the cell stress of glucose deprivation and methylene blue treatment by two distinct activation pathways.
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PMID:Acute activation of glucose uptake by glucose deprivation in L929 fibroblast cells. 1701 Apr 94

We measured changes in free and total plasma cortisol levels, plasma glucose, gill hsp70 levels, and growth in haddock (Melanogrammus aeglefinus) subjected to a long-term handling stress (15 s out of water, each day, for 4 weeks), and the effect of this long-term stress on the ability of haddock to respond to an acute stressor. The acute stressor was a single handling stress, and fish were sampled at 1, 6, and 12 h post-stress. During the long-term stress study, free and total plasma cortisol levels increased significantly (10-fold) in the stressed group after the second week. However, the percentage of free cortisol was already significantly elevated by the first week (control 17%, stressed 55%), and remained high during the second week (control 35% and stressed 65%). After 3 and 4 weeks of handling, both free and total cortisol declined in stressed fish to levels that were not significantly different from pre-stress values. Control fish grew significantly more than stressed fish (by 32% and 18%, respectively) over the 4 week study, and condition factor only increased in control fish. Although fish from the control group showed elevated total plasma cortisol levels (to 47 ng mL(-1)) 1 h after the acute stress, and the levels in stressed fish were comparable to those for the control fish, no significant increase in plasma cortisol was measured in the group subjected to the long-term stress. Free plasma cortisol levels did not increase significantly in either group following the acute stress. However, free plasma cortisol levels were significantly higher in long-term stress group, as compared with the control group, at 6 h post-stress. Plasma glucose and gill hsp70 levels were not altered by either the long-term stress or acute stressor. Our data indicate that cortisol (free and total), but not glucose or hsp70, appears to be adequate to assess short- and long-term stress in haddock.
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PMID:Changes in free and total plasma cortisol levels in juvenile haddock (Melanogrammus aeglefinus) exposed to long-term handling stress. 1704 29

Augmented cardiovascular responses to acute stress can predict cardiovascular disease in humans. Chronic systemic increases in glucocorticoids produce enhanced cardiovascular responses to psychological stress; however, the site of action is unknown. Recent evidence indicates that glucocorticoids can act within the dorsal hindbrain to modulate cardiovascular function. Therefore, we tested the hypothesis that the endogenous glucocorticoid corticosterone can act in the dorsal hindbrain to enhance cardiovascular responses to restraint stress in conscious rats. Adrenal-intact animals with indwelling arterial catheters were treated for 4 or 6 days with 3- to 4-mg pellets of corticosterone or silastic (sham pellets) implanted on the dorsal hindbrain surface. Corticosterone pellets were also implanted either on the surface of the dura or subcutaneously to control for the systemic effects of corticosterone (systemic corticosterone). The integrated increase in arterial pressure during 1 hour of restraint stress was significantly (P<0.05) greater in dorsal hindbrain corticosterone (912+/-98 mm Hg per 60 minutes) relative to dorsal hindbrain sham (589+/-57 mm Hg per 60 minutes) or systemic corticosterone (592+/-122 mm Hg per 60 minutes) rats. The plasma glucose response after 10 minutes of stress was also significantly higher in dorsal hindbrain corticosterone-treated rats relative to both other groups. There were no significant between-group differences in the heart rate or corticosterone responses to stress. There were no differences in baseline values for any measured parameters. We conclude that corticosterone can act selectively in the dorsal hindbrain in rats with normal plasma corticosterone levels to augment the arterial pressure response to restraint stress.
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PMID:Chronic activation of dorsal hindbrain corticosteroid receptors augments the arterial pressure response to acute stress. 1708 52

Three experiments were conducted to evaluate the effects of preslaughter physiological states mimicked by long- or short-term administration of corticosterone (CORT) and dietary energy sources on muscle glycogen contents and meat quality of broiler chickens. In experiment 1, the broilers were fed a high lipid diet (LD) or a normal diet (ND) that differed in carbohydrate (3.8%) and lipid (2.5%) contents from 21 d of age. From 28 d of age onwards, 50% of the chickens in each dietary treatment were subjected to CORT treatment (30 mg/kg of diet). At 7 and 11 d after CORT supplementation, musculus pectoralis major was sampled before and immediately after slaughter and analyzed for glycogen, pH, and R-value. In experiment 2, broilers, fed with the LD or ND diet from 21 d of age were subjected to 1 single s.c. injection of CORT (4 mg/kg of BW) for 3 h to mimicked acute stress at 46 d of age. In experiment 3, broiler chickens were supplied with water supplemented with glucose (30 g/L) for 1 wk before slaughter and were then subjected to the same CORT treatment as experiment 2. Blood and muscle samples were respectively obtained before and immediately after slaughter and analyzed for plasma glucose, urate and lactic acid, and muscle variables. Plasma concentrations of glucose and urate were significantly increased by acute CORT administration, whereas the lactic acid was not changed. Neither dietary energy source nor water glucose supplementation had any influence on the plasma variables. Dietary energy source or water glucose supplementation could not alter glycogen stores in musculus pectoralis major. Breast muscle glycogen stores were increased by stress mimicked by long-term CORT administration rather than by acute treatment. Preslaughter stress reactions had no relation to the depletion of breast muscle glycogen during the initial postmortem period. The initial breast muscle pH was significantly decreased by long-term CORT administration. The result suggests that short-term upregulation of circulating CORT is not involved in the elevated drip loss induced by preslaughter stress.
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PMID:Effects of diet and stress mimicked by corticosterone administration on early postmortem muscle metabolism of broiler chickens. 1729 68

Ninety juvenile yellowfin bream Acanthopagrus australis were angled from holding tanks, allowed to ingest nickel-plated, carbon-steel J-hooks and released (with their lines cut) into individual experimental tanks during 2 experiments in order to assess their (1) long-term (up to 105 d) health, mortality and rate of hook ejection and (2) short- and medium-term (< 42 d) temporal changes in health during hook ingestion. Equal numbers of control fish were scooped from holding tanks and similarly monitored in experimental tanks. Of 20 hook-ingested fish released during Expt 1, 3 died within 8 d, providing a non-significant mortality of 15%. Between Day 6 and Day 56 post-release, 13 of the surviving individuals ejected their hooks, which were typically oxidized to about 94% of their original weight and often broken into 2 pieces. At Day 105, there were no significant differences between the 20 control and 17 hook-ingested/-ejected fish in terms of their ability to digest and assimilate food (measured as changes in apparent digestibility coefficients), stress (measured as concentrations of plasma cortisol and glucose) or of morphological parameters that included weight (Wt) and maximum height (MH), maximum width (MW) and maximum girth (MG). During Expt 2, 3 individuals that still contained ingested hooks and 3 controls were sampled on each of 9 occasions between Day 3 and Day 42 post-release. All fish were sampled for blood cortisol and glucose and were then euthanized before being weighed and measured for total length (TL), MH, MW and MG. Hook-ingested individuals were also X-rayed to determine the position and orientation of hooks. There were no significant differences in plasma glucose between hook-ingested and control fish. Irrespective of the treatment of fish, concentrations of cortisol were elevated on some sampling occasions, indicating variable, acute stress. The MH and MG of fish were not significantly different between groups. Significant differences were detected for MG and Wt, with hook-ingested fish having weights similar to those of the control fish but a relatively greater MW (owing to stomach distension from ingested hooks) until 2 wk post-release, after which both morphological parameters generally declined. There was no significant temporal progression of hooks in the stomach of treatment fish; however, some hooks reorientated to positions that may have precluded passage along the digestive tract. We conclude that, for the J-hooks examined, cutting the line is an appropriate strategy that results in the greater majority of released hook-ingested yellowfin bream surviving with minimal negative long-term effects.
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PMID:Ingestion and ejection of hooks: effects on long-term health and mortality of angler-caught yellowfin bream Acanthopagrus australis. 1742 61

A dramatic change in stress responsiveness occurs during pubertal development such that stress-induced corticosterone secretion in prepubertal animals takes 45-60 min longer to return to baseline compared to adults. Though corticosterone is known to influence energy mobilization, it is presently unknown whether stressors affect other hormones important in energy utilization and metabolism differentially in animals before and after pubertal development. Therefore, we exposed prepubertal (28 days of age) and adult (77 days of age) male rats to a single 30 min session of restraint stress in either the light or dark phase of the animals' light-dark (LD) cycle and measured plasma glucose, insulin and thyroid hormones (thyroxine (T4) and triiodothyronine (T3)). We found similar stress-induced increases in plasma glucose levels in prepubertal and adult animals in the LD phase of the LD cycle. We also found that prepubertal animals have lower circulating insulin and total and free T4 levels, but higher total and free T3 levels compared to adults in both the light and dark phases (LD). Interestingly, insulin and thyroid hormone levels were unaffected by acute stress at either age or time of day. These data indicate that, despite prepubertal animals showing an extended glucocorticoid stress response after a single acute exposure to stress, glucose levels are similarly affected by acute stress in prepubertal and adult animals. Furthermore, though stage of development significantly affects the levels of peripheral metabolic hormones such as insulin, T4 and T3, acute stress does not appreciably influence their secretion before or after puberty.
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PMID:The effects of acute stress and pubertal development on metabolic hormones in the rat. 1745 71

Bioactivity-guided purification of n-BuOH soluble fraction from the ethanol extract of Evolvulus alsinoides resulted in the isolation of two new compounds, 2,3,4-trihydroxy-3-methylbutyl 3-[3-hydroxy-4-(2,3,4-trihydroxy-2-methylbutoxy)-phenyl]-2-propenoate (1) and 1,3-di-O-caffeoyl quinic acid methyl ester (2) along with six known compounds, caffeic acid (3), 6-methoxy-7-O-beta-glucopyranoside coumarin (4), 2-C-methyl erythritol (5), kaempferol-7-O-beta-glucopyranoside (6), kaempferol-3-O-beta-glucopyranoside (7) and quecetine-3-O-beta-glucopyranoside (8). The structure of new compounds 1 and 2 were elucidated by spectroscopic analysis, while known compounds were confirmed by direct comparison of their NMR data with those reported in literature. This is the first report of the presence of phenolic constituents in Evolvulus alsinoides. The isolated compounds 1-5 and 8 were screened for anti-stress activity in acute stress induced biochemical changes in adult male Sprague-Dawley rats. Stress exposure has resulted in significant increase of plasma glucose, adrenal gland weight, plasma creatine kinase (CK), and corticosterone levels. Compound 1 displayed most promising antistress effect by normalizing hyperglycemia, plasma corticosterone, CK and adrenal hypertrophy, while compounds 2 and 3 were also effective in normalizing most of these stress parameters, however compounds 4, 5 and 8 were ineffective in normalizing these parameters.
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PMID:Anti-stress constituents of Evolvulus alsinoides: an ayurvedic crude drug. 1747 66

The biochemical effects of acute and chronic psychological stress have been investigated in male Sprague-Dawley rats using a combination of 1H NMR spectral analysis of plasma and conventional hematological analyses. Animals were subjected to 35 consecutive days of 6-h sessions of stress, and following a 9 day break, were stressed for a further 6-h period. Plasma samples were collected at 0, 1, 3, and 6 h on days 1, 9, 21, 35, and 44, measured using 600 MHz 1H NMR spectroscopy, and analyzed by Principal Components Analysis. Time-dependent biochemical effects of psychological stress on a range of endogenous metabolites were evident and were correlated with the intensity of the stress response as defined by corticosterone and hematological parameters. Following acute stress, increases in the levels of glucose and ketone bodies, and decreases in the levels of acetate, alanine, isoleucine, lactate, leucine, valine, and lipoproteins, were observed. Chronic stress-induced increases in plasma levels of alanine, lactate (day 9), and leucine, valine, and choline (day 44) and decreases in acetate (day 9) and lipoprotein concentrations were observed. Positive correlations between plasma corticosterone level and glucose and glycerol, and between plasma lipoprotein concentrations and hemoglobin levels, were established using Projection to Latent Structures (PLS) analysis. This study indicates the potential of using NMR-based metabonomic strategies for the characterization of endogenous metabolic perturbations induced by psychological stressors and lifestyle choices.
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PMID:Metabonomic studies on the physiological effects of acute and chronic psychological stress in Sprague-Dawley rats. 1747 65

Substance P (SP) is involved in the pathophysiology of several psychiatric disorders and is considered a central stress neurotransmitter. Endogenous SP does not inhibit the initial extent of the HPA axis response to restraint stress, but reduces the duration of the stress suggesting that SP plays an important role in the transition between acute and chronic stress. Stress hormones can alter metabolic functions in white adipose tissue and liver. The HPA axis is the endocrine pathway that promotes lipolysis elevating free fatty acid levels (FFA) in blood, besides indirectly causing hyperglycemia. In the present study, changes in the blood levels of stress markers in the anxiogenic-like effects of SP, as evaluated on the elevated plus-maze (EPM), were studied in adult male rats. Serum corticosterone was used as the traditional stress marker, while the plasma FFA and glucose were used as alternative anxiety/stress markers. Our findings show: (a) elevated corticosterone levels, confirming the aversive situation induced by SP (behaviorally assessed in the EPM) and indicating SP as a "chemical" stressor; (b) elevated levels of FFA and glucose, indicators of stress-induced mobilization of energy substrates, confirming the stressor effect of SP; (c) FFA levels can be used as an accurate, sensitive and reliable index of acute stress situations, including in the anxiogenic-like effect of SP, with the FFA response being as good as corticosterone as a stress marker in this case; (d) NK1 receptors involvement in the underlying mechanisms of the behavioral and metabolic effects of SP. Finally, our study indicates that some of these physiological variables are positively related to the stressor intensity.
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PMID:Involvement of NK1 receptors in metabolic stress markers after the central administration of substance P. 1754 Apr 63


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