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)

Obese individuals are both insulin resistant and have high levels of circulating free fatty acids (FFAs). In cell culture, saturated but not unsaturated fatty acids induce endoplasmic reticulum (ER) stress. We hypothesized that chronic exposure to low dose fatty acids would significantly attenuate the acute stress response to a saturated fatty acid challenge and that unsaturated fatty acids (oleate) would be more protective than saturated fatty acids (palmitate). The ER stress response to palmitate was reduced after low dose fatty acid exposure in human hepatoma cells. Palmitate and oleate gave distinctive transcript responses, both acutely and after chronic low dose exposure. Differentially regulated pathways included lipid, cholesterol, fatty acid, and triglyceride metabolism, and IkappaB kinase and nuclear factor kappaB kinase inflammatory cascades. Oleate reduced palmitate-induced changes significantly more than low dose palmitate and completely blocked palmitate-induced phosphoinositide 3 kinase inhibitor (PIK3IP1) as well as induction of GADD45A and B. These changes are predicted to alter the PI3 kinase pathway and the pro-apoptotic p38 MAPK pathway. We recapitulated the oleate response by small interfering RNA-mediated block of PIK3IP1 stimulation with palmitate and significantly protected cells from palmitate-mediated ER stress. We show that transcriptional responses to oleate and palmitate are distinct, broad, and often discordant. We identified several potential candidates that may direct the transcriptional networks and demonstrate that PIK3IP1 partially accounts for the protective effects of oleate.
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PMID:Distinct gene expression profiles characterize cellular responses to palmitate and oleate. 2041 17

During acute psychological stress, the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system are activated. The released stress hormones influence glucose metabolism, can activate immune cells, and modulate subclinical inflammation. The aim of our study was to analyze the effect of acute psychological stress on glucose metabolism and the inflammatory status in patients with post-traumatic stress disorder (PTSD). We included 15 overweight male Bosnian war refugees with PTSD into the study (mean age 44+/-11 years, BMI 29.3+/-4.3 kg/m (2)). All subjects underwent an oral glucose tolerance test (OGTT) with either acute stress (trauma script exposure) or a resting period in a cross-over design. Blood was drawn over 2.5 h and metabolic markers were measured. Systemic levels of immune markers were determined using high-sensitive ELISA or bead-based multiplex assay. Immune gene expression was quantified by RT-PCR. After being exposed to acute stress, cortisol levels and heart frequency tended to be increased. Higher blood glucose and insulin levels after stress exposure were observed (p<0.05). Systemic levels of the chemokines interferon-gamma-inducible protein-10 and macrophage chemoattractant protein-1 were decreased compared to the control day (both p<0.05) and the expression of the proinflammatory regulator IKK beta was significantly reduced after stress exposure (p<0.001). In conclusion, acute stress induces postprandial blood glucose peaks and elevated insulin levels and a selective decrease of systemic immune markers and the proinflammatory regulator of the NF kappaB cascade, which are associated with type 2 diabetes. This points towards an independent effect of acute psychological stress on glucose metabolism and inflammation.
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PMID:Effects of acute psychological stress on glucose metabolism and subclinical inflammation in patients with post-traumatic stress disorder. 2066 27