Integrative transcriptomic and proteomic analyses of pathogenic Aeromonas hydrophila in response to stress hormone norepinephrine

2021 ◽  
Author(s):  
Ting Qin ◽  
Jun Xie ◽  
Bingwen Xi ◽  
Liangkun Pan
Keyword(s):  
Aeromonas Hydrophila ◽  
Stress Hormone ◽  
Response To Stress ◽  
Proteomic Analyses

scholarly journals Glucocorticoid/Adiponectin Axis Mediates Full Activation of Cold-Induced Beige Fat Thermogenesis

Biomolecules ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 1573
Author(s):  
Liping Luo ◽  
Lu Wang ◽  
Yan Luo ◽  
Estevan Romero ◽  
Xin Yang ◽  
...  
Keyword(s):  
Cold Stress ◽  
Mrna Levels ◽  
Stress Hormone ◽  
Adaptive Thermogenesis ◽  
White Adipocytes ◽  
Beige Fat ◽  
Response To Stress ◽  
Circulating Levels ◽  
Full Activation

Glucocorticoids (GCs), a class of corticosteroids produced by the adrenal cortex in response to stress, exert obesity-promoting effects. Although adaptive thermogenesis has been considered an effective approach to counteract obesity, whether GCs play a role in regulating cold stress-induced thermogenesis remains incompletely understood. Here, we show that the circulating levels of stress hormone corticosterone (GC in rodents) were significantly elevated, whereas the levels of adiponectin, an adipokine that was linked to cold-induced adaptive thermogenesis, were decreased 48 h post cold exposure. The administration of a glucocorticoid hydrocortisone downregulated adiponectin protein and mRNA levels in both WAT and white adipocytes, and upregulated thermogenic gene expression in inguinal fat. In contrast, mifepristone, a glucocorticoid receptor antagonist, enhanced adiponectin expression and suppressed energy expenditure in vivo. Mechanistically, hydrocortisone suppressed adiponectin expression by antagonizing PPARγ in differentiated 3T3-L1 adipocytes. Ultimately, adiponectin deficiency restored mifepristone-decreased oxygen consumption and suppressed the expression of thermogenic genes in inguinal fat. Taken together, our study reveals that the GCs/adiponectin axis is a key regulator of beige fat thermogenesis in response to acute cold stress.

Expression of the αB crystallin gene in response to stress hormone and oncogenes

1992 ◽  
Vol 55 ◽  
pp. 164
Author(s):  
R. Klemenz ◽  
R. Scheier ◽  
R. Schäfer ◽  
A. Aoyama
Keyword(s):  
Stress Hormone ◽  
Αb Crystallin ◽  
Response To Stress

Role of cortisol in the metabolic response to stress hormone infusion in the conscious dog

Metabolism ◽  
1996 ◽  
Vol 45 (5) ◽  
pp. 571-578 ◽  
Author(s):  
Toshihiko Fujiwara ◽  
Alan D. Cherrington ◽  
Doss N. Neal ◽  
Owen P. McGuinness
Keyword(s):  
Metabolic Response ◽  
Stress Hormone ◽  
Conscious Dog ◽  
Response To Stress

The effect of acute glucagon removal on the metabolic response to stress hormone infusion in the conscious dog

Metabolism ◽  
1994 ◽  
Vol 43 (10) ◽  
pp. 1310-1317 ◽  
Author(s):  
Owen P. McGuinness ◽  
Sam Murrell ◽  
Christopher Moran ◽  
Deanna Bracy ◽  
Alan D. Cherrington
Keyword(s):  
Metabolic Response ◽  
Stress Hormone ◽  
Conscious Dog ◽  
Response To Stress

scholarly journals Prenatal Programming of Human Neurological Function

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Curt A. Sandman ◽  
Elysia P. Davis ◽  
Claudia Buss ◽  
Laura M. Glynn
Keyword(s):  
Nervous System ◽  
Gray Matter Volume ◽  
Stress Hormones ◽  
Stress System ◽  
Stress Hormone ◽  
Fetal Exposure ◽  
Response To Stress ◽  
Cortisol Increase ◽  
Neuromuscular Development

The human placenta expresses the genes for proopiomelanocortin and the major stress hormone, corticotropin-releasing hormone (CRH), profoundly altering the “fight or flight” stress system in mother and fetus. As pregnancy progresses, the levels of these stress hormones, including maternal cortisol, increase dramatically. These endocrine changes are important for fetal maturation, but if the levels are altered (e.g., in response to stress), they influence (program) the fetal nervous system with long-term consequences. The evidence indicates that fetal exposure to elevated levels of stress hormones (i) delays fetal nervous system maturation, (ii) restricts the neuromuscular development and alters the stress response of the neonate, (iii) impairs mental development and increases fearful behavior in the infant, and (iv) may result in diminished gray matter volume in children. The studies reviewed indicate that fetal exposure to stress peptides and hormones exerts profound programming influences on the nervous system and may increase the risk for emotional and cognitive impairment.

Role of epinephrine and norepinephrine in the metabolic response to stress hormone infusion in the conscious dog

1997 ◽  
Vol 273 (4) ◽  
pp. E674-E681 ◽  
Author(s):  
Owen P. McGuinness ◽  
Vickie Shau ◽  
Eric M. Benson ◽  
Mike Lewis ◽  
Robert T. Snowden ◽  
...  
Keyword(s):  
Metabolic Response ◽  
Glucose Production ◽  
Stress Hormone ◽  
Glucose Levels ◽  
Hepatic Glucose Metabolism ◽  
Hepatic Glucose ◽  
Response To Stress ◽  
Arteriovenous Difference ◽  
Arterial Glucose

The role of epinephrine and norepinephrine in contributing to the alterations in hepatic glucose metabolism during a 70-h stress hormone infusion (SHI) was investigated in four groups of chronically catheterized (20-h-fasted) conscious dogs. SHI increased glucagon (∼5-fold), epinephrine (∼10-fold), norepinephrine (∼10-fold), and cortisol (∼6-fold) levels. Dogs received either all the hormones (SHI; n = 5), all the hormones except epinephrine (SHI−Epi; n = 6), or all the hormones except norepinephrine (SHI−NE; n = 6). In addition, six dogs received saline only (Sal). Glucose production (Ra) and gluconeogenesis were assessed after a 70-h hormone or saline infusion with the use of tracer ([3-3H]glucose and [U-14C]alanine) and arteriovenous difference techniques. SHI increased glucose levels (108 ± 2 vs. 189 ± 10 mg/dl) and Ra(2.6 ± 0.2 vs. 4.1 ± 0.3 mg ⋅ kg−1⋅ min−1) compared with Sal. The absence of an increase in epinephrine markedly attenuated these changes (glucose and Rawere 140 ± 6 mg/dl and 2.7 ± 0.4 mg ⋅ kg−1⋅ min−1, respectively). Only 25% of the blunted rise in Racould be accounted for by an attenuation of the rise in net hepatic gluconeogenic precursor uptake (0.9 ± 0.1, 1.5 ± 0.1, and 1.1 ± 0.2 mg ⋅ kg−1⋅ min−1for Sal, SHI, and SHI−Epi, respectively). The absence of an increase in norepinephrine did not blunt the rise in arterial glucose levels, Ra, or net hepatic gluconeogenic precursor uptake (they rose to 195 ± 21 mg/dl, 3.7 ± 0.5 mg ⋅ kg−1⋅ min−1, and 1.7 ± 0.2 mg ⋅ kg−1⋅ min−1, respectively). In summary, during chronic SHI, the rise in epinephrine exerts potent stimulatory effects on glucose production principally by enhancing hepatic glycogenolysis, although the rise in circulating norepinephrine has minimal effects.

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