Measuring endogenous corticosterone in laboratory mice - a mapping review, meta-analysis, and open source database

Mierden, Stevie van der; Leenaars, Cathalijn; Boyle, Erin C.; Ripoli, Florenza Lüder; Gass, Peter; Durst, Mattea; Goerlich-Jansson, Vivian C.; Jirkof, Paulin; Keubler, Lydia M.; Talbot, Steven R.; Habedank, Anne; Lewejohann, Lars; Tolba, René; Bleich, André

doi:10.14573/altex.2004221

Cited by 6 publications

(5 citation statements)

References 46 publications

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“…Collectively, the cold-induced HPA axis stress response seems generalizable across rodents and studies. Interestingly, we noticed a previously documented sex-dependent difference in corticosterone levels in 22 °C mice 45 , 46 , but not an associated sex-dependent difference in WGTT in 22 °C mice. This could mean that the effects of stress on gut motility are already saturated at the relatively lower stress levels observed in males at 22 °C, or that the effects of stress on changes in gut motility are dampened in female mice and require a higher stress level to achieve the same effect as in males.…”

Section: Discussionmentioning

confidence: 41%

Temperature-dependent differences in mouse gut motility are mediated by stress

Han,

Hudson-Paz,

Robinson

et al. 2024

Lab Anim

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Researchers have advocated elevating mouse housing temperatures from the conventional ~22 °C to the mouse thermoneutral point of 30 °C to enhance translational research. However, the impact of environmental temperature on mouse gastrointestinal physiology remains largely unexplored. Here we show that mice raised at 22 °C exhibit whole gut transit speed nearly twice as fast as those raised at 30 °C, primarily driven by a threefold increase in colon transit speed. Furthermore, gut microbiota composition differs between the two temperatures but does not dictate temperature-dependent differences in gut motility. Notably, increased stress signals from the hypothalamic–pituitary–adrenal axis at 22 °C have a pivotal role in mediating temperature-dependent differences in gut motility. Pharmacological and genetic depletion of the stress hormone corticotropin-releasing hormone slows gut motility in stressed 22 °C mice but has no comparable effect in relatively unstressed 30 °C mice. In conclusion, our findings highlight that colder mouse facility temperatures significantly increase gut motility through hormonal stress pathways.

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Section: Discussionmentioning

confidence: 41%

Temperature-dependent differences in mouse gut motility are mediated by stress

Han,

Hudson-Paz,

Robinson

et al. 2024

Lab Anim

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“…In our experiment, to avoid the effect of light on corticosterone secretion levels, we collected blood in the dark under a dim red light, but when the mouse cage was moved from the feeding room to the dissecting room, the blood drawing without pressure was not completed within 30 s. The sex, age, feeding environment, and timesince-lights-on had significant effects on the basal concentration of corticosterone. 54 In our research, mice were exposed to a light source at the level of the mouse activity of 400-450 Lux and mice as control were fed under strict light-dark conditions (light on at 8:00 h and light off at 20:00 h). Therefore, we speculate that the discrepancy between the expression rhythm of corticosterone in this study and previously reported may be due to the influence of stress exposure during blood drawing and exposure to high intensity light (400-450 lux) on the normal secretion rhythm of corticosterone.…”

Section: Discussionmentioning

confidence: 99%

“…A stress‐free blood draw needs to occur within 30 s from the moment the cage is picked up. In our experiment, to avoid the effect of light on corticosterone secretion levels, we collected blood in the dark under a dim red light, but when the mouse cage was moved from the feeding room to the dissecting room, the blood drawing without pressure was not completed within 30 s. The sex, age, feeding environment, and time‐since‐lights‐on had significant effects on the basal concentration of corticosterone 54 . In our research, mice were exposed to a light source at the level of the mouse activity of 400–450 Lux and mice as control were fed under strict light–dark conditions (light on at 8:00 h and light off at 20:00 h).…”

Section: Discussionmentioning

confidence: 99%

Circadian disturbances by altering the light–dark cycle negatively affects hematopoietic function of bone marrow in mice

Yang,

Zhao,

et al. 2024

The FASEB Journal

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Circadian rhythms in metabolically active tissues are crucial for maintaining physical health. Circadian disturbance (CD) can cause various health issues, such as metabolic abnormalities and immune and cognitive dysfunctions. However, studies on the role of CD in immune cell development and differentiation, as well as the rhythmic expression of the core clock genes and their altered expression under CD, remain unclear. Therefore, we exposed C57bl/6j mice to repeated reversed light–dark cycles for 90 days to research the effects of CD on bone marrow (BM) hematopoietic function. We also researched the effects of CD on endogenous circadian rhythms, temporally dependent expression in peripheral blood and myeloid leukocytes, environmental homeostasis within BM, and circadian oscillations of hematopoietic–extrinsic cues. Our results confirmed that when the light and dark cycles around mice were frequently reversed, the circadian rhythmic expression of the two main circadian rhythm markers, the hypothalamic clock gene, and serum melatonin, was disturbed, indicating that the body was in a state of endogenous CD. Furthermore, CD altered the temporally dependent expression of peripheral blood and BM leukocytes and destroyed environmental homeostasis within the BM as well as circadian oscillations of hematopoietic–extrinsic cues, which may negatively affect BM hematopoiesis in mice. Collectively, these results demonstrate that circadian rhythms are vital for maintaining health and suggest that the association between CD and hematopoietic dysfunction warrants further investigation.

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“…When studying muscle atrophy, researchers tend to select male mice, because they can live longer than female mice and do not have the high hormone variation observed in female mice. 33 , 34 It should be noted that average serum glucocorticoid concentrations in aged humans are higher than those reported for adult mice, 35 ,[S1] but would be probably be insufficient to produce the degree of muscle atrophy observed in the Dex treatment model. For the model of muscle aging, mice are generally used at 18 months or older, due to the increased expression of aging‐associated biomarkers.…”

Section: Discussionmentioning

confidence: 99%

Inhibiting 5‐lipoxygenase prevents skeletal muscle atrophy by targeting organogenesis signalling and insulin‐like growth factor‐1

Kim

Lee

et al. 2022

J cachexia sarcopenia muscle

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Background Skeletal muscle atrophy can occur in response to numerous factors, such as ageing and certain medications, and produces a major socio-economic burden. At present, there are no approved drugs for treating skeletal muscle atrophy. Arachidonate 5-lipoxygenase (Alox5) is a drug target for a number of diseases. However, pharmacological targeting of Alox5, and its role in skeletal muscle atrophy, is unclear. Methods The potential effects of gene knockdown and pharmacological targeting of Alox5 on skeletal muscle atrophy were investigated using cell-based models, animal models and human skeletal muscle primary cells. Malotilate, a clinically safe drug developed for enhancing liver regeneration and Alox5 inhibitor, was investigated as a repurposing candidate. Mechanism(s) of action in skeletal muscle atrophy was assessed by measuring the expression level or activation status of key regulatory pathways and validated using gene knockdown and RNA sequencing. Results Myotubes treated with the atrophy-inducing glucocorticoid, dexamethasone, were protected from catabolic responses by treatment with malotilate (+41.29%, P < 0.01). Similar anti-atrophy effects were achieved by gene knockdown of Alox5 (+30.4%, P < 0.05). Malotilate produced anti-atrophy effects without affecting the myogenic differentiation programme. In an in vivo model of skeletal muscle atrophy, malotilate treatment preserved muscle force/strength (grip strength: +35.72%, latency to fall: +553.1%, P < 0.05), increased mass and fibre crosssectional area (quadriceps: +23.72%, soleus: +33.3%, P < 0.01) and down-regulated atrogene expression (Atrogin-1: À61.58%, Murf-1: -66.06%, P < 0.01). Similar, beneficial effects of malotilate treatment were observed in an ageing muscle model, which also showed the preservation of fast-twitch fibres (Type 2a: +56.48%, Type 2b: +37.32%, P < 0.01). Leukotriene B4, a product of Alox5 activity with inflammatory and catabolic functions, was found to be elevated in skeletal muscle undergoing atrophy (quadriceps: +224.4%, P < 0.001). Cellular transcriptome analysis showed that targeting Alox5 up-regulated biological processes regulating organogenesis and increased the expression of insulin-like growth factor-1, a key anti-atrophy hormone (+226.5%, P < 0.05). Interestingly, these effects were restricted to the atrophy condition and not observed in normal skeletal muscle cultures with Alox5 inhibition. Human myotubes were also protected from atrophy by pharmacological targeting of Alox5 (+23.68%, P < 0.05). Conclusions These results shed new light on novel drug targets and mechanisms underpinning skeletal muscle atrophy. Alox5 is a regulator and drug target for muscle atrophy, and malotilate is an attractive compound for repurposing studies to treat this disease.

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Measuring endogenous corticosterone in laboratory mice - a mapping review, meta-analysis, and open source database

Cited by 6 publications

References 46 publications

Temperature-dependent differences in mouse gut motility are mediated by stress

Temperature-dependent differences in mouse gut motility are mediated by stress

Circadian disturbances by altering the light–dark cycle negatively affects hematopoietic function of bone marrow in mice

Inhibiting 5‐lipoxygenase prevents skeletal muscle atrophy by targeting organogenesis signalling and insulin‐like growth factor‐1

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