scholarly journals Altered Responses to Cold Environment in Urocortin 1 and Corticotropin-Releasing Factor Deficient Mice

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Bayan Chaker ◽  
Tareq A. Samra ◽  
Nabanita S. Datta ◽  
Abdul B. Abou-Samra
Keyword(s):  
Protein Metabolism ◽  
Core Body Temperature ◽  
Corticotropin Releasing Factor ◽  
Dexamethasone Treatment ◽  
Male And Female ◽  
Dramatic Decline ◽  
Urocortin 1 ◽  
Core Body ◽  
Deficient Mice

We examined core body temperature (CBT) of urocortin 1 (UCN1) and corticotropin releasing factor (CRF) knockout (KO) mice exposed to 4°C for 2 h. UCN1KO mice showed higher average CBT during cold exposure as compared to WT. The CBT of male and female WT mice dropped significantly to 34.1 ± 2.4 and 34.9 ± 3.1 C at 4°C, respectively. In contrast, the CBT of male and female UCN1KO mice dropped only slightly after 2 h at 4°C to 36.8 ± 0.7 and 38.1 ± 0.5 C, respectively. WT female and male UCN1KO mice showed significant acclimatization to cold; however, female UCN1KO mice did not show such a significant acclimatization. CRFKO mice showed a dramatic decline in CBT from 38.2 ±  0.4 at 22°C to 26.1 ± 9.8 at 4°C for 2 h. The CRF/UCN1 double KO (dKO) mice dropped their CBT to 32.5 ± 4.0 after 2 h exposure to 4°C. Dexamethasone treatment prevented the decline in CBT of the CRFKO and the dKO mice. Taken together, the data suggest a novel role for UCN1 in thermoregulation. The role of CRF is likely secondary to adrenal glucocorticoids, which have an important regulatory role on carbohydrate, fat, and protein metabolism.

scholarly journals Paradoxical Increase of Insulin Sensitivity Despite Blunted Adipose Tissue Browning in Genetic Ablation of IRP1 (OR09-08-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Mikyoung You ◽  
Jin-Seon Yook ◽  
Soonkyu Chung
Keyword(s):  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Iron Metabolism ◽  
Core Body Temperature ◽  
Serum Levels ◽  
Genetic Ablation ◽  
Ucp1 Expression ◽  
Core Body ◽  
Tissue Browning

Abstract Objectives Iron regulatory protein 1 (IRP1) plays a key regulator of cellular iron metabolism, systemic oxygen sensing, and erythropoiesis. Deletion of IRP1 leads to profound HIF2a-dependent abnormalities in erythropoiesis and iron metabolism. Previously, we demonstrated that modulation of adipose tissue iron metabolism is necessary for adipose tissue browning. However, the role of IRP1 in adipose tissue browning and its metabolic consequences are uncertain. This study aimed to investigate the role of IRP1 in regulating adipose tissue browning in a mouse model of genetic ablation of IPR1 (IRP1−/−). Methods The IRP1−/− mice and wildtype (WT) controls were kept either at room (25°C) or cold (6°C) temperature for 7 days. Adipose tissue browning was evaluated by UCP1 expression and prevalence of beige-like structure in inguinal fat. Thermogenic heat release captured by infrared camera and core body temperature was measured by a rectal thermometer. The modulation of iron metabolism was assessed by serum levels of ferritin, hematocrit, and erythropoietin levels by ELISA. To investigate the role of IRP1 on energy metabolism, IRP1−/− and WT controls were fed a high-fat diet (45%) for 14 weeks. Insulin sensitivity was determined by glucose and insulin tolerance test and HOMA-IR score. [3H]-2-deoxyglucose (DOG) was injected to determine the distribution of 3H-radioactivity was quantified. Results IRP1−/− mice dramatically increased serum levels of erythropoietin but decreased hepcidin. IRP1−/− developed polycythemia and reticulocytosis, which was not affected by cold exposure. IRP1−/− were completely blunted in cold-induced browning in the inguinal fat showing no changes in UCP1 and adipocyte morphology. Unexpectedly, IRP1−/− showed higher core body temperature and heat release than control independent of UCP1 expression. Chronic intake of HF diet paradoxically increased the insulin sensitivity regardless of obesity. 2-DOG distribution was significantly increased in red blood cells, suggesting that red blood cell-dependent energy expenditure significantly contributed to rapid glucose disposal. Conclusions Disruption of IRP1 blunted adipose tissue browning. The paradoxical rise in insulin sensitivity in IRP1−/− is likely due to red blood cells-mediated energy expenditure. Funding Sources None.

Assessing the role of nocturnal core body temperature dysregulation as a biomarker of neurodegeneration

2019 ◽  
Vol 29 (5) ◽  
Author(s):  
Arabella K. Raupach ◽  
Kaylena A. Ehgoetz Martens ◽  
Negar Memarian ◽  
George Zhong ◽  
Elie Matar ◽  
...  
Keyword(s):  
Body Temperature ◽  
Core Body Temperature ◽  
Core Body

Temporal phasing of locomotor activity, heart rate rhythmicity, and core body temperature is disrupted in VIP receptor 2-deficient mice

2011 ◽  
Vol 300 (3) ◽  
pp. R519-R530 ◽  
Author(s):  
Jens Hannibal ◽  
Hansen M. Hsiung ◽  
Jan Fahrenkrug
Keyword(s):  
Heart Rate ◽  
Locomotor Activity ◽  
Body Temperature ◽  
Circadian Rhythms ◽  
Wheel Running ◽  
Core Body Temperature ◽  
Running Activity ◽  
Wheel Running Activity ◽  
Core Body ◽  
Deficient Mice

Neurons of the brain's biological clock located in the hypothalamic suprachiasmatic nucleus (SCN) generate circadian rhythms of physiology (core body temperature, hormone secretion, locomotor activity, sleep/wake, and heart rate) with distinct temporal phasing when entrained by the light/dark (LD) cycle. The neuropeptide vasoactive intestinal polypetide (VIP) and its receptor (VPAC2) are highly expressed in the SCN. Recent studies indicate that VIPergic signaling plays an essential role in the maintenance of ongoing circadian rhythmicity by synchronizing SCN cells and by maintaining rhythmicity within individual neurons. To further increase the understanding of the role of VPAC2 signaling in circadian regulation, we implanted telemetric devices and simultaneously measured core body temperature, spontaneous activity, and heart rate in a strain of VPAC2-deficient mice and compared these observations with observations made from mice examined by wheel-running activity. The study demonstrates that VPAC2 signaling is necessary for a functional circadian clock driving locomotor activity, core body temperature, and heart rate rhythmicity, since VPAC2-deficient mice lose the rhythms in all three parameters when placed under constant conditions (of either light or darkness). Furthermore, although 24-h rhythms for three parameters are retained in VPAC2-deficient mice during the LD cycle, the temperature rhythm displays markedly altered time course and profile, rising earlier and peaking ∼4–6 h prior to that of wild-type mice. The use of telemetric devices to measure circadian locomotor activity, temperature, and heart rate, together with the classical determination of circadian rhythms of wheel-running activity, raises questions about how representative wheel-running activity may be of other behavioral parameters, especially when animals have altered circadian phenotype.

scholarly journals Methadone’s Effect on Hypothermia-Induced Shivering in Post Anesthetic Rat: Role of Nitric Oxide

2019 ◽  
Author(s):  
Alireza Mazarei ◽  
Mojtaba Nasimi ◽  
Nastaran Rahimi ◽  
Mehdi Sanatkar ◽  
Sina Tofigh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Core Body Temperature ◽  
Vehicle Group ◽  
Opioid Agonist ◽  
Cold Surface ◽  
Indirect Contact ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Core Body

Abstract- Post anesthesia shivering which happens in some patients during recovery time after general anesthesia is followed by central hypothermia and peripheral vasoconstriction. In this study, the effect of opioidergic/nitrergic systems were determined on post anesthesia shivering in rat. Animals were cooled gently on a cold surface with indirect contact with a mixture of ice and water. Animals were treated with saline; methadone (a full opioid agonist, 10 mg/kg); naltrexone (an opioid receptor antagonist, 10 mg/kg); L-NAME (a nonselective nitric oxide synthase (NOS) inhibitor, 10 mg/kg). The core body temperature and the frequency of basal state- and post anesthetic-shivering were recorded using a stainless steel rectal probe (MLT-1403, AD Instruments®) and electromyography (EMG) electrodes connected to Animal Bio Amp (FE136, AD Instruments®) signal conditioner, respectively. Methadone administration reduced the frequency of shivering after anesthesia, while injection of naltrexone and L-NAME increased post anesthetic shivering compared to vehicle group. Co-administration of L-NAME and methadone showed a significant decrease the frequency of post anesthetic shivering. Furthermore, the temperature of shivering onset was reduced following methadone administration, which was blocked by injection of both naltrexone and/or L-NAME. To conclude, the findings of this study revealed the protective impact of methadone on post anesthesia shivering-induced with hypothermia dominated to nitrergic pathway effects in rat.

scholarly journals Urocortins and Cholecystokinin-8 Act Synergistically to Increase Satiation in Lean But Not Obese Mice: Involvement of Corticotropin-Releasing Factor Receptor-2 Pathway

Endocrinology ◽  
2007 ◽  
Vol 148 (12) ◽  
pp. 6115-6123 ◽  
Author(s):  
G. Gourcerol ◽  
L. Wang ◽  
Y. H. Wang ◽  
M. Million ◽  
Y. Taché
Keyword(s):  
Corticotropin Releasing Factor ◽  
Vehicle Group ◽  
Afferent Activity ◽  
Wild Type ◽  
Rat Stomach ◽  
Urocortin 1 ◽  
Crf2 Receptor ◽  
Vagal Afferent ◽  
Deficient Mice

Interactions between gastrointestinal signals are a part of integrated systems regulating food intake (FI). We investigated whether cholecystokinin (CCK)-8 and urocortin systems potentiate each other to inhibit FI and gastric emptying (GE) in fasted mice. Urocortin 1 and urocortin 2 (1 μg/kg) were injected ip alone or with CCK (3 μg/kg) in lean, diet-induced obese (DIO) or corticotropin-releasing factor receptor-2 (CRF2)-deficient mice. Gastric vagal afferent activity was recorded from a rat stomach-vagus in vitro preparation. When injected separately, urocortin 1, urocortin 2, or CCK did not modify the 4-h cumulative FI in lean mice. However, CCK plus urocortin 1 or CCK plus urocortin 2 decreased significantly the 4-h FI by 39 and 27%, respectively, compared with the vehicle + vehicle group in lean mice but not in DIO mice. Likewise, CCK-urocortin-1 delayed GE in lean but not DIO mice, whereas either peptide injected alone at the same dose had no effect. CCK-urocortin 2 suppression of FI was observed in wild-type but not CRF2-deficient mice. Gastric vagal afferent activity was increased by intragastric artery injection of urocortin 2 after CCK at a subthreshold dose, and the response was reversed by devazepide. These data establish a peripheral synergistic interaction between CCK and urocortin 1 or urocortin 2 to suppress FI and GE through CRF2 receptor in lean mice that may involve CCK modulation of gastric vagal afferent responsiveness to urocortin 2. Such synergy is lost in DIO mice, suggesting a resistance to the satiety signaling that may contribute to maintain obesity.

Pathophysiology and management of fever

2016 ◽  
Author(s):  
Gabriele Bassi ◽  
Roberto Fumagalli
Keyword(s):  
Critically Ill ◽  
Single Case ◽  
Core Body Temperature ◽  
Intrinsic Resistance ◽  
Physiological Mechanisms ◽  
Inflammatory Conditions ◽  
Core Body ◽  
Fever Management ◽  
Clinical Strategy

Core body temperature is strictly regulated by autonomic and behavioural compensatory adaptations and an increase may represent a physiological stereotypical controlled response to septic and inflammatory conditions, or an uncontrolled drop in the hypothalamic thermoregulatory threshold. Fever has been demonstrated to be a potential mechanism of intrinsic resistance against infectious disease playing a pivotal role in the human evolution. High temperature may be detrimental during oxygen delivery-dependent conditions and in a neurological population. Despite this evidence, a definitive conclusion, between the association of fever and the outcome in critically-ill patients, is still lacking. The decision-making strategy in the context of fever management in critical care must be supported by single case assessment. This chapter summarizes the main physiological mechanisms of temperature control that physicians should consider when dealing with fever or deliberate hypothermia and analyses the main evidence in the role of fever in the critically ill in order to help bedside clinical strategy.

Role of C fibers in physiological responses to ozone in rats

1995 ◽  
Vol 78 (5) ◽  
pp. 1757-1763 ◽  
Author(s):  
M. Jimba ◽  
W. A. Skornik ◽  
C. R. Killingsworth ◽  
N. C. Long ◽  
J. D. Brain ◽  
...  
Keyword(s):  
Core Body Temperature ◽  
Dynamic Compliance ◽  
Airway Responsiveness ◽  
Pulmonary Mechanics ◽  
Neonatal Rats ◽  
Implanted Electrodes ◽  
C Fibers ◽  
Induced Changes ◽  
Core Body

The purpose of this study was to evaluate the role of C fibers in airway responsiveness after exposure to ozone (O3) in rats. The role of C fibers in the decreases in heart rate (HR) and core body temperature (Tc) that occur after inhalation of O3 was also examined. Neonatal rats were treated with capsaicin (Cap) or the vehicle used to dissolve capsaicin (Veh). Cap has been shown to cause permanent destruction of C fibers. When they reached adulthood, conscious minimally restrained rats were exposed to 2 ppm O3 or to air for 3 h. Two hours after the cessation of exposure, rats were anesthetized and instrumented for the measurement of pulmonary mechanics and airway responsiveness to inhaled aerosolized methacholine. O3 had no effect on baseline pulmonary conductance (GL) in either Veh or Cap rats but did cause a decrease in dynamic compliance (Cdyn) in Cap rats (P < 0.05). In Cap rats, O3 exposure caused a marked increase in airway responsiveness; the doses of inhaled aerosolized methacholine required to decrease GL and Cdyn by 50% were 6.5-fold and 9.8-fold lower in O3-compared with air-exposed rats (P < 0.005). In contrast, in Veh rats, O3 did not alter responsiveness. During O3 exposure, there was a profound, almost 50%, decrease in HR as measured with implanted electrodes. A decrease in Tc (measured with a rectal probe) of approximately 2.5 degrees C also occurred during O3 exposure. There was no significant effect of Cap pretreatment on the magnitude of these O3-induced changes in HR and Tc. Our results are consistent with the hypothesis that C fibers act to inhibit the development of hyperresponsiveness elicited by O3 inhalation but do not contribute to O3-induced changes in HR or Tc.

scholarly journals Role of Inflammatory Mediators in Resistance and Susceptibility to Pneumococcal Infection

2002 ◽  
Vol 70 (3) ◽  
pp. 1547-1557 ◽  
Author(s):  
Alison R. Kerr ◽  
June J. Irvine ◽  
Jennifer J. Search ◽  
Neill A. Gingles ◽  
Aras Kadioglu ◽  
...  
Keyword(s):  
Core Body Temperature ◽  
Inbred Mouse ◽  
Pneumococcal Infection ◽  
Mouse Strains ◽  
Isolated Lung ◽  
Cytokine Tumor Necrosis Factor ◽  
Core Body ◽  
Necrosis Factor

ABSTRACT Variations in the host response during pneumonia caused by Streptococcus pneumoniae in susceptible (CBA/Ca) and resistant (BALB/c) inbred mouse strains were investigated. Significant differences were detected in survival time, core body temperature, lung-associated and systemic bacterial loads, mast cell numbers, magnitude and location of cytokine production, lung disruption, and ability of isolated lung cells to release the cytokine tumor necrosis factor (TNF) alpha in vitro. Overall, the results indicate that the reduced capacity of CBA/Ca mice to induce rapid TNF activity within the airways following infection with S. pneumoniae may be a factor in their elevated susceptibility to pneumococcal pneumonia.

scholarly journals Dual orexin receptor antagonist induces changes in core body temperature in rats after exercise

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Tristan Martin ◽  
Yves Dauvilliers ◽  
Ouma-Chandrou Koumar ◽  
Valentine Bouet ◽  
Thomas Freret ◽  
...  
Keyword(s):  
Body Temperature ◽  
Receptor Antagonist ◽  
Core Body Temperature ◽  
Treadmill Running ◽  
Orexin Receptors ◽  
Dose Effects ◽  
Male Wistar Rats ◽  
Core Body ◽  
Dose Dependent

AbstractHypothalamic orexin neurons are involved in various physiological functions, including thermoregulation. The orexinergic system has been considered as a potent mediator of the exercise response. The present study describes how the antagonization of the orexinergic system by a dual orexin receptor antagonist (DORA) modifies the thermoregulatory process during exercise. Core Body Temperature (CBT) and Spontaneous Locomotor Activity (SLA) of 12 male Wistar rats were recorded after either oral administration of DORA (30 mg/kg or 60 mg/kg) or placebo solution, both at rest and in exercise conditions with treadmill running. DORA ingestion decreased SLA for 8 hours (p < 0.001) and CBT for 4 hours (p < 0.01). CBT (°C) response was independent of SLA. The CBT level decreased from the beginning to the end of exercise when orexin receptors were antagonized, with a dose-dependent response (39.09 ± 0.36 and 38.88 ± 0.28 for 30 and 60 mg/kg; p < 0.001) compared to placebo (39.29 ± 0.31; p < 0.001). CBT increased during exercise was also blunted after DORA administration, but without dose effects of DORA. In conclusion, our results favor the role of orexin in the thermoregulation under stress related to exercise conditions.

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