Activation of central melanocortin-4 receptor suppresses lipopolysaccharide-induced fever in rats

2003 ◽  
Vol 284 (6) ◽  
pp. R1595-R1603 ◽  
Author(s):  
Partha S. Sinha ◽  
Helgi B. Schiöth ◽  
Jeffrey B. Tatro
Keyword(s):  
Systemic Treatment ◽  
Core Body Temperature ◽  
Melanocortin Receptor ◽  
Melanocortin Receptors ◽  
Antipyretic Effect ◽  
Selective Agonist ◽  
Melanocortin 4 Receptor ◽  
Heat Conservation ◽  
Core Body ◽  
Escherichia Coli Lipopolysaccharide

Activation of central melanocortin receptors (MCR) inhibits fever, but the identity of the MCR subtype(s) mediating this antipyretic effect is unknown. To determine whether selective central melanocortin receptor-4 (MC4R) activation produces antipyretic effects, the MC4R selective agonist MRLOB-0001 (CO-His-d-Phe-Arg-Trp-Dab-NH2) was administered intracerebroventricularly to rats treated with Escherichia coli lipopolysaccharide (LPS, 30 μg/kg ip). Treatment with MRLOB-0001 (150 ng icv) did not lower core body temperature (Tc) in afebrile rats but did suppress LPS-induced increases in Tc and associated decreases in tail skin temperature (Tsk), an indicator of vasomotor thermoeffector function. In contrast, systemic treatment with MRLOB-0001 (150 ng iv) did not produce similar antipyretic effects. Coadministration of the selective MC4R antagonist HS014 (1 μg icv) blocked the antipyretic effects of MRLOB-0001. HS014 alone (1 μg icv) had no significant effect on LPS-induced increases in Tc or decreases in Tsk and in afebrile rats had no significant effects on Tc or Tsk. We conclude that pharmacological activation of central MC4R suppresses febrile increases in Tc and that inhibition of heat conservation pathways may contribute to this effect. These findings suggest that the central MC4R may mediate the long-recognized antipyretic effects of centrally administered melanocortins.

Systemic α-MSH suppresses LPS fever via central melanocortin receptors independently of its suppression of corticosterone and IL-6 release

1998 ◽  
Vol 275 (2) ◽  
pp. R524-R530 ◽  
Author(s):  
Qin-Heng Huang ◽  
Victor J. Hruby ◽  
Jeffrey B. Tatro
Keyword(s):  
Male Rats ◽  
Melanocortin Receptors ◽  
Antipyretic Effect ◽  
Melanocyte Stimulating Hormone ◽  
Melanocortin 4 Receptor ◽  
The Central Nervous System ◽  
Core Body ◽  
The Brain ◽  
Pituitary Adrenal Axis ◽  
Antipyretic Action

Systemically administered α-melanocyte-stimulating hormone (α-MSH) inhibits endotoxin (lipopolysaccharide; LPS)- or interleukin (IL)-1-induced fever and adrenocortical activation, but the sites of these actions and the mechanisms involved are unknown. The aims of this study were, first, to determine whether melanocortin receptors (MCR) located within the central nervous system mediate the suppressive effects of peripherally administered α-MSH on LPS-induced fever and activation of the pituitary-adrenal axis and, second, to determine whether systemic α-MSH suppresses the LPS-induced rise in plasma IL-6 levels, potentially contributing to its antipyretic effect. Male rats received Escherichia coli LPS (25 μg/kg ip). Core body temperatures (Tb) were determined hourly by radiotelemetry (0–8 h), and blood was withdrawn via venous catheters for plasma hormone immunoassays (0–2 h) and IL-6 bioassay (0–8 h). α-MSH (100 μg/kg ip) completely prevented the onset of LPS-induced fever during the first 3–4 h after LPS and suppressed fever throughout the next 4 h but did not affect Tb in afebrile rats treated with intraperitoneal saline rather than LPS. Intraperitoneal α-MSH also suppressed the LPS-induced rise in plasma IL-6, ACTH, and corticosterone (CS) levels. Intracerebroventricular injection of SHU-9119, a potent melanocortin-4 receptor (MC4-R)/MC3-R antagonist, completely blocked the antipyretic effect of intraperitoneal α-MSH during the first 4 h after LPS but had no effect on α-MSH-induced suppression of LPS-stimulated plasma IL-6 and CS levels. Taken together, the results indicate that the antipyretic effect of peripherally administered α-MSH during the early phase of fever is mediated by MCR within the brain. In contrast, the inhibition of LPS-induced increases in plasma CS and IL-6 levels by intraperitoneal α-MSH appears to be mediated by a different mechanism(s), and these effects do not contribute to its antipyretic action.

Postmortem body temperatures in the minke whale, Balaenoptera acutorostrata

1990 ◽  
Vol 68 (1) ◽  
pp. 140-143 ◽  
Author(s):  
Dag Vongraven ◽  
Morten Ekker ◽  
Arild R. Espelien ◽  
Frode J. Aarvik
Keyword(s):  
Body Temperature ◽  
Core Body Temperature ◽  
Thermal Gradients ◽  
Body Temperatures ◽  
Balaenoptera Acutorostrata ◽  
Dorsal Fin ◽  
Minke Whales ◽  
Temperature Regimes ◽  
Heat Conservation ◽  
Core Body

Postmortem temperature regimes were measured in 11 minke whales, Balaenoptera acutorostrata, at tissue depths varying from 1.5 (in the blubber) to 30 cm, at two different sites on the whales' sides, one in the flipper region (site A) and one in the dorsal fin region (site B). Body temperatures of instantaneously killed whales were assumed to represent those of living animals. Core body temperatures were 35.0 °C at site A and 35.6 °C at site B. Core body temperature and the size of the thermal core were affected by blubber thickness and the time between harpoon strike and death, but were not influenced by duration of pursuit prior to harpooning. Both intra- and inter-specific comparisons reveal that the thickness of the blubber layer is important for the maintenance of thermal gradients and, thereby, for heat conservation.

Core body temperature changes after sauna exposition in healthy subjects

2012 ◽  
Vol 26 (2) ◽  
Author(s):  
Joanna Pawlak ◽  
Paweł Zalewski ◽  
Jacek J. Klawe ◽  
Monika Zawadka ◽  
Anna Bitner ◽  
...  
Keyword(s):  
Body Temperature ◽  
Healthy Subjects ◽  
Core Body Temperature ◽  
Temperature Changes ◽  
Core Body

Nonphotic entrainment of the human circadian pacemaker

1998 ◽  
Vol 274 (4) ◽  
pp. R991-R996 ◽  
Author(s):  
Elizabeth B. Klerman ◽  
David W. Rimmer ◽  
Derk-Jan Dijk ◽  
Richard E. Kronauer ◽  
Joseph F. Rizzo ◽  
...  
Keyword(s):  
Circadian Rhythms ◽  
Light Exposure ◽  
Core Body Temperature ◽  
Biological Clock ◽  
Bright Light ◽  
Circadian Pacemaker ◽  
Temperature Rhythms ◽  
Blind Individuals ◽  
Nonphotic Entrainment ◽  
Core Body

In organisms as diverse as single-celled algae and humans, light is the primary stimulus mediating entrainment of the circadian biological clock. Reports that some totally blind individuals appear entrained to the 24-h day have suggested that nonphotic stimuli may also be effective circadian synchronizers in humans, although the nonphotic stimuli are probably comparatively weak synchronizers, because the circadian rhythms of many totally blind individuals “free run” even when they maintain a 24-h activity-rest schedule. To investigate entrainment by nonphotic synchronizers, we studied the endogenous circadian melatonin and core body temperature rhythms of 15 totally blind subjects who lacked conscious light perception and exhibited no suppression of plasma melatonin in response to ocular bright-light exposure. Nine of these fifteen blind individuals were able to maintain synchronization to the 24-h day, albeit often at an atypical phase angle of entrainment. Nonphotic stimuli also synchronized the endogenous circadian rhythms of a totally blind individual to a non-24-h schedule while living in constant near darkness. We conclude that nonphotic stimuli can entrain the human circadian pacemaker in some individuals lacking ocular circadian photoreception.

scholarly journals Pathophysiology of Fever and Application of Infrared Thermography (IRT) in the Detection of Sick Domestic Animals: Recent Advances

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2316
Author(s):  
Daniel Mota-Rojas ◽  
Dehua Wang ◽  
Cristiane Gonçalves Titto ◽  
Jocelyn Gómez-Prado ◽  
Verónica Carvajal-de la Fuente ◽  
...  
Keyword(s):  
Body Temperature ◽  
Infrared Thermography ◽  
Core Body Temperature ◽  
The Body ◽  
Farm Animals ◽  
Economic Losses ◽  
Febrile Response ◽  
Temperature Range ◽  
Stable Temperature ◽  
Core Body

Body-temperature elevations are multifactorial in origin and classified as hyperthermia as a rise in temperature due to alterations in the thermoregulation mechanism; the body loses the ability to control or regulate body temperature. In contrast, fever is a controlled state, since the body adjusts its stable temperature range to increase body temperature without losing the thermoregulation capacity. Fever refers to an acute phase response that confers a survival benefit on the body, raising core body temperature during infection or systemic inflammation processes to reduce the survival and proliferation of infectious pathogens by altering temperature, restriction of essential nutrients, and the activation of an immune reaction. However, once the infection resolves, the febrile response must be tightly regulated to avoid excessive tissue damage. During fever, neurological, endocrine, immunological, and metabolic changes occur that cause an increase in the stable temperature range, which allows the core body temperature to be considerably increased to stop the invasion of the offending agent and restrict the damage to the organism. There are different metabolic mechanisms of thermoregulation in the febrile response at the central and peripheral levels and cellular events. In response to cold or heat, the brain triggers thermoregulatory responses to coping with changes in body temperature, including autonomic effectors, such as thermogenesis, vasodilation, sweating, and behavioral mechanisms, that trigger flexible, goal-oriented actions, such as seeking heat or cold, nest building, and postural extension. Infrared thermography (IRT) has proven to be a reliable method for the early detection of pathologies affecting animal health and welfare that represent economic losses for farmers. However, the standardization of protocols for IRT use is still needed. Together with the complete understanding of the physiological and behavioral responses involved in the febrile process, it is possible to have timely solutions to serious problem situations. For this reason, the present review aims to analyze the new findings in pathophysiological mechanisms of the febrile process, the heat-loss mechanisms in an animal with fever, thermoregulation, the adverse effects of fever, and recent scientific findings related to different pathologies in farm animals through the use of IRT.

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