The vagus nerve in thermoregulation and energy metabolism

Székely, Miklós

doi:10.1016/s1566-0702(00)00217-4

Cited by 73 publications

(53 citation statements)

References 77 publications

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“…The authors explained this loss by the rats' failure to compensate for their attenuated water intake by an appropriate antidiuresis. However, the magnitude of the postlesion emaciation recorded in their study (and even in the current work) substantially exceeds normal daily food and water consumption for rats; it also exceeds by several times the body weight loss in starving rats (65). Such a dramatic weight loss, especially combined with the high body temperature, likely results from intensive substrate "burning" caused by disinhibition of nonshivering thermogenesis.…”

Section: Hyperthermia Induced By Ovlt Lesioncontrasting

confidence: 45%

The organum vasculosum laminae terminalis in immune-to-brain febrigenic signaling: a reappraisal of lesion experiments

Romanovsky

Sugimoto²,

Simons³

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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Romanovsky, Andrej A., Naotoshi Sugimoto, Christopher T. Simons, and William S. Hunter. The organum vasculosum laminae terminalis in immune-to-brain febrigenic signaling: a reappraisal of lesion experiments. Am J Physiol Regul Integr Comp Physiol 285: R420-R428, 2003. First published April 24, 2003 10.1152/ajpregu.00757. 2002The organum vasculosum laminae terminalis (OVLT) has been proposed to serve as the interface for blood-to-brain febrigenic signaling, because ablation of this structure affects the febrile response. However, lesioning the OVLT causes many "side effects" not fully accounted for in the fever literature. By placing OVLT-lesioned rats on intensive rehydration therapy, we attempted to prevent these side effects and to evaluate the febrile response in their absence. After the OVLT of Sprague-Dawley rats was lesioned electrolytically, the rats were given access to 5% sucrose for 1 wk to stimulate drinking. Sucrose consumption and body mass were monitored. The animals were examined twice a day for signs of dehydration and treated with isotonic saline (50 ml/kg sc) when indicated. This protocol eliminated mortality but not several acute and chronic side effects stemming from the lesion. The acute effects included adipsia and gross (14% of body weight) emaciation; chronic effects included hypernatremia, hyperosmolality, a suppressed drinking response to hypertonic saline, and previously unrecognized marked (by ϳ2°C) and long-lasting (Ͼ3 wk) hyperthermia. Because the hyperthermia was not accompanied by tail skin vasoconstriction, it likely reflected increased thermogenesis. After the rats recovered from the acute (but not chronic) side effects, their febrile response to IL-1␤ (500 ng/kg iv) was tested. The shamoperated rats developed typical monophasic fevers (ϳ0.5°C), the lesioned rats did not. However, the absence of the febrile response in the OVLT-lesioned rats likely resulted from the untreatable side effects. For example, hyperthermia at the time of pyrogen injection was high enough (39-40°C) to solely prevent fever from developing. Hence, the changed febrile responsiveness of OVLT-lesioned animals is given an alternative interpretation, unrelated to febrigenic signaling to the brain. fever; adipsia; third ventricle; median preoptic nucleus THERE IS LITTLE DOUBT that the febrile response is regulated by the central nervous system (CNS), but the mechanisms by which peripherally originating pyrogenic signals reach the brain remain unclear. At least four possibilities have been proposed. First, pyrogenic cytokines, such as IL-1␤, access the CNS by carriermediated transport across the blood-brain barrier (BBB) (2). Second, circulating pyrogens bind to the cerebral vascular endothelium and stimulate production of fever mediators, most importantly PGE 2 , by endothelial cells; endotheliocytes release PGE 2 into the brain tissue (10). Third, pyrogens act on neural terminals in peripheral tissues and convey febrigenic signals to the CNS via sensory fibers, e.g., those of the vagus nerve (7, 74). Fourt...

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Section: Hyperthermia Induced By Ovlt Lesioncontrasting

confidence: 45%

The organum vasculosum laminae terminalis in immune-to-brain febrigenic signaling: a reappraisal of lesion experiments

Romanovsky

Sugimoto²,

Simons³

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Since vagal afferents are thought to serve important homeostatic functions [16], the present study was designed to investigate the hypothesis that neonatal CAP treatment results in compensatory adjustments by redundant endocrine factors involved in the regulation of energy balance and glucose homeostasis. Important for consideration of the data in the present study is that body weights of our CAP and VEH rats were not different, nor were there any overt differences in weights of organs and tissues relevant to nutrient balance.…”

Section: Discussionmentioning

confidence: 99%

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

Wall

Wielinga

Strubbe

et al. 2006

Physiology & Behavior

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Several mechanisms involved in ingestive behavior and neuroendocrine activity rely on vagal afferent neuronal signaling. Seemingly contradictory to this idea are observations that vagal afferent neuronal ablation by neonatal capsaicin (CAP) treatment has relatively small effects on glucose homeostasis and long-term regulation of energy balance. It may be proposed that humoral endocrine factors and/or their sensitivities compensate for the loss of vagal afferent information, particularly when subjects face disturbances in ambient fuel levels. Therefore, male adult rats neonatally treated with CAP or with the vehicle (VEH) underwent intravenous glucose tolerance tests (IVGTTs) during which blood fuel levels, and circulating adipose, pancreatic, and adrenal hormones were assessed. CAP rats displayed similar hyperglycemia as VEH rats, but with markedly reduced plasma insulin and corticosterone responses. These results indicate that CAP rats have increased insulin sensitivity during hyperglycemic episodes, and lower plasma levels of corticosterone in CAP rats relative to VEH rats could underlie this effect. After the IVGTT, CAP rats had increased plasma adiponectin and reduced plasma resistin levels, and these alterations in adipose hormones might be relevant for post-ingestive metabolic processes. In a second experiment, anorexigenic efficacies of cholecystokinin and leptin were assessed. While VEH rats, but not CAP rats, responded with reduced food intake to i.p. injected cholecystokinin, only CAP rats responded to i.v. infused leptin with a reduction in food intake. It is concluded that reduced HPA axis activity and/or increased leptin signaling could underlie compensations in fuel handling and energy balance following CAP treatment.

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“…This inhibition may constitute a connection between the organs supplying the body with chemical energy (GIT) and the organs burning (BAT) and dissipating (skin blood vessels) this energy. If the nonthermal TRPV1-mediated signals indeed originate in the GIT, they may be involved in thermoregulatory adjustments to changes in the feeding status such as diet-induced thermogenesis and postprandial hyperthermia in mammals (Székely, 2000;Gobel et al, 2001), starvation-associated hypome- FIG. 10.…”

Section: Physiological and Pathological Significancementioning

confidence: 99%

The Transient Receptor Potential Vanilloid-1 Channel in Thermoregulation: A Thermosensor It Is Not

et al. 2009

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The vagus nerve in thermoregulation and energy metabolism

Cited by 73 publications

References 77 publications

The organum vasculosum laminae terminalis in immune-to-brain febrigenic signaling: a reappraisal of lesion experiments

The organum vasculosum laminae terminalis in immune-to-brain febrigenic signaling: a reappraisal of lesion experiments

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

The Transient Receptor Potential Vanilloid-1 Channel in Thermoregulation: A Thermosensor It Is Not

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