scholarly journals Activation of TRPV1 in nucleus tractus solitarius reduces brown adipose tissue thermogenesis, arterial pressure, and heart rate

2018 ◽  
Vol 315 (1) ◽  
pp. R134-R143 ◽  
Author(s):  
Mazher Mohammed ◽  
Christopher J. Madden ◽  
Michael C. Andresen ◽  
Shaun F. Morrison
Keyword(s):  
Heart Rate ◽  
Adipose Tissue ◽  
Arterial Pressure ◽  
Vagus Nerve ◽  
Brown Adipose Tissue ◽  
Nucleus Tractus Solitarius ◽  
Trpv1 Channels ◽  
Brown Adipose ◽  
Skin Cooling ◽  
Vagal Afferent

The sympathetic nerve activity (SNA) to brown adipose tissue (BAT) regulates BAT thermogenesis to defend body temperature in cold environments or to produce fever during immune responses. The vagus nerve contains afferents that inhibit the BAT SNA and BAT thermogenesis evoked by skin cooling. We sought to determine whether activation of transient receptor potential vanilloid 1 (TRPV1) channels in the nucleus tractus solitarius (NTS), which are prominently expressed in unmyelinated vagal afferents, would affect cold-evoked BAT thermogenesis, cardiovascular parameters, or their vagal afferent-evoked responses. In urethane-chloralose-anesthetized rats, during skin cooling, nanoinjection of the TRPV1-agonist resiniferatoxin in NTS decreased BAT SNA (from 695 ± 195% of baseline during cooling to 103 ± 8% of baseline after resiniferatoxin), BAT temperature (−0.8 ± 0.1°C), expired CO2 (−0.3 ± 0.04%), mean arterial pressure (MAP; −20 ± 5 mmHg), and heart rate (−44 ± 11 beats/min). Pretreatment of NTS with the TRPV1 antagonist capsazepine prevented these resiniferatoxin-mediated effects. Intravenous injection of the TRPV1 agonist dihydrocapsaicin also decreased all the measured variables (except MAP). Bilateral cervical or subdiaphragmatic vagotomy attenuated the decreases in BAT SNA and thermogenesis evoked by nanoinjection of resiniferatoxin in NTS but did not prevent the decreases in BAT SNA and BAT thermogenesis evoked by intravenous dihydrocapsaicin. We conclude that activation of TRPV1 channels in the NTS of vagus nerve intact rats inhibits BAT SNA and decreases BAT metabolism, blood pressure, and heart rate. In contrast, the inhibition of BAT thermogenesis following systemic administration of dihydrocapsaicin does not require vagal afferent activity, consistent with a nonvagal pathway through which systemic TRPV1 agonists can inhibit BAT thermogenesis.

scholarly journals Central efferent pathways mediating skin cooling-evoked sympathetic thermogenesis in brown adipose tissue

2007 ◽  
Vol 292 (1) ◽  
pp. R127-R136 ◽  
Author(s):  
Kazuhiro Nakamura ◽  
Shaun F. Morrison
Keyword(s):  
Heart Rate ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Receptor Agonist ◽  
Excitatory Amino Acid ◽  
Defense Responses ◽  
Hypothalamic Nucleus ◽  
Brown Adipose ◽  
Skin Cooling ◽  
Efferent Pathways

Control of thermoregulatory effectors by the autonomic nervous system is a critical component of rapid cold-defense responses, which are triggered by thermal information from the skin. However, the central autonomic mechanism driving thermoregulatory effector responses to skin thermal signals remains to be determined. Here, we examined the involvement of several autonomic brain regions in sympathetic thermogenic responses in brown adipose tissue (BAT) to skin cooling in urethane-chloralose-anesthetized rats by monitoring thermogenic [BAT sympathetic nerve activity (SNA) and BAT temperature], metabolic (expired CO2), and cardiovascular (arterial pressure and heart rate) parameters. Acute skin cooling, which did not reduce either rectal (core) or brain temperature, evoked increases in BAT SNA, BAT temperature, expired CO2, and heart rate. Skin cooling-evoked thermogenic, metabolic, and heart rate responses were inhibited by bilateral microinjections of bicuculline (GABAA receptor antagonist) into the preoptic area (POA), by bilateral microinjections of muscimol (GABAA receptor agonist) into the dorsomedial hypothalamic nucleus (DMH), or by microinjection of muscimol, glycine, 8-OH-DPAT (5-HT1A receptor agonist), or kynurenate (nonselective antagonist for ionotropic excitatory amino acid receptors) into the rostral raphe pallidus nucleus (rRPa) but not by bilateral muscimol injections into the lateral/dorsolateral part or ventrolateral part of the caudal periaqueductal gray. These results implicate the POA, DMH, and rRPa in the central efferent pathways for thermogenic, metabolic, and cardiac responses to skin cooling, and suggest that these pathways can be modulated by serotonergic inputs to the medullary raphe.

Modulation of brown adipose tissue-mediated thermogenesis by lesions to the nucleus tractus solitarius in the rat

1991 ◽  
Vol 546 (2) ◽  
pp. 203-210 ◽  
Author(s):  
Doreen M. Fyda ◽  
Keith E. Cooper ◽  
Warren L. Veale
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Nucleus Tractus Solitarius ◽  
Brown Adipose

scholarly journals Inhibition of brown adipose tissue thermogenesis by neurons in the ventrolateral medulla and in the nucleus tractus solitarius

2010 ◽  
Vol 299 (1) ◽  
pp. R277-R290 ◽  
Author(s):  
Wei-Hua Cao ◽  
Christopher J. Madden ◽  
Shaun F. Morrison
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Receptor Agonist ◽  
Nucleus Tractus Solitarius ◽  
Ventrolateral Medulla ◽  
Prostaglandin E ◽  
Experimental Conditions ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Raphe Pallidus

Neurons in the ventrolateral medulla (VLM) and in the nucleus tractus solitarius (NTS) play important roles in the regulation of cardiovascular and other autonomic functions. In the present study, we demonstrate an inhibition of brown adipose tissue (BAT) thermogenesis evoked by activation of neurons in the VLM, as well as by neurons in the intermediate NTS, of chloralose/urethane-anesthetized, artificially ventilated rats. Activation of neurons in either rostral VLM or caudal VLM with N-methyl-d-aspartate (12 nmol) reversed the cold-evoked increase in BAT sympathetic nerve activity (SNA), BAT temperature, and end-expired CO2. Disinhibition of neurons in either VLM or NTS with the GABAA receptor antagonist, bicuculline (30 pmol), reversed the increases in BAT SNA, BAT temperature, and end-expired CO2 that were elicited 1) by cold defense; 2) during the febrile model of nanoinjection of prostaglandin E2 into the medial preoptic area; 3) by activation of neurons in the dorsomedial hypothalamus or in the rostral raphe pallidus (rRPa); or 4) by the μ-opioid receptor agonist fentanyl. Combined, but not separate, inhibitions of neurons in the VLM and in the NTS, with the GABAA receptor agonist, muscimol (120 pmol/site), produced increases in BAT SNA, BAT temperature, and expired CO2, which were reversed by nanoinjection of glycine (30 nmol) into the rRPa. These findings suggest that VLM and NTS contain neurons whose activation inhibits BAT thermogenesis, that these neurons receive GABAergic inputs that are active under these experimental conditions, and that neurons in both sites contribute to the tonic inhibition of sympathetic premotor neuronal activity in the rRPa that maintains a low level of BAT thermogenesis in normothermic conditions.

scholarly journals A high-fat diet impairs cooling-evoked brown adipose tissue activation via a vagal afferent mechanism

2016 ◽  
Vol 311 (2) ◽  
pp. E287-E292 ◽  
Author(s):  
Christopher J. Madden ◽  
Shaun F. Morrison
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
Control Diet ◽  
Neural Mechanism ◽  
Afferent Input ◽  
High Fat ◽  
Bat Activity ◽  
Brown Adipose ◽  
Vagal Afferent

In dramatic contrast to rats on a control diet, rats maintained on a high-fat diet (HFD) failed to activate brown adipose tissue (BAT) during cooling despite robust increases in their BAT activity following direct activation of their BAT sympathetic premotor neurons in the raphe pallidus. Cervical vagotomy or blockade of glutamate receptors in the nucleus of the tractus solitarii (NTS) reversed the HFD-induced inhibition of cold-evoked BAT activity. Thus, a HFD does not prevent rats from mounting a robust, centrally driven BAT thermogenesis; however, a HFD does alter a vagal afferent input to NTS neurons, thereby preventing the normal activation of BAT thermogenesis to cooling. These results, paralleling the absence of cooling-evoked glucose uptake in the BAT of obese humans, reveal a neural mechanism through which consumption of a HFD contributes to reduced energy expenditure and thus to weight gain.

scholarly journals Centrally Administered Resistin Enhances Sympathetic Nerve Activity to the Hindlimb but Attenuates the Activity to Brown Adipose Tissue

Endocrinology ◽  
2011 ◽  
Vol 152 (7) ◽  
pp. 2626-2633 ◽  
Author(s):  
S. Kosari ◽  
J. A. Rathner ◽  
F. Chen ◽  
S. Kosari ◽  
E. Badoer
Keyword(s):  
Cardiovascular Disease ◽  
Heart Rate ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Sympathetic Nerve ◽  
Energy Homeostasis ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Obesity And Diabetes ◽  
Brown Adipose

Resistin, an adipokine, is believed to act in the brain to influence energy homeostasis. Plasma resistin levels are elevated in obesity and are associated with metabolic and cardiovascular disease. Increased muscle sympathetic nerve activity (SNA) is a characteristic of obesity, a risk factor for diabetes and cardiovascular disease. We hypothesized that resistin affects SNA, which contributes to metabolic and cardiovascular dysfunction. Here we investigated the effects of centrally administered resistin on SNA to muscle (lumbar) and brown adipose tissue (BAT), outputs that influence cardiovascular and energy homeostasis. Overnight-fasted rats were anesthetized, and resistin (7 μg) was administered into the lateral cerebral ventricle (intracerebroventricular). The lumbar sympathetic nerve trunk or sympathetic nerves supplying BAT were dissected free, and nerve activity was recorded. Arterial blood pressure, heart rate, body core temperature, and BAT temperature were also recorded. Responses to resistin or vehicle were monitored for 4 h after intracerebroventricular administration. Acutely administered resistin increased lumbar SNA but decreased BAT SNA. Mean arterial pressure and heart rate, however, were not significantly affected by resistin. BAT temperature was significantly reduced by resistin, and there was a concomitant fall in body temperature. The findings indicate that resistin has differential effects on SNA to tissues involved in metabolic and cardiovascular regulation. The decreased BAT SNA and the increased lumbar SNA elicited by resistin suggest that it may contribute to the increased muscle SNA and reduced energy expenditure observed in obesity and diabetes.

scholarly journals Vagus Nerve Stimulation Increases Energy Expenditure: Relation to Brown Adipose Tissue Activity

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e77221 ◽  
Author(s):  
Guy H. E. J. Vijgen ◽  
Nicole D. Bouvy ◽  
Loes Leenen ◽  
Kim Rijkers ◽  
Erwin Cornips ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
Vagus Nerve ◽  
Brown Adipose Tissue ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Brown Adipose ◽  
Brown Adipose Tissue Activity

scholarly journals Butyrate reduces appetite and activates brown adipose tissue via the gut-brain neural circuit

Gut ◽  
2017 ◽  
Vol 67 (7) ◽  
pp. 1269-1279 ◽  
Author(s):  
Zhuang Li ◽  
Chun-Xia Yi ◽  
Saeed Katiraei ◽  
Sander Kooijman ◽  
Enchen Zhou ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Neural Circuit ◽  
Nucleus Tractus Solitarius ◽  
Fat Oxidation ◽  
Metabolic Effects ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Underlying Mechanisms

ObjectiveButyrate exerts metabolic benefits in mice and humans, the underlying mechanisms being still unclear. We aimed to investigate the effect of butyrate on appetite and energy expenditure, and to what extent these two components contribute to the beneficial metabolic effects of butyrate.DesignAcute effects of butyrate on appetite and its method of action were investigated in mice following an intragastric gavage or intravenous injection of butyrate. To study the contribution of satiety to the metabolic benefits of butyrate, mice were fed a high-fat diet with butyrate, and an additional pair-fed group was included. Mechanistic involvement of the gut-brain neural circuit was investigated in vagotomised mice.ResultsAcute oral, but not intravenous, butyrate administration decreased food intake, suppressed the activity of orexigenic neurons that express neuropeptide Y in the hypothalamus, and decreased neuronal activity within the nucleus tractus solitarius and dorsal vagal complex in the brainstem. Chronic butyrate supplementation prevented diet-induced obesity, hyperinsulinaemia, hypertriglyceridaemia and hepatic steatosis, largely attributed to a reduction in food intake. Butyrate also modestly promoted fat oxidation and activated brown adipose tissue (BAT), evident from increased utilisation of plasma triglyceride-derived fatty acids. This effect was not due to the reduced food intake, but explained by an increased sympathetic outflow to BAT. Subdiaphragmatic vagotomy abolished the effects of butyrate on food intake as well as the stimulation of metabolic activity in BAT.ConclusionButyrate acts on the gut-brain neural circuit to improve energy metabolism via reducing energy intake and enhancing fat oxidation by activating BAT.

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