Tissue-specific increase in norepinephrine turnover by central interleukin-1, but not by interleukin-6, in rats

1994 ◽  
Vol 266 (2) ◽  
pp. R400-R404 ◽  
Author(s):  
A. Terao ◽  
M. Oikawa ◽  
M. Saito
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Interleukin 1 ◽  
Corticosterone Level ◽  
Plasma Corticosterone ◽  
Interscapular Brown Adipose Tissue ◽  
Norepinephrine Turnover ◽  
Brown Adipose ◽  
Intracerebroventricular Injections ◽  
Sympathetic Nervous

To examine the effects of brain cytokines on the sympathetic nervous system, norepinephrine (NE) turnover in peripheral organs (spleen, lung, diaphragm, pancreas, heart, liver, kidney, and interscapular brown adipose tissue) was assessed after intraperitoneal or intracerbroventricular administrations of human recombinant interleukin (IL)-1 beta and IL-6 in rats. An intraperitoneal injection of IL-1 (1 microgram/rat) accelerated NE turnover in the spleen, lung, diaphragm, and pancreas without appreciable effects in other organs examined. When IL-1 was injected intracerebroventricularly at much lower doses (1-100 ng/rat), a dose-dependent increase in NE turnover was observed in the spleen, lung, diaphragm, and pancreas. IL-6 did not affect NE turnover in every organ examined, even when it was given at much higher doses, 100 micrograms/rat and 100 ng/rat for intraperitoneal and intracerebroventricular injections, respectively. In contrast to tissue NE turnover, plasma corticosterone level was increased after the administration of IL-6 as well as IL-1, regardless of the site of administration. These results suggest that central IL-1, but not IL-6, increases sympathetic nerve activity in some specific organs, whereas both cytokines are effective for adrenocortical activation. A possible role of the sympathetic nervous system in physiological and immune responses to central IL-1 was discussed.

Diminished sympathetic nervous system activity in genetically obese (ob/ob) mouse

1983 ◽  
Vol 245 (2) ◽  
pp. E148-E154 ◽  
Author(s):  
J. B. Young ◽  
L. Landsberg
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Cold Exposure ◽  
Feedback Regulation ◽  
Turnover Rates ◽  
Interscapular Brown Adipose Tissue ◽  
Peripheral Tissues ◽  
Brown Adipose ◽  
Sympathetic Nervous ◽  
Long Acting

The genetically obese (ob/ob) mouse exhibits defective thermoregulatory responses to cold exposure. Pathophysiological explanations for this phenomenon have focused on abnormalities in intracellular metabolism or insensitivity of peripheral tissues to the thermogenic effects of catecholamines. Because the sympathetic nervous system (SNS) is subject to feedback regulation, a peripheral impairment in thermogenesis should be associated with a compensatory increase in SNS activity. To examine SNS activity in the ob/ob mouse, norepinephrine (NE) turnover was measured in heart and interscapular brown adipose tissue (IBAT) of ob/ob and lean mice. The results from studies utilizing radiolabeled NE or inhibition of NE biosynthesis with alpha-methyl-p-tyrosine to measure NE turnover demonstrated reductions in SNS activity of 33-56% in heart and of 45-73% in IBAT in ob/ob mice at ambient temperature (22 degrees C) compared with measurements in lean controls. During cold exposure (4 degrees C) NE turnover increased in heart and IBAT to a similar extent in both ob/ob and lean mice, but NE turnover rates in heart, and probably in IBAT as well, remained lower in the obese mice than in the lean despite the gradual development of hypothermia in the ob/ob mice during this period. Administration of naltrexone, a long-acting opiate antagonist, failed to reverse the suppression of SNS activity observed in the ob/ob mice. These data indicate that diminished SNS activity in ob/ob mice may be an additional factor contributing to the defective thermogenesis characteristic of these animals.

Norepinephrine turnover in iron deficiency at three environmental temperatures

1988 ◽  
Vol 255 (1) ◽  
pp. R90-R96 ◽  
Author(s):  
J. Beard ◽  
B. Tobin ◽  
S. M. Smith
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nervous System Activity ◽  
Interscapular Brown Adipose Tissue ◽  
System Activity ◽  
Nervous System Activity ◽  
Brown Adipose ◽  
Iron Deficient ◽  
Sympathetic Nervous ◽  
Environmental Temperatures

Iron-deficient anemic rats had a significant elevation in urinary norepinephrine (NE) after 7 days at 30 and 24 degrees C, but not at 10 degrees C, compared with control animals. NE turnover studies were performed to examine sympathetic nervous system activity in a tissue-specific fashion. NE content in myocardium decreased by nearly 50% in hypertrophied iron-deficient hearts at all three temperatures, whereas fractional turnover rates were compensatorily increased. In contrast, interscapular brown adipose tissue NE turnover was significantly reduced to 30% of normal in iron-deficient animals at both 30 and 10 degrees C. Serum triiodothyronine concentrations were similar to controls at 30 degrees C but were decreased at lower temperatures. Serum tetraiodothyronine concentrations were lower in iron-deficient animals at all three environmental temperatures. We conclude that increased sympathetic nervous system activity compensatory to temperatures below thermoneutrality is less well controlled in iron-deficient animals than in controls, and at a low environmental temperature this may possibly explain the poor thermoregulatory capacity of iron-deficient animals. A generalized hypernoradrenergic state is not supported by our NE turnover study and does not explain the elevated urine NE concentrations.

Effects of chronic lard feeding on sympathetic nervous system activity in the rat

1994 ◽  
Vol 267 (5) ◽  
pp. R1320-R1328 ◽  
Author(s):  
J. B. Young ◽  
P. A. Daly ◽  
K. Uemura ◽  
F. Chaouloff
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Nerves ◽  
Plasma Norepinephrine ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Chronic Ingestion ◽  
Sympathetic Nervous ◽  
Specific Stimulation ◽  
Kidney Liver

The level of sympathetic nervous system (SNS) activity in obesity is controversial, with reports claiming either increased or decreased SNS activity. The following studies examined SNS activity in a dietary form of obesity, ingestion of a lard-enriched diet for 4 wk. Plasma norepinephrine (NE) levels were 61% higher in rats fed the lard-enriched diet than in chow-fed controls at 20 degrees C (200 +/- 24 pg/ml vs. 124 +/- 6, P < 0.005) and remained elevated after 1 h of cold exposure (4 degrees C). [3H]NE turnover was markedly increased in heart, but not in interscapular brown adipose tissue (IBAT), kidney, liver, skeletal muscle, or spleen of rats fed the high-fat diet. By contrast, ingestion of a diet similarly enriched with sucrose raised rates of [3H]NE turnover in IBAT as well as in heart. Thus chronic ingestion of a lard-enriched diet induces region-specific stimulation of SNS activity that is greater in heart than in IBAT. Whereas the absence of an SNS response to lard in IBAT may contribute to weight gain in these animals, activation of cardiac sympathetic nerves may promote development of hypertension in this model of obesity.

Increased sympathetic nervous system activity in rats fed a low-protein diet

1985 ◽  
Vol 248 (5) ◽  
pp. R627-R637 ◽  
Author(s):  
J. B. Young ◽  
L. N. Kaufman ◽  
M. E. Saville ◽  
L. Landsberg
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Deficient Diet ◽  
Interscapular Brown Adipose Tissue ◽  
Caloric Density ◽  
Low Protein ◽  
Brown Adipose ◽  
Sympathetic Nervous

To examine the state of sympathetic nervous system (SNS) function in animals fed a protein-restricted diet, [3H] norepinephrine ([3H]-NE) turnover was measured in heart and interscapular brown adipose tissue (IBAT) of rats fed synthetic diets of equal caloric density containing 22% protein (as casein) or 7% protein (the difference being made up by sucrose). Because dietary availability of tyrosine is a potential mediator of SNS responses to protein ingestion, a third diet (7% protein supplemented with tyrosine) was also tested. After 12 days dietary preparation [3H]-NE turnover was increased 35-70% in heart by 7% protein feeding and 93-103% in IBAT. When smaller animals were fed the synthetic diets for 4-5 wk, sympathetic stimulation in those given the protein-restricted formula was also apparent, although demonstration of this response was complicated by comparative problems due to the marked differences in body size between normal and protein-restricted groups. Addition of tyrosine (sufficient to normalize plasma and brain tyrosine levels) was without effect on the stimulation of NE turnover induced by the protein-deficient diet. Similarly, augmented urinary NE excretion observed in animals consuming the 7% protein diet was unaffected by supplemental tyrosine. Urinary dopamine excretion, however, was uniquely and strikingly elevated with restoration of dietary tyrosine to animals fed the low-protein diet. Thus isocaloric substitution of sucrose for casein in the diet activates the SNS in heart and IBAT, a response unrelated to limitation of dietary tyrosine.

CNS origins of the sympathetic nervous system outflow to brown adipose tissue

1999 ◽  
Vol 276 (6) ◽  
pp. R1569-R1578 ◽  
Author(s):  
Maryam Bamshad ◽  
C. Kay Song ◽  
Timothy J. Bartness
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Sympathetic Nervous System ◽  
Brown Adipose Tissue ◽  
Pseudorabies Virus ◽  
Critical Role ◽  
Hypothalamic Nucleus ◽  
Brown Adipose ◽  
Sympathetic Nervous ◽  
Diet Induced Thermogenesis

Brown adipose tissue (BAT) plays a critical role in cold- and diet-induced thermogenesis. Although BAT is densely innervated by the sympathetic nervous system (SNS), little is known about the central nervous system (CNS) origins of this innervation. The purpose of the present experiment was to determine the neuroanatomic chain of functionally connected neurons from the CNS to BAT. A transneuronal viral tract tracer, Bartha’s K strain of the pseudorabies virus (PRV), was injected into the interscapular BAT of Siberian hamsters. The animals were killed 4 and 6 days postinjection, and the infected neurons were visualized by immunocytochemistry. PRV-infected neurons were found in the spinal cord, brain stem, midbrain, and forebrain. The intensity of labeled neurons in the forebrain varied from heavy infections in the medial preoptic area and paraventricular hypothalamic nucleus to few infections in the ventromedial hypothalamic nucleus, with moderate infections in the suprachiasmatic and lateral hypothalamic nuclei. These results define the SNS outflow from the brain to BAT for the first time in any species.

Regulation of brown adipose tissue lipogenesis by thyroid hormone and the sympathetic nervous system

1993 ◽  
Vol 265 (2) ◽  
pp. E252-E258 ◽  
Author(s):  
W. J. Yeh ◽  
P. Leahy ◽  
H. C. Freake
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Thyroid Hormone ◽  
Sympathetic Nervous System ◽  
Brown Adipose Tissue ◽  
Fatty Acid Synthase ◽  
Northern Analysis ◽  
Brown Adipose ◽  
Sympathetic Nervous

Thyroid hormone regulates lipogenesis differently in rat liver and brown adipose tissue (BAT). In the hypothyroid state, lipogenesis is suppressed in liver but enhanced in BAT. Here we investigated the mechanisms underlying increased lipogenesis in hypothyroid BAT. Housing the animals at 28 degrees C decreased lipogenesis in hypothyroid BAT to euthyroid levels. Denervation resulted in a 90% reduction in lipogenesis in hypothyroid BAT such that levels were lower than in euthyroid tissue. Thyroid hormone treatment of hypothyroid rats stimulated fatty acid synthesis in denervated BAT, as in liver, but decreased it in intact BAT. Steady-state levels of mRNA encoding acetyl-CoA carboxylase, fatty-acid synthase, and spor 14 were measured in similar animals by Northern analysis. The expression of these mRNAs mirrored the lipogenic data, showing that both thyroid hormone and the sympathetic nervous system work at a pretranslational level in this tissue. These data suggest that the increased BAT lipogenesis found with hypothyroidism is mediated by the sympathetic nervous system to counter the reduction in metabolic rate in these animals.

scholarly journals Interleukin-1 receptor antagonist treatment in acute ischaemic stroke does not alter systemic markers of anti-microbial defence

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 1039
Author(s):  
Laura McCulloch ◽  
Stuart M. Allan ◽  
Hedley C. Emsley ◽  
Craig J. Smith ◽  
Barry W. McColl
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Receptor Antagonist ◽  
Inflammatory Responses ◽  
Interleukin 1 ◽  
Plasma Concentrations ◽  
Classical Pathway ◽  
Stroke Patients ◽  
Complement Components ◽  
Sympathetic Nervous

Background: Blockade of the cytokine interleukin-1 (IL-1) with IL-1 receptor antagonist (IL-1Ra) is a candidate treatment for stroke entering phase II/III trials, which acts by inhibiting harmful inflammatory responses.  Infection is a common complication after stroke that significantly worsens outcome and is related to stroke-induced deficits in systemic immune function thought to be mediated by the sympathetic nervous system.  Therefore, immunomodulatory treatments for stroke, such as IL-1Ra, carry a risk of aggravating stroke-associated infection. Our primary objective was to determine if factors associated with antibody-mediated antibacterial defences were further compromised in patients treated with IL-1Ra after stroke. Methods: We assessed plasma concentrations of immunoglobulin isotypes and complement components in stroke patients treated with IL-1Ra or placebo and untreated non-stroke controls using multiplex protein assays. Activation of the sympathetic nervous system (SNS) was determined by measuring noradrenaline, a major SNS mediator. Results:  There were significantly lower plasma concentrations of IgM, IgA, IgG1 and IgG4 in stroke-patients compared to non-stroke controls, however there were no differences between stroke patients treated with placebo or IL-1Ra. Concentrations of complement components associated with the classical pathway  were increased and those associated with the alternative pathways decreased in stroke patients, neither being affected by treatment with IL-1Ra.  Noradrenaline concentrations were increased after stroke in both placebo and IL-1Ra-treated stroke patients compared to non-stroke controls.  Conclusion: These data show treatment with IL-1Ra after stroke does not alter circulating immunoglobulin and complement concentrations and is therefore unlikely to further aggravate stroke-associated infection susceptibility through reduced availability of these key anti-microbial mediators.

scholarly journals Hypothalamic administration of sargahydroquinoic acid elevates peripheral thermogenic signaling and ameliorates high fat diet-induced obesity through the sympathetic nervous system

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Doyeon Kim ◽  
Yuna Lee ◽  
Hyeung-Rak Kim ◽  
Yeo Jin Park ◽  
Hongik Hwang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Signaling Pathways ◽  
High Fat Diet ◽  
Energy Homeostasis ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Sympathetic Nervous

AbstractSargassum serratifolium (C. Agardh) C.Agardh, a marine brown alga, has been consumed as a food and traditional medicine in Asia. A previous study showed that the meroterpenoid-rich fraction of an ethanolic extract of S. serratifolium (MES) induced adipose tissue browning and suppressed diet-induced obesity and metabolic syndrome when orally supplemented. Sargahydroquinoic acid (SHQA) is a major component of MES. However, it is unclear whether SHQA regulates energy homeostasis through the central nervous system. To examine this, SHQA was administrated through the third ventricle in the hypothalamus in high-fat diet-fed C57BL/6 mice and investigated its effects on energy homeostasis. Chronic administration of SHQA into the brain reduced body weight without a change in food intake and improved metabolic syndrome-related phenotypes. Cold experiments and biochemical analyses indicated that SHQA elevated thermogenic signaling pathways, as evidenced by an increase in body temperature and UCP1 signaling in white and brown adipose tissues. Peripheral denervation experiments using 6-OHDA indicated that the SHQA-induced anti-obesity effect is mediated by the activation of the sympathetic nervous system, possibly by regulating genes associated with sympathetic outflow and GABA signaling pathways. In conclusion, hypothalamic injection of SHQA elevates peripheral thermogenic signaling and ameliorates diet-induced obesity.

scholarly journals Altered norepinephrine turnover in the brown fat of rats with chronic renal failure.

1994 ◽  
Vol 4 (11) ◽  
pp. 1896-1900 ◽  
Author(s):  
R Bigazzi ◽  
E Kogosov ◽  
V M Campese
Keyword(s):  
Renal Failure ◽  
Nervous System ◽  
Chronic Renal Failure ◽  
Turnover Rate ◽  
Turnover Rates ◽  
Sprague Dawley ◽  
Norepinephrine Turnover ◽  
Brown Adipose ◽  
Sympathetic Nervous ◽  
Nerve Discharge

Disturbances of the sympathetic nervous system (SNS) have been described in chronic renal failure, but their role in the metabolic derangements of uremia has not been well established. In these studies, SNS activity has been measured in the ventromedial hypothalamic (VMH) nuclei and in the intercostal brown adipose tissue (IBAT) of Sprague Dawley 5/6 nephrectomized or sham-operated rats. SNS activity was determined by calculating the norepinephrine (NE) turnover rate (in picograms per milligram per hour) 3, 6, and 12 h after the inhibition of NE synthesis with L-methyltyrosine. The endogenous NE concentration was significantly (P < 0.01) higher in the VMH (14,567 +/- 1,130 pg/mg wet wt) and IBAT (17,902 +/- 2,308 pg/mg wet wt) of uremic than control rats (9,600 +/- 1,110 and 5,752 +/- 320 pg/mg wet wt, respectively). The turnover rates of NE in the VMH (582 +/- 146 pg/mg per hour) and in the IBAT (1,432 +/- 179 pg/mg/hr) of uremic rats were significantly faster (P < 0.01) than in control rats (192 +/- 96 and 173 +/- 58 pg/mg per hour, respectively). These studies demonstrate a significant increase in NE turnover in the VMH nuclei and IBAT of uremic rats. It is suggested that increased efferent sympathetic nerve discharge from the VMH to the IBAT may play a role in the pathogenesis of malnutrition in uremia.

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