Progesterone does not alter sympathetic activity in tissues involved in energy balance

1996 ◽  
Vol 134 (4) ◽  
pp. 508-512
Author(s):  
Marisa Puerta ◽  
César Venero ◽  
Carmen Castro ◽  
María Abelenda
Keyword(s):  
Nervous System ◽  
Energy Balance ◽  
Food Intake ◽  
Sympathetic Nervous System ◽  
Sympathetic Activity ◽  
Female Rats ◽  
Noradrenaline Content ◽  
Brown Adipose ◽  
Energy Stores ◽  
Sympathetic Nervous

Puerta M, Venero C, Castro C, Abelenda M. Progesterone does not alter sympathetic activity in tissues involved in energy balance. Eur J Endocrinol 1996;134:508–12. ISSN 0804–4643 Female rats acclimated to thermoneutrality to avoid cold influences received progesterone by means of subcutaneous implants. They increased their food intake and body weight above the values recorded in control animals. None the less, despite the enhanced food intake, no sign of activation of the sympathetic nervous system was observed, as judged by the unaltered noradrenaline content, half-life and turnover rate in brown adipose tissue, pancreas and heart. This indicates that progesterone increases food intake but prevents non-energy-conservation processes regulated by the sympathetic nervous system from taking place. Thus, it facilitates in two different ways the building up of energy stores. Because overfeeding induced by palatable diets increases the sympathetic tone to the organs studied, it is suggested that the central mechanisms regulating energy balance are probably influenced in a different manner by progesterone than by the sensory properties of palatable diets. M Puerta, Departamento de Biología Animal II (Fisiología Animal), Facultad de Ciencias Biológicas, Universidad Complutense de Madrid, E-28040 Madrid, Spain

Melanocortin-4 receptor mRNA is expressed in sympathetic nervous system outflow neurons to white adipose tissue

2005 ◽  
Vol 289 (5) ◽  
pp. R1467-R1476 ◽  
Author(s):  
C. Kay Song ◽  
Raven M. Jackson ◽  
Ruth B. S. Harris ◽  
Denis Richard ◽  
Timothy J. Bartness
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Energy Balance ◽  
Food Intake ◽  
Sympathetic Nervous System ◽  
White Adipose Tissue ◽  
Sympathetic Outflow ◽  
Lipid Mobilization ◽  
Melanocortin 4 Receptor ◽  
Sympathetic Nervous

Energy balance results from the coordination of multiple pathways affecting energy expenditure and food intake. Candidate neuropeptides involved in energy balance are the melanocortins. Several species, including Siberian hamsters studied here, decrease and increase food intake in response to stimulation and blockade of the melanocortin 4-receptor (MC4-R). In addition, central application of the MC3/4-R agonist melanotan-II decreases body fat (increases lipolysis) beyond that accounted for by its ability to decrease food intake. Because an increase in the sympathetic nervous system drive to white adipose tissue (WAT) is the principal initiator of lipolysis, we tested whether the sympathetic outflow circuitry from brain to WAT contained MC4-R mRNA expressing cells. This was accomplished by labeling the sympathetic outflow to inguinal WAT using the pseudorabies virus (PRV), a transneuronal retrograde viral tract tracer, and then processing the brain for colocalization of PRV immunoreactivity with MC4-R mRNA, the latter assessed by in situ hybridization. MC4-R mRNA was impressively colocalized in PRV-labeled cells (approximately greater than 60%) in many brain areas across the neuroaxis, including those typically implicated in lipid mobilization (e.g., hypothalamic paraventricular, suprachiasmatic, arcuate and dorsomedial nuclei, lateral hypothalamic area), as well as those not traditionally identified with lipolysis (e.g., preoptic area, subzona incerta of the lateral hypothalamus, periaqueductal gray, solitary nucleus). These data provide compelling neuroanatomical evidence that could underlie a direct central modulation of the sympathetic outflow to WAT by the melanocortins through the MC4-Rs resulting in changes in lipid mobilization and adiposity.

Impairment of trophic response of brown fat to cold in guanethidine-treated rats

1982 ◽  
Vol 242 (3) ◽  
pp. C159-C165 ◽  
Author(s):  
G. Mory ◽  
D. Ricquier ◽  
M. Nechad ◽  
P. Hemon
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Protein A ◽  
Chronic Administration ◽  
Phospholipid Content ◽  
Noradrenaline Content ◽  
Brown Adipose ◽  
Sympathetic Nervous ◽  
Binding To Mitochondria

The aim of the present study was to investigate the role of the sympathetic nervous system in the trophic response of brown adipose tissue (BAT) to chronic cold exposure. The hyperplasia and the development of the mitochondria characterizing this response are usually considered as mainly controlled by the sympathetic activity in BAT, but this has never been clearly demonstrated. In the present work rats were sympathectomized by chronic administration of guanethidine and then exposed to cold during two weeks. The treatment induced a strong reduction of the noradrenaline content of BAT. The trophic response of the tissue to cold was largely impaired: no increase of the tissue weight, weak increase in the DNA, protein, and phospholipid content of the tissue. The development of the mitochondria was almost abolished. The increase in the proportion of the 32,000-dalton protein, a protein which regulates heat production by BAT, was suppressed and the GDP-binding to mitochondria, which is an index of BAT thermogenic capacity, was not increased as in normal cold-adapted rats. The ultrastructure of the tissue remained the same as in warm-adapted animals. It is concluded that the sympathetic nervous system plays an essential role in the control of the trophic response of BAT to the cold.

scholarly journals Central Administration of Leptin Inhibits Food Intake and Activates the Sympathetic Nervous System in Rhesus Macaques1

1999 ◽  
Vol 84 (2) ◽  
pp. 711-717 ◽  
Author(s):  
Mads Tang-Christensen ◽  
Peter J. Havel ◽  
Rebecca R. Jacobs ◽  
Philip J. Larsen ◽  
Judy L. Cameron
Keyword(s):  
Nervous System ◽  
Food Intake ◽  
Sympathetic Nervous System ◽  
Central Administration ◽  
Sympathetic Nervous

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.

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.

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 Roles for the sympathetic nervous system, renal nerves, and CNS melanocortin-4 receptor in the elevated blood pressure in hyperandrogenemic female rats

2015 ◽  
Vol 308 (8) ◽  
pp. R708-R713 ◽  
Author(s):  
Rodrigo Maranon ◽  
Roberta Lima ◽  
Frank T. Spradley ◽  
Jussara M. do Carmo ◽  
Howei Zhang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Female Rats ◽  
Elevated Blood Pressure ◽  
Renal Nerves ◽  
Female Rat ◽  
Elevated Blood ◽  
Melanocortin 4 Receptor ◽  
Sympathetic Nervous

Women with polycystic ovary syndrome (PCOS) have hyperandrogenemia and increased prevalence of risk factors for cardiovascular disease, including elevated blood pressure. We recently characterized a hyperandrogenemic female rat (HAF) model of PCOS [chronic dihydrotestosterone (DHT) beginning at 4 wk of age] that exhibits similar characteristics as women with PCOS. In the present studies we tested the hypotheses that the elevated blood pressure in HAF rats is mediated in part by sympathetic activation, renal nerves, and melanocortin-4 receptor (MC4R) activation. Adrenergic blockade with terazosin and propranolol or renal denervation reduced mean arterial pressure (MAP by telemetry) in HAF rats but not controls. Hypothalamic MC4R expression was higher in HAF rats than controls, and central nervous system MC4R antagonism with SHU-9119 (1 nmol/h icv) reduced MAP in HAF rats. Taking a genetic approach, MC4R null and wild-type (WT) female rats were treated with DHT or placebo from 5 to 16 wk of age. MC4R null rats were obese and had higher MAP than WT control rats, and while DHT increased MAP in WT controls, DHT failed to further increase MAP in MC4R null rats. These data suggest that increases in MAP with chronic hyperandrogenemia in female rats are due, in part, to activation of the sympathetic nervous system, renal nerves, and MC4R and may provide novel insights into the mechanisms responsible for hypertension in women with hyperandrogenemia such as PCOS.

Sympathetic nervous system contributes to the age-related impairment of flow-mediated dilation of the superficial femoral artery

2006 ◽  
Vol 291 (6) ◽  
pp. H3122-H3129 ◽  
Author(s):  
Dick H. J. Thijssen ◽  
Patricia de Groot ◽  
Miriam Kooijman ◽  
Paul Smits ◽  
Maria T. E. Hopman
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Femoral Artery ◽  
Superficial Femoral Artery ◽  
Sympathetic Activity ◽  
Cold Pressor Test ◽  
Young Men ◽  
Older Men ◽  
Flow Mediated Dilation ◽  
Sympathetic Nervous

The physiological aging process is associated with endothelial dysfunction, as assessed by flow-mediated dilation (FMD). Aging is also characterized by increased sympathetic tone. Therefore, the aim of the present study is to assess whether acute changes in sympathetic activity alter FMD in the leg. For this purpose, the FMD of the superficial femoral artery was determined in 10 healthy young (22 ± 1 yr) and 8 healthy older (69 ± 1 yr) men in three different conditions: 1) at baseline, 2) during reduction of sympathetic activity, and 3) during sympathetic stimulation. Reduction of sympathetic activity was achieved by performing a maximal cycling exercise, leading to postexercise attenuation of the sympathetic responsiveness in the exercised limb. A cold pressor test was used to increase sympathetic activity. Nitroglycerin (NTG) was used to assess endothelium-independent vasodilation in all three conditions. Our results showed that, in older men, the FMD and NTG responses were significantly lower compared with young men ( P = 0.001 and P = 0.02, respectively). In older men, sympathetic activity significantly affected the FMD response [repeated-measures (RM) ANOVA: P = 0.01], with a negative correlation between the level of sympathetic activity and FMD ( R = −0.41, P = 0.049). This was not the case for NTG responses (ANOVA; P = 0.48). FMD and NTG responses in young men did not differ among the three conditions (RM-ANOVA: P = 0.32 and P = 0.31, respectively). In conclusion, in older men, FMD of the femoral artery is impaired. Local attenuation of the sympathetic responsiveness partly restores the FMD in these subjects. In contrast, in young subjects, acute modulation of the sympathetic nervous system activity does not alter flow-mediated vasodilation in the leg.

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.

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