scholarly journals Rikkunshito, a Japanese Kampo Medicine, Ameliorates Decreased Feeding Behavior via Ghrelin and Serotonin 2B Receptor Signaling in a Novelty Stress Murine Model

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Chihiro Yamada ◽  
Yayoi Saegusa ◽  
Koji Nakagawa ◽  
Shunsuke Ohnishi ◽  
Shuichi Muto ◽  
...  
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Receptor Activation ◽  
Antagonistic Activity ◽  
Acylated Ghrelin ◽  
Receptor Antagonists ◽  
Water Treated Control ◽  
Cumulative Food Intake

We investigated the effects of rikkunshito (RKT), a ghrelin signal enhancer, on the decrease in food intake after exposure to novelty stress in mice. RKT administration (500 mg/kg,per os) improved the decrease in 6 h cumulative food intake. In control mice, the plasma acylated ghrelin levels significantly increased by 24 h fasting. In contrast, the acylated ghrelin levels did not increase by fasting in mice exposed to the novelty stress. RKT administration to the novelty stress mice showed a significant increase in the acylated ghrelin levels compared with that in the distilled-water-treated control mice. Food intake after administering serotonin 2B (5-HT2B) receptor antagonists was evaluated to clarify the role of 5-HT2Breceptor activation in the decrease in feeding behavior after novelty stress. SB215505 and SB204741, 5-HT2Breceptor antagonists, significantly improved the decrease in food intake after exposure to novelty stress. A component of RKT, isoliquiritigenin, prevented the decrease in 6 h cumulative food intake. Isoliquiritigenin showed 5-HT2Breceptor antagonistic activityin vitro.In conclusion, the results suggested that RKT improves the decrease in food intake after novelty stress probably via 5-HT2Breceptor antagonism of isoliquiritigenin contained in RKT.

Liver X Receptor Activation Impairs Neutrophil Functions and Aggravates Sepsis

2019 ◽  
Vol 221 (9) ◽  
pp. 1542-1553 ◽  
Author(s):  
Fabrício O Souto ◽  
Fernanda V S Castanheira ◽  
Silvia C Trevelin ◽  
Braulio H F Lima ◽  
Guilherme Cesar Martelossi Cebinelli ◽  
...  
Keyword(s):  
Multiorgan Failure ◽  
Bacterial Load ◽  
Cecal Ligation ◽  
Neutrophil Infiltration ◽  
Receptor Activation ◽  
Messenger Ribonucleic Acid ◽  
X Receptors ◽  
Lxr Agonists

Abstract Background Liver X receptors (LXRs) are nuclear receptors activated by oxidized lipids and were previously implicated in several metabolic development and inflammatory disorders. Although neutrophils express both LXR-α and LXR-β, the consequences of their activation, particularly during sepsis, remain unknown. Methods We used the model of cecal ligation and puncture (CLP) to investigate the role of LXR activation during sepsis. Results In this study, we verified that LXR activation reduces neutrophil chemotactic and killing abilities in vitro. Mice treated with LXR agonists showed higher sepsis-induced mortality, which could be associated with reduced neutrophil infiltration at the infectious foci, increased bacteremia, systemic inflammatory response, and multiorgan failure. In contrast, septic mice treated with LXR antagonist showed increased number of neutrophils in the peritoneal cavity, reduced bacterial load, and multiorgan dysfunction. More important, neutrophils from septic patients showed increased ABCA1 messenger ribonucleic acid levels (a marker of LXR activation) and impaired chemotactic response toward CXCL8 compared with cells from healthy individuals. Conclusions Therefore, our findings suggest that LXR activation impairs neutrophil functions, which might contribute to poor sepsis outcome.

scholarly journals Expression of Taste Receptor 2 Subtypes in Human Testis and Sperm

2020 ◽  
Vol 9 (1) ◽  
pp. 264 ◽  
Author(s):  
Laura Governini ◽  
Bianca Semplici ◽  
Valentina Pavone ◽  
Laura Crifasi ◽  
Camilla Marrocco ◽  
...  
Keyword(s):  
Taste Receptor ◽  
Receptor Activation ◽  
Taste Buds ◽  
The Body ◽  
Semen Parameters ◽  
Human Testis ◽  
Taste Receptors ◽  
Organ Systems

Taste receptors (TASRs) are expressed not only in the oral cavity but also throughout the body, thus suggesting that they may play different roles in organ systems beyond the tongue. Recent studies showed the expression of several TASRs in mammalian testis and sperm, indicating an involvement of these receptors in male gametogenesis and fertility. This notion is supported by an impaired reproductive phenotype of mouse carrying targeted deletion of taste receptor genes, as well as by a significant correlation between human semen parameters and specific polymorphisms of taste receptor genes. To better understand the biological and thus clinical significance of these receptors for human reproduction, we analyzed the expression of several members of the TAS2Rs family of bitter receptors in human testis and in ejaculated sperm before and after in vitro selection and capacitation. Our results provide evidence for the expression of TAS2R genes, with TAS2R14 being the most expressed bitter receptor subtype in both testis tissue and sperm cells, respectively. In addition, it was observed that in vitro capacitation significantly affects both the expression and the subcellular localization of these receptors in isolated spermatozoa. Interestingly, α-gustducin and α-transducin, two Gα subunits expressed in taste buds on the tongue, are also expressed in human spermatozoa; moreover, a subcellular redistribution of both G protein α-subunits to different sub-compartments of sperm was registered upon in vitro capacitation. Finally, we shed light on the possible downstream transduction pathway initiated upon taste receptor activation in the male reproductive system. Performing ultrasensitive droplets digital PCR assays to quantify RNA copy numbers of a distinct gene, we found a significant correlation between the expression of TAS2Rs and TRPM5 (r = 0.87), the cation channel involved in bitter but also sweet and umami taste transduction in taste buds on the tongue. Even if further studies are needed to clarify the precise functional role of taste receptors for successful reproduction, the presented findings significantly extend our knowledge of the biological role of TAS2Rs for human male fertility.

scholarly journals Influence of serotonergic transmission and postsynaptic 5-HT2C action on the feeding behavior of Coturnix japonica (Galliformes: Aves)

2005 ◽  
Vol 65 (4) ◽  
pp. 589-595 ◽  
Author(s):  
P. L. Cedraz-Mercez ◽  
A. C. Almeida ◽  
R. H. Costa-e-Sousa ◽  
D. Badauê-Passos Jr. ◽  
L. R. Castilhos ◽  
...  
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Serotonin Release ◽  
Significant Inhibition ◽  
Current Data ◽  
Coturnix Japonica ◽  
Behavior Control ◽  
Control Groups

We investigated the role of 5-HT2C receptors and serotonergic transmission in the feeding behavior control of quails. Administration of serotonin releaser, fenfluramine (FEN) and 5-HT2C agonists, mCPP and MK212, 1.0 and 3.3 mg/Kg induced significant inhibition of food intake in previously fasted fowls (0.71 ± 0.18 g and 0.47 ± 0.2 g; 0.49 ± 0.22 g and 0.48 ± 0.29 g; 0.82 ± 0.13 g and 0.71 ± 0.16 g, respectively). Control groups ranged from 2.89 ± 0.21 g to 2.97 ± 0.22 g, 60 min after reintroduction of food, P < 0.0001). Similar results were obtained with normally fed quails. Both serotonin releaser and 5-HT2C agonists, in a 3.3 mg/Kg dose, induced hypophagy (FEN, 0.78 ± 0.08 g; mCPP, 0.89 ± 0.07 g; MK212, 1.25 ± 0.17 g vs. controls, 2.05 ± 0.12 g, 120 min after food was presented, P < 0.0001 to P < 0.01). Previous administration of 5-HT2C antagonist, LY53857 (5.0 mg/Kg) blocked the hypophagic response induced by 5-HT2C agonists 60 min after food was reintroduced. Current data show a modulatory role of serotonin release and postsynaptic 5-HT2C receptors in the feeding behavior of quails.

Abstract P249: ICV Infusion Of AgRP Modulates Feeding Behavior And Energy Expenditure In Mice

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Vanessa Oliveira ◽  
Kirthikaa Balapattabi ◽  
John J Reho ◽  
Sebastiao D Silva ◽  
Chetan N Patil ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Feeding Behavior ◽  
Body Mass ◽  
High Dose ◽  
Digestive Efficiency ◽  
Genetic Ablation ◽  
Total Food Intake ◽  
Intracerebroventricular Infusion

A subset of Agouti-related protein (AgRP) neurons within the arcuate nucleus express angiotensin type 1a receptors (AT1A), and genetic ablation of AT1A in these cells disinhibits AgRP gene expression and attenuates energy expenditure (EE) in mice. To further understand the role of AgRP in metabolic control, and to establish relevant dosing schedules in this species, here we tested the effect of intracerebroventricular infusion (icv) of recombinant AgRP on metabolic functions in C57BL/6J male mice. First, we examined the effects of AgRP(82-132) (21 days, 1 or 10 nmol/d, icv) or artificial cerebrospinal fluid (aCSF) using metabolic cages. High dose AgRP reduced body mass (aCSF n=12, +0.8±0.6 vs 1 nmol/d n=14, +0.6±0.6 vs 10 nmol/d n=11, -1.5±0.5 p<0.05 g/21d), without affecting food intake (15.1±1.2 vs 14.1±1.1 vs 16.3±1.1 kcal/d) or digestive efficiency (85.2±0.5 vs 84.5±0.7 vs 85.1±0.6 %), but a significant reduction in energy efficiency (+3.8±2.0 vs +2.7±2.8 vs -5.9±2.2 p<0.05 mg/kcal) indicated increased total EE. Next, we examined the effect of AgRP(82-132) (14 days, 1 nmol/d, icv) using a multiplexed system (Promethion, Sable). AgRP had no effect on body mass (25.1±1.2, n=8 vs 26.7±0.5, n=8), overall body composition (by NMR), heat production (Weir, 24h: 0.485±0.015 vs 0.490±0.022 kcal/h), or respiratory exchange ratio (0.88±0.01 vs 0.89±0.01). AgRP increased total food intake (10.1±0.6, n=8 vs 11.9±0.5, n=8, kcal/d, p=0.03) through a synergistic effect on number of meals and median meal mass. We conclude that AgRP (1-10 nmol/d, 2-3 wk, icv) infusion causes subtle changes in feeding behavior without effect on digestive efficiency. In contrast, EE is paradoxically increased by AgRP when infused at a high dose (10 nmol/d). We postulate that these differences may reflect differential accessibility of the peptide to relevant feeding vs autonomic control regions of the hypothalamus when infused into the cerebral ventricles, and/or compensatory increases in EE secondary to changes in feeding behavior. Future studies to deconvolute the role of AgRP in the control of EE in mice will require site-specific delivery of the peptide to relevant target regions or manipulation of its receptor in those regions. Funding: HL134850, HL084207

scholarly journals Antagonism and synergism in Gardnerella vaginalis strains isolated from women with bacterial vaginosis

2010 ◽  
Vol 59 (8) ◽  
pp. 891-897 ◽  
Author(s):  
G. S. Teixeira ◽  
K. L. K. Soares-Brandão ◽  
K. M. G. R. Branco ◽  
J. L. M. Sampaio ◽  
R. M. D. Nardi ◽  
...  
Keyword(s):  
Bacterial Vaginosis ◽  
Chemical Nature ◽  
Growth Conditions ◽  
Antagonistic Activity ◽  
Gardnerella Vaginalis ◽  
Ecological Role ◽  
Micro Organisms

Antagonistic and synergistic substances are important for interactions between micro-organisms associated with human body surfaces, either in healthy or in diseased conditions. In the present study, such compounds produced by Gardnerella vaginalis strains isolated from women with bacterial vaginosis (BV) were detected in vitro and the antagonistic ones were partially characterized. Among 11 G. vaginalis strains tested, all showed antagonistic activity against at least one of the 22 indicator bacteria assayed. Interestingly, for some of these strains, antagonism reverted to synergism, favouring one of the indicator strains (Peptostreptococcus anaerobius) when the growth medium was changed. Partial characterization of antagonistic substances suggested a bacteriocin-like chemical nature. Depending on growth conditions, G. vaginalis isolated from women with BV produced antagonistic or synergistic compounds for other bacterial components of the vaginal ecosystem. This is the first report to our knowledge of the production of antagonistic and/or synergistic substances by G. vaginalis. This ability may be a pivotal factor in understanding BV and the ecological role of this bacterium in the vaginal environment.

Role of ET-1 in the regulation of coronary circulation

2003 ◽  
Vol 81 (6) ◽  
pp. 570-577 ◽  
Author(s):  
Michel Lavallée ◽  
Eric Thorin
Keyword(s):  
Coronary Vessels ◽  
Receptor Activation ◽  
Primary Objective ◽  
No Production ◽  
Metabolic Demand ◽  
Resistance Vessels ◽  
Secondary Phenomenon

Given that circulating ET levels in heart failure, in particular, may reach physiological threshold for coronary constrictor responses, the primary objective of the present review is to consider coronary vessels as an important target for circulating and locally produced endothelin(s). In healthy vessels, ET-1 causes biphasic coronary responses characterized by a transient dilation of large and small arteries followed by a sustained constriction. ETB receptors are pivotal in the early dilation of resistance vessels, whereas dilation of conductance vessels may be a secondary phenomenon triggered by flow increases. Exogenous ET-1 causes coronary constriction almost exclusively through ETA receptor activation. Human and canine large epicardial coronary vessels display significant baseline ET-1 dependent tone in vitro and in vivo, an ETA-dependent process. In contrast, ETB receptors located on smooth muscle cells are apparently less important for producing constrictor responses. NO production may serve as an important counter-regulatory mechanism to limit ET-dependent effects on coronary vessels. Conversely, in a dysfunctional endothelium, the loss of NO may augment ET-1 production and activity. By lifting the ET-dependent burden from coronary vessels, ET receptor blockade should help to ensure a closer match between cardiac metabolic demand and coronary perfusion.Key words: endothelin, ET receptors, coronary vessels, coronary blood flow, nitric oxide, shear stress, atherosclerosis, humans, animals.

scholarly journals A potent neuropeptide Y antagonist, 1229U91, suppressed spontaneous food intake in Zucker fatty rats

1998 ◽  
Vol 274 (5) ◽  
pp. R1500-R1504 ◽  
Author(s):  
A. Ishihara ◽  
T. Tanaka ◽  
A. Kanatani ◽  
T. Fukami ◽  
M. Ihara ◽  
...  
Keyword(s):  
Food Intake ◽  
Neuropeptide Y ◽  
Feeding Behavior ◽  
Physiological Role ◽  
Abnormal Behavior ◽  
Zucker Rats ◽  
Intracerebroventricular Administration ◽  
Feeding Suppression ◽  
Npy Antagonist

Neuropeptide Y (NPY) is one of the most potent orexigenic substances known. 1229U91 was found to be a potent and selective NPY antagonist. To elucidate a physiological role of NPY in hyperphagia in obese animals, we studied the effect of 1229U91 on spontaneous food intake in obese and lean Zucker rats. The food intake of Zucker rats was suppressed by intracerebroventricular administration of 1229U91 more potently in obese than in lean animals without abnormal behavior (31.7 and 67.3% inhibition at doses of 10 and 30 μg, respectively, in Zucker fatty rats and 22.2% inhibition at 30 μg in lean rats). This compound markedly suppressed NPY-induced food intake at 30 μg but did not affect galanin-induced food intake, suggesting that the feeding suppression seen in Zucker fatty and lean rats is pharmacologically and behaviorally specific. These results suggest that NPY is involved in feeding behavior in Zucker fatty rats and that NPY contributes to feeding to a greater degree in Zucker fatty than in lean rats. The hyperphagia in Zucker fatty rats may be due to the abnormal overactivation of the NPYergic system.

Fatty acid oxidation affects food intake by altering hepatic energy status

1999 ◽  
Vol 276 (4) ◽  
pp. R1046-R1053 ◽  
Author(s):  
Mark I. Friedman ◽  
Ruth B. Harris ◽  
Hong Ji ◽  
Israel Ramirez ◽  
Michael G. Tordoff
Keyword(s):  
Fatty Acid ◽  
Food Intake ◽  
Feeding Behavior ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Energy Status ◽  
Hepatic Fatty Acid ◽  
Hepatic Fatty Acid Oxidation

Inhibition of fatty acid oxidation stimulates feeding behavior in rats. To determine whether a decrease in hepatic fatty acid oxidation triggers this behavioral response, we compared the effects of different doses of methyl palmoxirate (MP), an inhibitor of fatty acid oxidation, on food intake with those on in vivo and in vitro liver and muscle metabolism. Administration of 1 mg/kg MP selectively decreased hepatic fatty acid oxidation but did not stimulate food intake. In contrast, feeding behavior increased in rats given 5 or 10 mg/kg MP, which inhibited hepatic fatty acid oxidation to the same extent as did the low dose but in addition suppressed fatty acid oxidation in muscle and produced a marked depletion of liver glycogen. Dose-related increases in food intake tracked dose-related reductions in liver ATP content, ATP-to-ADP ratio, and phosphorylation potential. The findings suggest that a decrease in hepatic fatty acid oxidation can stimulate feeding behavior by reducing hepatic energy production.

scholarly journals A reassessment of the role of serotonergic system in the control of feeding behavior

2005 ◽  
Vol 77 (1) ◽  
pp. 103-111 ◽  
Author(s):  
Magda A. Medeiros ◽  
Ricardo H. Costa-e-Sousa ◽  
Emerson L. Olivares ◽  
Wellington S. Côrtes ◽  
Luís C. Reis
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Feeding Behavior ◽  
The Body ◽  
Serotonergic System ◽  
Initial Increase ◽  
Energetic Balance ◽  
Electrolytic Lesions ◽  
Fasted Rats

The role of serotonergic system in the feeding behaviorwas appraised by electrolytic lesions in the dorsal raphe nucleus (DRN) and administration of para-chlorophenylalanine (PCPA, 3 mg/5 mul, icv). Chronic evaluations were accomplished through 120 and 360 days in PCPA-injected and DRN-lesioned rats, respectively. Acute food intake was evaluated in fasted rats and submitted to injection of PCPA and hydroxytryptophan (LHTP, 30 mg/kg, ip). DRN-lesioned rats exhibited 22-80% increase in food intake up to sixth month, whereas the obesity was evident and sustained by whole period. In PCPA-injected rats was observed an initial increase in the food intake followed by hypophagy from 25th to 30th day and a transitory increase of body weight from 5th to 60th day. In the acute study, the LHTP reverted partially the PCPA-induced increase in food intake of fasted rats suggesting a sustained capacity of decarboxylation of precursor by serotonergic neurons. Slow restoration of the levels of food intake in DRN-lesioned rats reveals a neuroplasticity in the systems that regulate feeding behavior. A plateau on the body weight curve in lesioned rats possibly represents the establishment of a new and higher set point of energetic balance.

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