scholarly journals Az ösztrogénmetabolom biológiai és klinikai jelentősége lokális folyamatokban

2017 ◽  
Vol 158 (24) ◽  
pp. 929-937
Author(s):  
Krisztián Kovács ◽  
Barna Vásárhelyi ◽  
Katalin Mészáros ◽  
Attila Patócs ◽  
Gellért Karvaly
Keyword(s):  
Biological Activity ◽  
Clinical Significance ◽  
Physiological Role ◽  
Tissue Homeostasis ◽  
Diagnostic Significance ◽  
Peripheral Tissues ◽  
Breakdown Process ◽  
Specific Manner ◽  
Related Compounds

Abstract: Considerable knowledge has been gathered on the physiological role of estrogens. However, fairly little information is available on the role of compounds produced in the breakdown process of estrone and estradiol wich may play a role in various diseases associated with estrogen impact. To date, approximately 15 extragonadal estrogen-related compounds have been identified. These metabolites may exert protective, or, instead, pro-inflammatory and/or pro-oncogenic activity in a tissue-specific manner. Systemic and local estrogen metabolite levels are not necesserily correlated, which may promote the diagnostic significance of the locally produced estrogen metabolites in the future. The aim of the present study is a bibliographic review of the extragonadal metabolome in peripheral tissues, and to highlight the role of the peripheral tissue homeostasis of estrogens as well as the non-hormonal biological activity and clinical significance of the estrogen metabolome. Orv Hetil. 2017; 158(24): 929–937.

Peripheral muscarinic control of norepinephrine release in the cardiovascular system

1980 ◽  
Vol 239 (6) ◽  
pp. H713-H720 ◽  
Author(s):  
E. Muscholl
Keyword(s):  
Physiological Role ◽  
Sympathetic Nerves ◽  
Adrenergic Nerve ◽  
Sequence Of Events ◽  
Adrenergic Response ◽  
Adrenergic Nerve Terminals ◽  
Muscarinic Cholinergic ◽  
Related Compounds ◽  
Stimulation Of

Activation of muscarinic cholinergic receptors located at the terminal adrenergic nerve fiber inhibits the process of exocytotic norepinephrine (NE) release. This neuromodulatory effect of acetylcholine and related compounds has been discovered as a pharmacological phenomenon. Subsequently, evidence for a physiological role of the presynaptic muscarinic inhibition was obtained on organs known to be innervated by the autonomic ground plexus (Hillarp, Acta. Physiol. Scand. 46, Suppl. 157: 1-68, 1959) in which terminal adrenergic and cholinergic axons run side by side. Thus, in the heart electrical vagal stimulation inhibits the release of NE evoked by stimulation of sympathetic nerves, and this is reflected by a corresponding decrease in the postsynaptic adrenergic response. On the other hand, muscarinic antagonists such as atropine enhance the NE release evoked by field stimulation of tissues innervated by the autonomic ground plexus. The presynaptic muscarine receptor of adrenergic nerve terminals probably restricts the influx of calcium ions that triggers the release of NE. However, the sequence of events between recognition of the muscarinic compound by the receptor and the process of exocytosis still remains to be clarified.

scholarly journals Emerging Role of l-Dopa Decarboxylase in Flaviviridae Virus Infections

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 837 ◽  
Author(s):  
Frakolaki ◽  
Kalliampakou ◽  
Kaimou ◽  
Moraiti ◽  
Kolaitis ◽  
...  
Keyword(s):  
Viral Replication ◽  
Viral Infections ◽  
Physiological Role ◽  
Inverse Correlation ◽  
Dopa Decarboxylase ◽  
Hcv Rna ◽  
Virus Infections ◽  
Peripheral Tissues ◽  
Functional Complex

l-dopa decarboxylase (DDC) that catalyzes the biosynthesis of bioactive amines, such as dopamine and serotonin, is expressed in the nervous system and peripheral tissues, including the liver, where its physiological role remains unknown. Recently, we reported a physical and functional interaction of DDC with the major signaling regulator phosphoinosite-3-kinase (PI3K). Here, we provide compelling evidence for the involvement of DDC in viral infections. Studying dengue (DENV) and hepatitis C (HCV) virus infection in hepatocytes and HCV replication in liver samples of infected patients, we observed a negative association between DDC and viral replication. Specifically, replication of both viruses reduced the levels of DDC mRNA and the ~120 kDa SDS-resistant DDC immunoreactive functional complex, concomitant with a PI3K-dependent accumulation of the ~50 kDa DDC monomer. Moreover, viral infection inhibited PI3K-DDC association, while DDC did not colocalize with viral replication sites. DDC overexpression suppressed DENV and HCV RNA replication, while DDC enzymatic inhibition enhanced viral replication and infectivity and affected DENV-induced cell death. Consistently, we observed an inverse correlation between DDC mRNA and HCV RNA levels in liver biopsies from chronically infected patients. These data reveal a novel relationship between DDC and Flaviviridae replication cycle and the role of PI3K in this process.

Endogenous NUCB2/Nesfatin-1 Regulates Energy Homeostasis Under Physiological Conditions in Male Rats

2020 ◽  
Vol 52 (09) ◽  
pp. 676-684
Author(s):  
Anna-Maria Wilz ◽  
Kerstin Wernecke ◽  
Lena Appel ◽  
Johanna Kahrs ◽  
Riccardo Dore ◽  
...  
Keyword(s):  
Paraventricular Nucleus ◽  
Calcium Binding ◽  
Energy Homeostasis ◽  
Physiological Role ◽  
Male Rats ◽  
Peripheral Tissues ◽  
Downstream Target ◽  
Food And Water Intake ◽  
Pharmacological Blockade

AbstractNesfatin-1 is the proteolytic cleavage product of Nucleobindin 2, which is expressed both in a number of brain nuclei (e. g., the paraventricular nucleus of the hypothalamus) and peripheral tissues. While Nucleobindin 2 acts as a calcium binding protein, nesfatin-1 was shown to affect energy homeostasis upon central nervous administration by decreasing food intake and increasing thermogenesis. In turn, Nucleobindin 2 mRNA expression is downregulated in starvation and upregulated in the satiated state. Still, knowledge about the physiological role of endogenous Nucleobindin 2/nesfatin-1 in the control of energy homeostasis is limited and since its receptor has not yet been identified, rendering pharmacological blockade impossible. To overcome this obstacle, we tested and successfully established an antibody-based experimental model to antagonize the action of nesfatin-1. This model was then employed to investigate the physiological role of endogenous Nucleobindin 2/nesfatin-1. To this end, we applied nesfatin-1 antibody into the paraventricular nucleus of satiated rats to antagonize the presumably high endogenous Nucleobindin 2/nesfatin-1 levels in this feeding condition. In these animals, nesfatin-1 antibody administration led to a significant decrease in thermogenesis, demonstrating the important role of endogenous Nucleobindin 2/nesfatin-1in the regulation of energy expenditure. Additionally, food and water intake were significantly increased, confirming and complementing previous findings. Moreover, neuropeptide Y was identified as a major downstream target of endogenous Nucleobindin 2/nesfatin-1.

scholarly journals The Inhibitory Role of B7-H4 in Antitumor Immunity: Association with Cancer Progression and Survival

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Changjun He ◽  
Haiquan Qiao ◽  
Hongchi Jiang ◽  
Xueying Sun
Keyword(s):  
Cancer Progression ◽  
Antitumor Immunity ◽  
Human Cancer ◽  
Physiological Role ◽  
T Cell Response ◽  
Soluble Form ◽  
Peripheral Tissues ◽  
Inhibitory Role ◽  
Pertinent Data

B7-H4 is one of the most recently identified members of B7 superfamily of costimulatory molecules serving as an inhibitory modulator of T-cell response. B7-H4 is broadly expressed in human peripheral tissues and inducibly expressed in immune cells. The expression of B7-H4 has been observed in various types of human cancer tissues, and its soluble form has been detected in blood samples from cancer patients. However, its precise physiological role is still elusive, as its receptor has not been identified and the expression levels are not consistent. This paper summarizes the pertinent data on the inhibitory role of B7-H4 in antitumor immunity and its association with cancer progression and survival in human patients. The paper also discusses the clinical significance of investigating B7-H4 as potential markers for cancer diagnosis and prognosis, and as therapeutic targets.

THYROXINE: STUDIES CONCERNING ITS INTRINSIC PHYSIOLOGICAL ACTIVITY

1978 ◽  
Vol 88 (1) ◽  
pp. 87-93 ◽  
Author(s):  
Anne du Breuil ◽  
Valerie Anne Galton
Keyword(s):  
Biological Activity ◽  
Thyroid Hormone ◽  
Cold Exposure ◽  
Physiological Activity ◽  
Peripheral Tissues ◽  
Physiological Action ◽  
Thyroid Hormone Biosynthesis ◽  
Hormone Biosynthesis

ABSTRACT The importance of the monodeiodination of T4 to T3 in the physiological action of T4 was explored by assessing the role of T4 in maintaining propylthiouracil (PTU)-treated rats during exposure to 4°C. (PTU inhibits both thyroid hormone biosynthesis and T4 to T3 conversion in peripheral tissues.) Firstly, the effects of cold exposure on the metabolism of T4 in control and PTU-treated rats equilibrated with [125I]T4 (2 μg/100 g b. w./day) were determined. PTU was administered in the food (2 mg/g food). In control rats, no significant changes in T4 metabolism occurred during 3 days at 4°C. Urinary 125I was greatly decreased in PTU-treated rats. Exposure of these rats to cold resulted in some increase but values were still 50 % below normal. Secondly, four groups of rats were exposed to cold: control; PTU-treated; T4-treated; PTU + T4-treated. Control and T4-treated rats survived. PTU-treated rats died unless T4 was administered. Radioimmunoassay of T4 and T3 indicated significant concentrations of T3 in sera of rats from all but the PTU + T4 group. These results suggest that T4 permits survival in the cold-exposed PTU-treated rat without being converted to T3 and thus they support the concept that T4 has intrinsic biological activity.

scholarly journals ANGPTL8 in metabolic homeostasis: more friend than foe?

Open Biology ◽  
2021 ◽  
Vol 11 (9) ◽  
Author(s):  
Chang Guo ◽  
Chenxi Wang ◽  
Xia Deng ◽  
Jianqiang He ◽  
Ling Yang ◽  
...  
Keyword(s):  
Metabolic Disorders ◽  
Metabolic Diseases ◽  
Hepatic Glucose Production ◽  
Physiological Role ◽  
Glucose Production ◽  
Peripheral Tissues ◽  
Glucose And Lipid Metabolism ◽  
Hepatic Glucose

ANGPTL8 is an important cytokine, which is significantly increased in type 2 diabetes mellitus (T2DM), obesity and metabolic syndrome. Many studies have shown that ANGPTL8 can be used as a bio-marker of these metabolic disorders related diseases, and the baseline ANGPTL8 level has also been found to be positively correlated with retinopathy and all-cause mortality in patients with T2DM. This may be related to the inhibition of lipoprotein lipase activity and the reduction of circulating triglyceride (TG) clearance by ANGPTL8. Consistently, inhibition of ANGPTL8 seems to prevent or improve atherosclerosis. However, it is puzzling that ANGPTL8 seems to have a directing function for TG uptake in peripheral tissues; that is, ANGPTL8 specifically enhances the reserve and buffering function of white adipose tissue, which may alleviate the ectopic lipid accumulation to a certain extent. Furthermore, ANGPTL8 can improve insulin sensitivity and inhibit hepatic glucose production. These contradictory results lead to different opinions on the role of ANGPTL8 in metabolic disorders. In this paper, the correlation between ANGPTL8 and metabolic diseases, the regulation of ANGPTL8 and the physiological role of ANGPTL8 in the process of glucose and lipid metabolism were summarized, and the physiological/pathological significance of ANGPTL8 in the process of metabolic disorder was discussed.

scholarly journals Estrogen Receptors Alpha and Beta Mediate Synaptic Transmission in the PFC and Hippocampus of Mice

2021 ◽  
Vol 22 (3) ◽  
pp. 1485
Author(s):  
Mingyue Zhang ◽  
Hannah Weiland ◽  
Michael Schöfbänker ◽  
Weiqi Zhang
Keyword(s):  
Estrogen Receptor ◽  
Synaptic Transmission ◽  
Estrogen Receptors ◽  
Hippocampal Slices ◽  
Physiological Role ◽  
Glutamatergic Transmission ◽  
Postsynaptic Currents ◽  
Specific Manner ◽  
The Brain

Distinct from ovarian estradiol, the steroid hormone 17ß-estradiol (E2) is produced in the brain and is involved in numerous functions, particularly acting as a neurosteroid. However, the physiological role of E2 and the mechanism of its effects are not well known. In hippocampal slices, 17ß-estradiol has been found to cause a modest increase in fast glutamatergic transmission; because some of these effects are rapid and acute, they might be mediated by membrane-associated receptors via nongenomic action. Moreover, activation of membrane estrogen receptors can rapidly modulate neuron function in a sex-specific manner. To further investigate the neurological role of E2, we examined the effect of E2, as an estrogen receptor (ER) agonist, on synaptic transmission in slices of the prefrontal cortex (PFC) and hippocampus in both male and female mice. Whole-cell recordings of spontaneous excitatory postsynaptic currents (sEPSC) in the PFC showed that E2 acts as a neuromodulator in glutamatergic transmission in the PFC in both sexes, but often in a cell-specific manner. The sEPSC amplitude and/or frequency responded to E2 in three ways, namely by significantly increasing, decreasing or having no response. Additional experiments using an agonist selective for ERß, diarylpropionitrile (DPN) showed that in males the sEPSC and spontaneous inhibitory postsynaptic currents sIPSC responses were similar to their E2 responses, but in females the estrogen receptor ß (ERß) agonist DPN did not influence excitatory transmission in the PFC. In contrast, in the hippocampus of both sexes E2 potentiated the gluatmatergic synaptic transmission in a subset of hippocampal cells. These data indicate that activation of E2 targeting probably a estrogen subtypes or different downstream signaling affect synaptic transmission in the brain PFC and hippocampus between males versus females mice.

scholarly journals Leptin Regulates Hypothalamus-Pituitary-Thyroid Axis via TRH in Energy Expenditure During Fasting: The Study on TRH Deficient Mouse

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A851-A851
Author(s):  
Yuri Kondo ◽  
Atsushi Ozawa ◽  
Takuya Watanabe ◽  
Masayuki Yoshioka ◽  
Sayaka Yamada ◽  
...  
Keyword(s):  
Biological Activity ◽  
Energy Expenditure ◽  
Mrna Expression ◽  
Anterior Pituitary ◽  
Physiological Role ◽  
Expression Level ◽  
Mrna Expression Level ◽  
Central Hypothyroidism ◽  
Serum Tsh

Abstract Objectives: The hypothalamic-pituitary-thyroid (HPT) axis plays a significant role in the regulation of energy expenditure. Previous reports demonstrated that thyroid hormones are critically involved in metabolic process, and hypothyroidism was induced by fasting. The mechanism by which TRH neurons sense alterations in peripheral energy stores is supposed to be regulated by leptin, an adipose tissue-derived hormone. Leptin was initially considered as a hormone to prevent obesity, it was later showed that the major role of leptin is to signal the switch from the fed to the starved state at the hypothalamic level. Recently, we generated TRH-deficient mice (TRH-/-). The mice exhibit tertiary/central hypothyroidism with characteristic elevation of serum TSH level and diminished TSH biological activity. In this study, we used TRH-/- to investigate the physiological role of TRH in fasting energy expenditure, including the mechanism regulated by leptin. Methods: Twelve-week-old male F2 hybrid ICR mice were used in this study. (1) Wild-type mice (WT) and TRH-/- were fasted up to 50 hrs. Blood samples were collected from tail veins at various points. Anterior pituitary samples were obtained from euthanized mice before and after 16 hrs fasting. (2) Serum free T4 (FT4) and TSH levels assessed. (3) The expression level of TSHβ mRNA in anterior pituitary were detected using qPCR assays. (4) We repeated these experiments using mice with leptin administration; leptin (0.5μg/g•BW) was administrated every 6 hours starting at after 2 hours fasting. Results: In WT, the level of FT4 was decreased chronologically during fasting to approximately 50% at 50 hrs after fasting. Serum TSH decreased to 70% and the expression level of TSHβ mRNA in anterior pituitary also decreased to 30% compared to before fasting. Administration of leptin recovered the level of FT4 to basal level. However, the level of serum TSH and TSHβ mRNA in pituitary were not recovered to basal levels. By contrast, in TRH-/-, the level of FT4 were also decreased after fasting indicating that the decrease of FT4 by fasting was independent of TRH. However, the level of FT4 was not recovered by leptin suggesting that the recovery of FT4 by leptin was TRH dependent. Serum TSH level decreased to 75% after fasting, and no recovery to basal level with leptin administration was observed in TRH-/- same as WT. In TRH-/-, the pituitary TSHβ mRNA expression level was about 50% of WT before fasting. It did not correlate with the serum TSH level. In addition, no increase in TSHβ mRNA expression level by leptin administration was observed in TRH-/-. These findings suggested that the TSHβ mRNA expression level in the pituitary is completely TRH-dependent in TRH-/-. Conclusion: Fasting-induced hypothyroxinemia was independent of TRH. Leptin regulates H-P-T axis via TRH during fasting-induced energy expenditure. Leptin may modulate the biological activity of TSHβ.

Clinical significance and treatment options of increased lipoprotein(a)

2014 ◽  
Vol 155 (16) ◽  
pp. 607-614 ◽  
Author(s):  
Noémi Zsíros ◽  
György Paragh ◽  
Mariann Harangi
Keyword(s):  
Cardiovascular Diseases ◽  
Clinical Significance ◽  
Physiological Function ◽  
Treatment Options ◽  
Physiological Role ◽  
Lipoprotein A

Lipoprotein(a) has been shown to be associated with an increased incidence of cardiovascular diseases for decades. However, only recent research revealed more about its physiological function and its role in the development of cardiovascular diseases. The authors summarize the physiological role of lipoprotein(a), causes and treatment of elevated lipoprotein(a) level, and the association between lipoprotein(a) and cardiovascular diseases. Orv. Hetil., 2014, 155(16), 607–614.

scholarly journals THE CLINICAL ROLE OF COMPONENT DIAGNOSTICS OF PEANUT ALLERGY AMONG CHILDREN WITH ALLERGIC DISEASES

2014 ◽  
Vol 11 (6) ◽  
pp. 41-46
Author(s):  
A M Shulyaeva ◽  
A N Pampura ◽  
T S Okuneva ◽  
E I Shabelnikova
Keyword(s):  
Clinical Significance ◽  
Allergic Diseases ◽  
Specific Ige ◽  
Diagnostic Significance ◽  
Clinical Role ◽  
Ara H1 ◽  
Peanut Allergens ◽  
Method Of Measurement

Background. To determine the clinical significance of IgEmediated sensibilization to recombinant peanut allergens. Materials and methods. We examined 30 children with allergic diseases and sensibilization to whole peanut allergen. All children passed through allergological examination, including determination of specific IgE (method of Measurement CAP 100 Phadia, Switzerland) to recombinant peanut allergens: Ara h1, Ara h2, Ara h3, Ara and Ara h8, h9. Results. A wide variation of combinations of sensibilization to various peanut allergens was found. Sensibilization to rAra hi allergen was found in 40% of cases, to rAra h2 - in 36,6%, to rAra h3 - in 33%, to rAra h8 - in 60%, to rAra h9 in 56,6% of cases. Their clinical significance was 36,6% (rAra hi), 26% (rAra h2), 23% (rAra h3), 33% (rAra h8), 36% (rAra h9). Monosensibilization to peanut allergens rAra hi, 8 and 9 was identified in 26,6% of cases. The interrelation of rAra h2 and rAra h8 with atopic dermatitis and rAra h3 with asthma was found. Conclusion. Component diagnostics of peanut allergens has high diagnostic significance in further administration of elimination diets.

Sign in / Sign up

Export Citation Format

Share Document