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Friday, 13 December 2013
The Effects of Hormone Histamine (2)
Histamine, found within granules of basophils and mast cells (>90% of body stores) is a biogenic amine and an organic nitrogen compound that occurs to various degrees in many foods such as cherries to about 0.17-13.46 ng/g, bananas and grapes, rice and cereals, herbs, olive oil, wine, beer, etc.. In healthy persons, dietary histamine can be rapidly detoxified by amine oxidases, whereas persons with low amine oxidase activity are at risk of histamine toxicity(a). the hormone, as a neurotransmitter is involved in regulating physiological function in the gut and immune response to foreign pathogens.
10. Histamine and schizophrenia
In a study of a strong hyperactivity of histamine neurons induced in rodent brain by administration of methamphetamine or NMDA-receptor antagonists, Dr. Arrang JM. at the Unité de Neurobiologie et Pharmacologie Moléculaire, found that H3-receptor antagonists/inverse agonists display antipsychotic-like properties in animal models of the disease. Because of the limited predictability value of most animal models and the paucity of drugs affecting histaminergic transmission that were tried so far in human, the evidence remains therefore largely indirect, but supports a role of histamine neurons in schizophrenia(10).
11. Histamine and eating behavior
Interest in the histaminergic system as a potential target for the treatment of feeding disorders is driven by the unsatisfactory history of the pharmacotherapy of obesity, researchers at the found that the appetitive phase requires a high and yet optimal arousal state, and the histaminergic system is crucial for sustaining a high degree of arousal during motivated behavior. Histamine H(1) receptors in the brain are crucial for the regulation of the diurnal rhythm of food intake and the regulation of obesity; however, from a therapeutic standpoint, no brain-penetrating H(1) receptor agonists have been identified that would have antiobesity effects. Despite conflicting preclinical data, insights are emerging into the potential role of histamine H(3) receptors as a target of antiobesity therapeutics(11)
12. Histamine and the effects on nasal mucous membrane
In the study to examine the reliability of suppression of the histamine wheal and flare reaction in the skin to predict an antihistamine's clinical efficacy in two common allergic diseases seasonal allergic rhinitis and chronic idiopathic urticaria, showed that although histamine is one mediator in the allergic response in the skin and nasal mucosa, many other agents are important modulators of the allergic response. In addition, the major structural and functional differences that exist between the nasal mucosa and the skin affect the type of local response. These manifest themselves as differences between the responses to antigen and histamine challenge in the skin and the nose. The allergic responses in these tissues are not simply the consequence of one chemical but are the result of a cascade of interactions among various cells and mediators. The clinical manifestations of these complex interactions obviously cannot be fully replicated by injection of one chemical mediator, histamine, into the outer layer of the skin. Studies with antihistamines have shown that certain drugs, such as cetirizine, are more suppressive than others (loratadine, terfenadine) in controlling the histamine-induced wheal and flare reaction in the skin. When the clinical efficacy of these medications is compared in clinical trials in seasonal allergic rhinitis and chronic idiopathic urticaria, all are equally efficacious in controlling symptoms(12).
13. Histamine and smooth muscle cells
Acoording to the study by The University of Tennessee, histamine markedly induces protein kinase D (PKD) activation in human aortic smooth muscle cells (HASMCs). PKD belongs to a family of serine/threonine protein kinases, and its function in vascular disease is largely unknown. Histamine-induced PKD phosphorylation is dependent on the activation of histamine receptor 1 (H1) and protein kinase C (PKC). PKD2 predominantly mediates histamine-induced TF expression via the p38 MAPK pathway, while PKD1 mediates histamine-induced TF expression through a p38 MAPK-independent pathway. PKD is a new component in histamine signaling in live cells and that PKD has a novel function in the histamine signaling pathway leading to gene expression, as evidenced by TF expression. Importantly, our data reveal a regulatory link from histamine to PKD and TF, providing new insights into the mechanisms of coagulation and the development of atherothrombosis(13).
14. Histamine and variant angina and acute coronary syndromes
Histamine can induce coronary vasospasm, leading to variant angina and acute myocardial infarction, according to the study by Cardiovascular Research, Physiology Institute, University of Zurich, histamine induces expression of TF, but not TF pathway inhibitor, in vascular cells via activation of the H1, but not H2, receptor. This effect is mediated by the MAP kinases p38, ERK, and JNK. This observation may open novel perspectives in the treatment of variant angina and acute coronary syndromes(14).
15. Histamine and endumetrium
In the study to investigate whether histamine was taken up by perivascular adrenergic nerves and released by periarterial nerve stimulation (PNS) to induce vascular responses, showed that histamine treatment for 20 min induced PNS-induced vasoconstriction followed by vasodilation without affecting CGRP-induced vasodilation. Chlorpheniramine, guanethidine, combination of histamine and desipramine, and endothelium-removal abolished PNS-induced vasodilation in histamine-treated preparations. These results suggest that histamine taken up by and released from adrenergic nerves by PNS causes endothelium-dependent vasodilation in rat mesenteric arteries(15).
16. Histamine H4 receptor and CNS
Histamine is a biogenic amine that mediates multiple physiological processes, including immunomodulatory effects in allergic and inflammatory reactions, and also plays a key regulatory role in experimental allergic encephalomyelitis, the autoimmune model of multiple sclerosis. According to the Immunobiology Program, University of Vermont, H(4)R plays a role in determining the frequency of T regulatory (T(R)) cells in secondary lymphoid tissues, and regulates T(R) cell chemotaxis and suppressor activity. Moreover, the lack of H(4)R leads to an impairment of an anti-inflammatory response due to fewer T(R) cells in the CNS during the acute phase of the disease and an increase in the proportion of Th17 cells(16).
17. Histamine-induced vasodilation and vasoconstriction
In the study to examine the vascular response to histamine in rat perfused mesenteric vascular beds with active tone, suggested that histamine induced endothelium-dependent vasodilation via endothelium histamine H(1) receptors and endothelium-independent vasodilation via smooth muscle histamine H(2) receptors. It is also suggested that the histamine-induced endothelium-independent vasoconstriction and vasodilation are mediated by histamine H(1) receptors and perivascular nerves(17).
18. Histamine on Monocyte Adhesion to Vascular Endothelial Cells
The histamine level is high during allergic attacks, and patients with allergy may have chronic inflammatory conditions at which tumor necrosis factor (TNF)-α is extensively released by macrophages. In the study in vitro static and microfluidic flow assays conducted to investigate the combined influence of histamine and TNF-α on adhesion of monocytic THP-1 cells to human umbilical vein endothelial cells (HUVEC), showed that the number of crawling and firmly adherent THP-1 cells was higher on TNF-α + histamine activated HUVEC than on HUVEC activated by TNF-α alone. This synergistic effect of histamine and TNF-α is caused by the increased endothelial surface expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin. Since the exposure of TNF-α-activated endothelium to histamine favors monocyte recruitment, it may be a serious risk factor for atherosclerosis and other inflammatory disorders(18).
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(18) http://www.ncbi.nlm.nih.gov/pubmed/23053728 Sources