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cholinergic
كولينِيُّ الفِعْل
Dernière mise à jour : 1970-01-01
Fréquence d'utilisation : 1
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a cholinergic.
حقنة تحفيز
Dernière mise à jour : 2016-10-27
Fréquence d'utilisation : 2
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in addition to muscle weakness or fasciculations, some or all of the signs of a cholinergic crisis may develop
وبالإضافة إلى ضعف العضلات أو الارتجافات الحزمية، قد تطور بعض أو كافة أعراض النوبة الكولينية
as a consequence, an increased activity in the cholinergic system associated with improved cognitive function can be achieved in patients with dementia of the alzheimer type
ونتيجة لذلك، يمكن حدوث نشاط زائد في النظام الكوليني مصحوبًا بتحسن في الوظائف الإدراكية للمرضى الذين يعانون من أحد أنواع الزهايمر
effects included a dose dependent inhibition of cholinesterase in plasma, erythrocytes and brain, with other symptoms of cholinergic toxicity such as convulsions, reduced body weight or body weight gain.
وشملت التأثيرات تثبيطاً مرتبطاً بالجرعة لأنزيمات الكولينيستيراز في البلاسما والكريات الحمر والدماغ، ترافقه أعراض أخرى من أعراض التسمم الكوليني، كالاختلاجات وتناقص وزن الجسم أو تناقص زيادة الوزن.
eight male volunteers were given a daily oral dose of 0.25 mg/kg bw/day for 28 days without effect on cholinergic signs or erythrocyte acetylcholinesterase activity.
وأعطي ثمانية من المتطوعين الذكور جرعة فموية يومية قدرها 0,25 ملغ/كغ من وزن الجسم يومياً لمدة 28 يوماً دون أن يؤثر ذلك على مؤشرات نشاط الكولين أو نشاط أنزيمات الكولينيستيراز في الكريات الحمر.
longer-term modifi cation may occur via infl uences on β cell mass and differentiation.11 given insulin’s pivotal role in glucose utilisation and metabolism, it is not surprising that glucose has multiple infl uences on insulin biosynthesis and secretion. however, other factors such as amino acids, fatty acids, acetylcholine, pituitary adenylate cyclase-activating polypeptide (pacap), glucose-dependent insulinotropic polypeptide (gip), glucagon-like peptide-1 (glp-1), and several other agonists, together in combination, also infl uence these processes.10 mechanisms of insulin secretion increased levels of glucose induce the “fi rst phase” of glucose-mediated insulin secretion by release of insulin from secretory granules in the β cell. glucose entry into the β cell is sensed by glucokinase, which phosphorylates glucose to glucose-6-phosphate (g6p), generating atp.12 closure of k+ -atp-dependent channels results in membrane depolarization and activation of voltage dependent calcium channels leading to an increase in intracellular calcium concentration; this triggers pulsatile insulin secretion.13 augmentation of this response occurs by both a k+ -atp channel-independent ca2+-dependent pathway and k+ -atp channel-independent ca2+-independent pathways of glucose action.10 other mediators of insulin release include activation of phospholipases and protein kinase c (e.g. by acetycholine) and by stimulation of adenylyl cyclase activity and activation of β cell protein kinase a, which potentiates insulin secretion. this latter mechanism may be activated by hormones, such as vasoactive intestinal peptide (vip), pacap, glp-1, and gip. these factors appear to play a signifi cant role in the second phase of glucose mediated insulin secretion, after refi lling of secretory granules translocated from reserve pools.10 regulation and mechanisms of insulin secretion at the cellular level synthesis and secretion of insulin is regulated by both nutrient and non-nutrient secretagogues, in the context of environmental stimuli and the interplay of other hormones.8 nutrient secretagogues such as glucose appear to trigger insulin secretion from the β cell by increasing intracellular atp and closing of k+ -atp channels as outlined above. generation of cyclic amp and other cellular energy intermediates is also augmented, further enhancing insulin release. glucose does not require insulin action to enter the β cell (nor do fructose, mannose or galactose).8 non-nutrient secretagogues may act via neural stimuli such as cholinergic and adrenergic pathways, or through peptide hormones and cationic amino acids. neural stimuli 1. cholinergic transmission it has been well recognised that vagus nerve stimulation results in pancreatic insulin secretion. this is thought to mediate the so-called “cephalic phase” of insulin secretion, occurring when food is seen, smelled or acutely ingested. islet cell cholinergic muscarinic receptors activate phospholipase c, with subsequent intracellular events activating protein kinase c, phospholipase a2 and mobilizing intracellular calcium. insulin secretion by these mechanisms does not occur in the fasting state or if blood glucose levels are low, but may augment the anabolic response to feeding.8 2. adrenergic pathway catecholamines, through α2-adrenoceptors, typically inhibit insulin release during stress and exercise. the pancreas also has β-adrenoceptors, which enhance insulin secretion via camp, but this effect appears to be minor. the α2-mediated effects appear to act downstream to those of nutrient secretogogues.8 peptide hormones a number of peptide hormones infl uence insulin secretion. the gut hormones glp-114 and somatostatin enhance and inhibit insulin action respectively. their secretion is stimulated by nutrients in the gut. their mechanisms of action appear to be, at least in part, mediated by camp generation and activation of a camp-responsive protein kinase.8 leptin and adiponectin appear to act in a similar fashion whereas acylation-stimulating protein appears to work via glucose phosphorylation, calcium infl ux and protein kinase c.15 amino acids the insulinotropic effect of the cationic amino acid arginine is well established. l-ornithine has similar effects. arginine’s action is associated with an increase in potassium permeability without any effect on proinsulin biosynthesis. uptake of arginine into the β cell is associated with depolarization of the cell membrane and gating of voltage dependent calcium channels.8 leucine, an essential branched chain amino acid, is a potent enhancer of insulin secretion, allosterically stimulating glutamate dehydrogenase and forming α-ketoglutarate via the krebs cycle to generate atp.12 the major pathways and infl uences on insulin secretion are presented schematically in figure 1. factors infl uencing β cell mass longer term regulation of insulin secretion may be mediated via effects on β cell mass. growth hormone, prolactin, placental lactogen and glp-1 not only increase glucose- stimulated insulin release and insulin gene expression, but also increase β cell proliferation.11,14 for a comprehensive review on this topic see nielsen and serup.16 physiology of insulin secretion glucose is the principal stimulus for insulin secretion, though
