INT1322
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
To determine insulin secretory reserve after islet transplant, we performed studies of glucose potentiation of arginine-induced insulin secretion (GPAIS) in eight recipients of intrahepatic islet autotransplants. | |||||||||||||||
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To evaluate possible synergistic interactions between these inhibitory agents upon the regulation of insulin release in man, we examined the effects of PGE, epinephrine and the long-acting met-enkephalin analogue FK 33-824, given alone or in combination, upon glucose-induced insulin secretion in normal man. | |||||||||||||||
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Similarly, the negative effect of FK 33-824 upon glucose-induced insulin secretion was reversed by sodium salicylate. | |||||||||||||||
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Prostaglandin E (PGE), epinephrine and metenkephalin are three endogenous substances normally present in the endocrine pancreas which have been reported to inhibit glucose-induced insulin secretion in normal humans. | |||||||||||||||
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The inhibitory effect of epinephrine (15 ng/kg/min) upon glucose-induced insulin secretion was partially reversed by sodium salicylate, an inhibitor of endogenous prostaglandin synthesis, which increased but not normalized, either the acute insulin response and the glucose disappearance rates. | |||||||||||||||
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This study seems to indicate that hyperproduction of endogenous opioid peptides in obesity increases insulin secretion stimulated by food intake, whereas it does not appreciably affect insulin production stimulated by circulating glucose or aminoacids. | |||||||||||||||
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To evaluate the hypothesis that an increased sensitivity to these endogenous substances may play a role in defective insulin secretion in diabetes, we evaluated the effects of three blocking drugs upon the impaired insulin response to glucose in Type II diabetic subjects, as well as glucose-induced insulin secretion in normal humans. | |||||||||||||||
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Interactions between naloxone, phentolamine and lysine acetylsalicylate upon glucose induced insulin release. | |||||||||||||||
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In diabetics, acute insulin responses to glucose were significantly increased by all the agents tested (naloxone, phentolamine and lysine acetylsalicylate), but only the cyclooxygenase inhibitor significantly augmented second phase insulin secretion and glucose disappearance rates. | |||||||||||||||
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Acute insulin response to glucose (mean change 3-10 min insulin), second phase insulin secretion (change 10-60 min), as well as glucose disappearance rates (%/min) were significantly increased in the diabetics receiving the two higher doses of naloxone (2 and 4 mg, respectively). | |||||||||||||||
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Approved by the FDA in 2005 as an adjunct therapy for type 2 diabetes, exenatide given as twice-daily injections enhances insulin release in response to elevated blood glucose levels, inhibits glucagon secretion after meals, slows the rate of gastric emptying (which reduces nutrient absorption into the bloodstream), and increases satiety thereby promoting reduced food intake [54]. | |||||||||||||||
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Under these conditions, glucose stimulated insulin release. | |||||||||||||||
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Again, with no possibility of further action on the K(ATP) channel, glucose stimulated insulin release. | |||||||||||||||
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The results reveal that harmane, pinoline, and norharmane cause a dose- and glucose-dependent increase in insulin secretion but show that this response differs in a number of ways from that elicited by the well-characterized I(3)-agonist, efaroxan. | |||||||||||||||
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On the contrary, 0.2 mg/kg (i.e. 12-14 mg per subject as total amount) given to 3 women and 6 men led to a glucose-induced insulin release significantly lower than that recorded in basal conditions, with corresponding greater plasma glucose elevation. | |||||||||||||||
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Evidence has been presented that an endogenous I(3) ligand may exist, because extracts of brain contain an active principle that stimulates insulin secretion in a manner consistent with the involvement of I(3) sites. | |||||||||||||||
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Quinine is known to cause deterioration in patients with myasthenia gravis and erythema multiforme, to stimulate insulin release in patients receiving treatment for falicparum malaria, and to be responsible at times for ataxia following moderate overdosage. | |||||||||||||||
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High carbohydrate diets, by increasing the insulin secretion, may worsen insulin resistance in diabetic patients and increase the inflammatory and prothrombotic tendencies in this patient population. | |||||||||||||||
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Parasympathetic cholinergic influence was studied using 500 mumol/l carbamylcholine, which increased insulin secretion. | |||||||||||||||
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We found that IPC insulin release increased markedly following a step increase of glucose from 2.8 to 25 mM (see Figure 4Q). | |||||||||||||||
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General Comments
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