S
Stewart A. Metz
Researcher at Veterans Health Administration
Publications - 10
Citations - 329
Stewart A. Metz is an academic researcher from Veterans Health Administration. The author has contributed to research in topics: Insulin & Phospholipase C. The author has an hindex of 6, co-authored 10 publications receiving 321 citations. Previous affiliations of Stewart A. Metz include Anschutz Medical Campus & Royal Melbourne Hospital.
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Journal ArticleDOI
Induction of Defective Insulin Secretion and Impaired Glucose Tolerance by Clonidine Selective Stimulation of Metabolic Alpha-adrenergic Pathways
TL;DR: It is concluded that clonidine causes hyperglycemia and inhibits insulin secretion through an alpha-adrenergic mechanism and appears to selectively stimulate metabolic adrenergic pathways different from those operative in vasomotor regulation.
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Lysophosphatidylinositol, but not lysophosphatidic acid, stimulates insulin release
Stewart A. Metz,Stewart A. Metz +1 more
TL;DR: Dunlop et al. as discussed by the authors showed that lysophosphatidylinositol is shown to promote insulin release in a manner having characteristics of physiologic exocytosis-that is, it is dose-dependent, saturable, reversible, inhibitable and unassociated with detrimental effects on subsequent islet functioning.
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Autonomic Epilepsy: Clonidine Blockade of Paroxysmal Catecholamine Release and Flushing
TL;DR: This patient represents a rare case of autonomic epilepsy with the seizure focus in the temporal lobe and an epileptic pathogenesis was suggested by stereotypic olfactory and epigastric prodromata before spells, and abolition of paroxysms with the anticonvulsant carbamazepine.
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Production of phosphatidylethanol by phospholipase D phosphatidyl transferase in intact or dispersed pancreatic islets: evidence for the in situ metabolism of phosphatidylethanol.
Stewart A. Metz,Stewart A. Metz,Stewart A. Metz,Marjorie Dunlop,Marjorie Dunlop,Marjorie Dunlop +5 more
TL;DR: In view of the recent findings that phosphatidic acid (or exogenous phospholipase D) has potent insulinotropic effects, this pathway could play a role in stimulus-secretion coupling and stimulation of transphosphatidylation at the expense of hydrolysis could contribute to the inhibition of secretion caused by ethanol.
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Prostaglandin E2 Metabolite Levels During Diabetic Ketoacidosis
TL;DR: It is suggested that elevated PGE-m levels early in the onset of DKA may represent a host-defense mechanism, and P GE-m, glucagon, and catecholamine levels promptly return to normal levels when insulin therapy is reinstituted.