Drug-Induced Diabetes

Dollery, C. T.; Pentecost, B L; Samaan, Naguib A.

doi:10.1016/s0140-6736(62)90567-6

Cited by 129 publications

(28 citation statements)

References 5 publications

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“…Diazoxide, an antihypertensive benzothiadiazine (1), produces hyperglycemia in vivo (2)(3)(4)(5)(6)(7)(8)(9) and is presently used in the management of intractable hypoglycemia in man (5). It would appear that this hyperglycemic ac-tion is exerted through both pancreatic (6)(7)(8)(9) and extrapancreatic effects (10,11).…”

Section: Introductionmentioning

confidence: 99%

Diazoxide effects on biphasic insulin release: “adrenergic” suppression and enhancement in the perifused rat pancreas

Burr¹,

Marliss²,

Stauffacher³

et al. 1971

J. Clin. Invest.

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A B S T R A C T An in vitro system for perifusion of rat pancreas has been used to investigate the effects of diazoxide on glucose-induced insulin release. Administration of diazoxide with a stimulating concentration of glucose produced a dose-dependent suppression of insulin release. This effect was partly reversed by phentolamine. In the presence of nonstimulatory-concentrations of glucose, diazoxide plus phentolamine, but neither alone, stimulated a biphasic release of insulin similar to that observed with 1-isopropyl norepinephrine. A prior period of perifusion with a low concentration of diazoxide enhanced the primary component of subsequent glucose-stimulated insulin release, an effect inhibited by addition of either phentolamine or propranolol to the diazoxide during this "prestimulation" period. These effects are similar to those observed with epinephrine. By contrast with epinephrine however, increasing the concentration of diazoxide during the period before glucose stimulation enhanced both the primary and secondary components of subsequent glucoseinduced insulin release. These data suggest that at least some of the direct effects of diazoxide on the pancreas are mediated through a-and P-adrenergic receptor mechanisms.

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Section: Introductionmentioning

confidence: 99%

Diazoxide effects on biphasic insulin release: “adrenergic” suppression and enhancement in the perifused rat pancreas

Burr¹,

Marliss²,

Stauffacher³

et al. 1971

J. Clin. Invest.

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show abstract

“…Diazoxide 1 is an antihypertensive agent with potent hyperglycemic activity, particularly when used in combination with trichlormethiazide 2 (3)(4)(5). The mode of action by which these compounds exert a temporary diabetogenic effect has not been established.…”

mentioning

confidence: 99%

Benzothiadiazine suppression of insulin release from normal and abnormal islet tissue in man.

Fajans¹,

Floyd²,

Knopf³

et al. 1966

J. Clin. Invest.

152

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“…Like many vasodilatory antihypertensive drugs, diazoxide induces fluid retention (Dollery et al, 1962). Whether or not the reduction in blood pressure, hence filtration rate, is the sole reason for salt and water retention, both this propensity and that related to hyperglycaemia seem to be offset or reduced by the presence of a natriuretic sulphamoyl group resident in the chlorothiazide but not the diazoxide structure.…”

mentioning

confidence: 99%

Chlorothiazide.

Kh¹

1982

Brit J Clinical Pharma

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Drug-Induced Diabetes

Cited by 129 publications

References 5 publications

Diazoxide effects on biphasic insulin release: “adrenergic” suppression and enhancement in the perifused rat pancreas

Diazoxide effects on biphasic insulin release: “adrenergic” suppression and enhancement in the perifused rat pancreas

Benzothiadiazine suppression of insulin release from normal and abnormal islet tissue in man.

Chlorothiazide.

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