The effect of adrenergic blocking agents on plasma insulin and blood glucose during urethan or epinephrine induced hyperglycemia

Kansal, Prakash C.; Buse, Maria G.

doi:10.1016/0026-0495(67)90085-6

Cited by 20 publications

(5 citation statements)

References 10 publications

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“…Infusion of adrenaline or noradrenaline inhibits the rise in plasma insulin that would otherwise occur in response to hyperglycemia, produced either by the adrenaline itself or by administered glucose (PORTE et aI., 1966;PORTE and WILLIAMS, 1966;KARAM et aI., 1966;HERTELENDY et aI., 1966;KRIS et aI., 1966;CAMPBELL and RASTOGI, 1966). a-Adrenergic blockade with phentolamine prevents the inhibition and permits a rise in plasma insulin concentration (PORTE, 1967a;KANSAL and BUSE, 1967) whereas p-adrenergic blockade (with propranolol) potentiates the inhibition (POR-TE, 1967 a): stimulation of p-adrenergic receptors (with isopropylnoradrenaline) increases plasma insulin concentration (PORTE, 1967b).…”

Section: C) Role Of Catecholamines In the Regulation Of Insulin Secrementioning

confidence: 95%

Effects of Catecholamines on Metabolism

Himms‐Hagen¹

1972

Catecholamines

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Section: C) Role Of Catecholamines In the Regulation Of Insulin Secrementioning

confidence: 95%

Effects of Catecholamines on Metabolism

Himms‐Hagen¹

1972

Catecholamines

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“…Islet preparations were allowed to incubate at 370C in tissue culture medium 199 with 15% fetal bovine serum under 95% air/5% CO2 for [16][17][18] h with two to three medium changes. This method results in relative enrichment of islets because much of the exocrine tissue undergoes autolysis and islet harvesting is facilitated (14).…”

Section: Superoxide Dismutase Derivatizationsmentioning

confidence: 99%

Protective Role of Superoxide Dismutase against Diabetogenic Drugs

Gandy¹,

Buse²,

Crouch³

1982

J. Clin. Invest.

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125

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A B S T R A C T Copper-zinc superoxide dismutase (SOD) is present in relatively high concentrations in the ,-cells of human islets. The activity of the extracted enzyme is partially inhibited upon incubation with the diabetogenic drugs alloxan, streptozotocin, or Vacor. The role of this enzyme in protecting a-cells against chemically induced diabetes was further investigated.Incubation of intact canine islets with alloxan (0.2 mg/ml) and 4 mM glucose decreased the insulin secretory response by 87% during subsequent exposure to 28 mM glucose. Concomitantly the SOD-specific activity (units of enzyme activity per milligram immunoreactive SOD) decreased 50% in alloxan-exposed islets. When islets were protected from alloxan toxicity by including 28 mM glucose with alloxan, the insulin secretory response and SOD specific activity remained identical to controls. Thus, SOD specific activity correlates with maintenance of ,B-cell function.To test the effectiveness of SOD against streptozotocin in vitro, canine islets were incubated 10 min with or without streptozotocin (0.1 mg/ml) with 4 mM glucose; their functional integrity was tested subsequently as the insulin secretory response to 28 mM glucose. Exposure to streptozotocin alone decreased the response by 70%; inclusion of SOD (1.5 mg/ml) before and during exposure to streptozotocin completely prevented this effect. Cyanide-inactivated SOD was not effective.The potential of SOD to prevent streptozotocin-induced diabetes was tested in rats in vivo. SOD injected 10 s or 50 min before streptozotocin prevented or significantly attenuated diabetes. Injection of SOD and streptozotocin simultaneously was much less effective, and cyanide-inactivated SOP was ineffective. No protection was afforded by injection of SOD 12 or 24 h before streptozotocin.

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“…This effect is weaker in animals in the postprandial state probably because of the lack of effect on insulin secretion; it is, however, weak when compared to that of endogenous catecholamines. Although in mammals phentolamine reduces the hyperglycaemic effect of epinephrine (Porte 1967;Kansal and Buse 1967), no direct effect of the a blocker has been noted on basal glucose level (Buse, Johnson, Kuperminc and Buse 1970). This is not the case in the duck where plasma glucose drops very sharply in animals in the postprandial state, and less in fasted ones.…”

Section: ) Alpha Adrenergic Receptors and Glucose Metabolismmentioning

confidence: 86%

Modulation by the Nutritional State of Adrenergic Receptor Mediated Effects on Insulin Secretion in Ducks

Gross¹,

Mialhe²

1982

Horm Metab Res

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The effects of exogenous (IV Norepinephrine (NE)) and endogenous alpha adrenergic activity (IV phentolamine (PH)) were studied in the duck. Our aim was first to compare their importance in animals fed for 1 1/2 hours and fasted for 24 and 48 hours, and then to assess the relative importance of alpha versus beta adrenergic receptor mediated effects during the development of a 48-hour-fast. NE reduces plasma IRI levels after a fast but not in the postprandial state. PH while ineffective in animals fed for 1 1/2 hours brings fasting IRI values to levels observed in the former group. Twenty-four hour fasted ducks are sensitive to both alpha adrenergic stimulation and beta adrenergic blockade which have additive effects; so, insulin secretion is controlled by 2 distinct mechanisms: a beta stimulating and an alpha inhibiting one. The importance of one component versus the other is modulated by the nutritional state: indeed, a double alpha and beta equimolar adrenergic blockade reveals that during the transition from the postprandial state to a 48-hour-fast, there is a progressive reversal in the importance of one adrenergic component versus the other. The effects of alpha adrenergic stimulation or blockade occur independently of simultaneous glucose variations. This is not the case for A cell function: an alpha adrenergic receptor stimulating effect on glucagon secretion exists, but A cell remains primarily sensitive to plasma glucose level. alpha Adrenergic activity has no direct effect on plasma free fatty acids (FFA) level but plays a role in plasma glucose level regulation especially in animals in the postprandial state.

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The effect of adrenergic blocking agents on plasma insulin and blood glucose during urethan or epinephrine induced hyperglycemia

Cited by 20 publications

References 10 publications

Effects of Catecholamines on Metabolism

Effects of Catecholamines on Metabolism

Protective Role of Superoxide Dismutase against Diabetogenic Drugs

Modulation by the Nutritional State of Adrenergic Receptor Mediated Effects on Insulin Secretion in Ducks

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