Insulin Secretion in Heart Failure

Sharma, B; Majid, P A; Pakrashi, Brojesh C.; Dykes, J. R. W.; Sh, Taylor

doi:10.1136/bmj.2.5706.396

Cited by 25 publications

(10 citation statements)

References 9 publications

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“…One physiological role of such a system may be to protect normal individuals from ketoacidosis during periods of great stress such as burns, severe congestive heart fail-ure, and myocardial infarction. Although these states have been associated with increased catechol output (11)(12)(13) and severe inhibition of acute insulin release (14)(15)(16), the maintenance of normal or elevated basal insulin levels appears adequate to suppress lipolysis and may account for the rarity of ketoacidosis in these conditions.…”

Section: Discussionmentioning

confidence: 99%

Epinephrine: selective inhibition of the acute insulin response to glucose

Lerner¹,

Porte²

1971

J. Clin. Invest.

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A B S T R A C T An epinephrine infusion of 6 gsg/min decreased the rapid insulin response to a 5 g glucose pulse by 96% (P < 0.001) compared with the preinfusion control. In contrast when an identical epinephrine infusion was superimposed on a prolonged glucose infusion, elevated steady-state insulin levels did not decrease, but increased from 26.9 ±6 (mean -+SD, UU/ml) to 56.8 ±15 AU/ml (P < 0.05) in parallel with the epinephrineinduced hyperglycemia. Thus epinephrine inhibition of insulin secretion was observed during acute but not chronic glucose stimulation. To evaluate further the insulin responses during a prolonged glucose infusion, a 5 g glucose pulse was given iefore and 60 min later during a concomitant epinephrine infusion. Although the acute insulin response to the first glucose pulse was observed during the elevated steady-state glucose and insulin levels associated with the glucose infusion, epinephrine again inhibited the acute insulin response to the subsequent 5 g glucose pulse by 91% (P < 0.01 ). Thus epinephrine appears to inhibit selectively the rapid insulin response to glucose but not to influence insulin output stimulated by prolonged hyperglycemia. These observations provide further evidence for a model of insulin secretion which includes a small storage pool available for immediate release to a glucose challenge and a more slowly responding pool regulating insulin secretion in the basal and steady state.

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Section: Discussionmentioning

confidence: 99%

Epinephrine: selective inhibition of the acute insulin response to glucose

Lerner¹,

Porte²

1971

J. Clin. Invest.

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“…Though many factors may regulate insulin secretion, the dominating control exercised by the sympathetic nervous system is seen in a number of clinical situations. In patients with greatly increased sympathetic nervous activity due to cardiogenic shock (Allison et al, 1969;Taylor et al, 1969), severe heart failure (Sharma et al, 1970), hypothermia (Baum and Porte, 1968), and phaeochromocytoma (Wilber et al, 1966;Spergel et al, 1968;Colwell, 1969;Porte, 1969) the secretion of insulin is completely suppressed even though the blood glucose concentration is greatly raised. The insulin suppression in these patients is maintained even when challenged by such a potent insulinogenic stimulus as intravenous tolbutamide Majid et al, 1970;Sharma et al, 1970).…”

Section: Discussionmentioning

confidence: 99%

“…The normal insulin secretion response to glucose and tolbutamide is suppressed in patients with severe power failure of the heart, whether this is due to cardiogenic shock after myocardial infarction (Allison et al, 1969;Taylor et al, 1969), severe congestive heart failure (Sharma et al, 1970), or pumping failure after open-heart surgery . Evidence has suggested that one of the major factors responsible for this suppression of insulin secretion was the greatly increased sympathetic stimulation found in such patients Majid et al, 1970;Sharma et al, 1970).…”

Section: Introductionmentioning

confidence: 99%

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Autonomic Control of Insulin Secretion and the Treatment of Heart Failure

Majid¹,

Saxton²,

Dykes³

et al. 1970

BMJ

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The families studied in the present work yield VA -0-65 for post-phenobarbitone phenylbutazone half-life corrected for height. These results are clearly of much the same order. The same genes do not control the two characters, since the postphenobarbitone phenylbutazone half-life data have been adjusted to a standard height. Therapeutic ImplicationsSome drugs are known to show a correlation between plasma level and (1) therapeutic effect and (2) occurrence of toxic (or adverse) effects. Bruck et al. (1954) showed that various toxic effects were more common in patients receiving phenylbutazone whose blood levels exceeded 100 pg./ml. than in those with concentrations below this level. On the other hand, subjective improvement in rheumatoid arthritics was more frequent above blood phenylbutazone concentrations of 50 pg./ml. than below this level. The variability in phenylbutazone half-life is therefore relevant in regard to the consequences of phenylbutazone therapy. It is also relevant that for a pharmacological phenomenon in a population of patients, Vp may be increased by additions to VE owing, for example, to disease, differing modes of administration, etc. On the other hand, VG cannot be diminished. Thus possibly in the future attention to the variability between persons may result in the development of improved therapeutics.

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“…This is of considerable clinical interest in the light of the recent finding that insulin secretion is suppressed in patients with severe heart failure (Sharma, Majid, Pakrashi, Dykes & Taylor, 1970;Majid, Saxton, Dykes, Galvin & Taylor, 1970), particularly as digitalis glycosides are frequently employed in the treatment of these patients. However, as the relief of heart failure itself results in significant improvement in insulin secretion (Sharma et al, 1970; the direct importance of these glycosides in the relief of insulin suppression in such patients is difficult to define. Triner et al (1969) also suggested that the mechanism whereby ouabain exerted its hypoglycaemic activity was either by suppression of release of catecholamines or by interference with their metabolic effects.…”

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confidence: 97%

Effect of Ouabain on Insulin Secretion in Man

et al. 1972

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S U M M A R Y1. The effect of an intravenous infusion of ouabain 0.25 pg min-' kg-' for 1 h on plasma insulin and blood glucose concentrations in peripheral venous blood and on urinary excretion of catecholamines was studied in six normal adult males. Ouabain had no effect on insulin and glucose concentrations but resulted in a significant decrease in urinary catecholamine excretion.2. The effect of a single intravenous injection of 0.01 mg of ouabain/kg on the response of insulin secretion to intravenous tolbutamide was studied in four normal adult males. Ouabain had no significant effect on the increase of plasma insulin which followed tolbutamide.3. These results indicate that improvement in insulin secretion observed during digitalis-induced remission in heart failure is probably due to the improved circulatory state of the patient and not to a direct insulin secretogogue effect. 4.The mechanisms responsible for decreased catecholamine excretion after ouabain in normal man are unexplained.

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Insulin Secretion in Heart Failure

Cited by 25 publications

References 9 publications

Epinephrine: selective inhibition of the acute insulin response to glucose

Epinephrine: selective inhibition of the acute insulin response to glucose

Autonomic Control of Insulin Secretion and the Treatment of Heart Failure

Effect of Ouabain on Insulin Secretion in Man

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