Elevation of Plasma Epinephrine Levels Produced by Glucagon<i>in Vivo</i>

Sarcione, Edward J.; Back, Nathan; Sokal, Joseph E.; Mehlman, Ben; Knoblock, Edward C.

doi:10.1210/endo-72-4-523

Cited by 66 publications

(18 citation statements)

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“…Hypoglycemia is a stimulus for the release of glucagon [18] and it has been postulated that the adrenal medullary response to hypoglycemia was caused by the increase in circulating glucagon [14,15]. In our study, when the cats were killed 1 h after the injection of insulin or glucagon, the decreases of adrenaline and noradrenaline were similar, being independent from the changes in plasma glucose and adrenal corticosteroids.…”

Section: Discussionsupporting

confidence: 62%

“…It has been suggested that the increase in the adrenal medullary secretion produced by hypoglycemia may not be due to the depression in blood glucose per se [14,[21][22][23]. Hypoglycemia is a stimulus for the release of glucagon [18] and it has been postulated that the adrenal medullary response to hypoglycemia was caused by the increase in circulating glucagon [14,15].…”

Section: Discussionmentioning

confidence: 99%

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Effects of Insulin, Glucagon and Adrenocorticotrophin on the Levels of Corticosteroids, Noradrenaline, Adrenaline and Ascorbic Acid in the Adrenal Glands of Cats

Lloréns

Borrell

1973

Horm Res

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The concentration of noradrenaline, adrenaline, corticosteroids and ascorbic acid in the adrenal glands of intact cats was studied after administration of adrenocorticotrophin (ACTH), insulin or glucagon. The animals were injected intraperitoneally with either hormone and killed 1or 3 h later. Significant increases of corticosteroids were found in all experiments after ACTH or insulin but a significant decrease was observed 1 h after glucagon administration. Adrenal ascorbic acid decreased significantly 1 and 3 h after ACTH but only 1 h after treatment with insulin, and glucagon, or when both hormones were given simultaneously. A significant increase in the content of adrenaline was found 3 h after single ACTH injection in the absence of significant variation of the levels of noradrenaline in the adrenal gland. Significant decreases of noradrenaline and adrenaline were found 1 and 3 h after insulin as well as 1 h after glucagon administration. A decrease of catecholamines was also obtained following the simultaneous administration of insulin and glucagon. These findings suggest that the decrease in adrenaline may be secondary to the significant decrease in adrenal noradrenaline; they also indicate that in the intact cat the glucocorticoid levels may regulate the methylation of noradrenaline without being, however, the only factor involved in the control of adrenaline production by the adrenal gland.

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Effects of Insulin, Glucagon and Adrenocorticotrophin on the Levels of Corticosteroids, Noradrenaline, Adrenaline and Ascorbic Acid in the Adrenal Glands of Cats

Lloréns

Borrell

1973

Horm Res

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“…This statement is based on the observation that the results in the two groups did not differ significantly in regard to hepatic glucose and cAMP release. There may be two reasons (34)(35)(36) which also stimulate hepatocellular cAMP formation (2). To determine if the glucagonnlediated rise in plasma cAMP could be attributed to secondary catecholamine release, Broadus et al compared a 100 ng/kg/min glucagon infusion with a 450 pmol/kg/ min epinephrine infusion (13).…”

Section: Results and Commentsmentioning

confidence: 99%

Effect of Glucagon on Net Splanchnic Cyclic AMP Production in Normal and Diabetic Men

Liljenquist¹,

Bomboy²,

Lewis³

et al. 1974

J. Clin. Invest.

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A B S T R A C T Glucagon activates hepatic adenylate cyclase, thereby increasing acutely the liver content of cyclic AMP (cAMP) as well as the release of cAMP into the hepatic vein. Insulin, on the other hand, antagonizes this glucagon-mediated cAMP production, thus providing a hypothetical mechanism through which insulin might correct some of the metabolic abnormalities of diabetes.To study this hormonal interaction in man, net splanchnic cAMP production (NScAMPP) was investigated in normal and insulin-dependent diabetic men under basal conditions and in response to intravenous glucagon, 50 ng/kg/nmin for 2 h.In normals (n = 19), basal hepatic vein cAMP concentration was 23.6±1.1 nM and NScAMPP was 1.7±0.6 nmol/min. Glucagon stimulated NScAMPP in four normal subjects to a peak of 99.6±43 nmol/min at 25 min with a subsequent fall to 12.4±5.1 nmol/min by 90 min despite continuing glucagon infusion. Endogenous insulin secretion was stimulated as indicated by rising levels of immunoreactive insulin and C-peptide (connecting peptide) immunoreactivity, raising the possibility that endogenous insulin might be responsible for the fall in NScAMPP that followed the initial spike.In the diabetics (n = 8), basal hepatic vein cAMP concentration was 24.7±1.2 nM and NScAMPP was undetectable. Glucagon stimulated NScAMPP in five diabetics to a peak of 169.9±42.6 with a subsequent fall to 17.4±3.9 nmol/min by 90 min even though endogenous

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“…Glucagon in pharmacological doses, has long been known to stimulate adrenal cathecholamine release (50)(51)(52) and both epinephrine and norepinephrine are known lipolytic agents in man (9). Indeed, the initial and transient rise in circulating FFA noted after large bolus injections of glucagon has been attributed to glucagoninduced mobilization of catecholamines (23,53,54).…”

Section: Discussionmentioning

confidence: 99%

Effects of Glucagon on Lipolysis and Ketogenesis in Normal and Diabetic Men

Liljenquist¹,

Bomboy²,

Lewis³

et al. 1974

J. Clin. Invest.

138

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A B S T R A C T The effect of glucagon (50 ng/kg/min) on arterial glycerol concentration and net splanchnic production of total ketones and glucose was studied after an overnight fast in four normal and five insulin-dependent diabetic men. Brachial artery and hepatic vein catheters were inserted and splanchnic blood flow determined using indocyanine green. The glucagon infusion resulted in a mean circulating plasma level of 4,420 pg/mI.In the normal subjects, the glucagon infusion resulted in stimulation of insulin secretion indicated by rising levels of immunoreactive insulin and C-peptide immunoreactivity. Arterial glycerol concentration (an index of lipolysis) declined markedly and net splanchnic total ketone production was virtually abolished. In contrast, the diabetic subjects secreted no insulin (no rise in C-peptide immunoreactivity) in response to glucagon. Arterial glycerol and net splanchnic total ketone production in these subjects rose significantly (P = < 0.05) when compared with the results in four diabetics who received a saline infusion after undergoing the same catheterization procedure.Net splanchnic glucose production rose markedly during glucagon stimulation in the normals and diabetics despite the marked rise in insulin in the normals. Thus, the same level of circulating insulin which markedly suppressed lipolysis and ketogenesis in the normals failed to inhibit the glucagon-mediated increase in net splanchnic glucose production. It is concluded (a) that glucagon at high concentration is capable of stimulating lipolysis and ketogenesis in insulin-deficient diabetic man; (b) that insulin, mole for mole, has more antilipolytic activity in man than glucagon has lipolytic activity; and (c) that glucagon, on a molar basis, has greater stimulatory activity than insulin has inhibitory activity on hepatic glucose release.

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Elevation of Plasma Epinephrine Levels Produced by Glucagonin Vivo

Cited by 66 publications

References 0 publications

Effects of Insulin, Glucagon and Adrenocorticotrophin on the Levels of Corticosteroids, Noradrenaline, Adrenaline and Ascorbic Acid in the Adrenal Glands of Cats

Effects of Insulin, Glucagon and Adrenocorticotrophin on the Levels of Corticosteroids, Noradrenaline, Adrenaline and Ascorbic Acid in the Adrenal Glands of Cats

Effect of Glucagon on Net Splanchnic Cyclic AMP Production in Normal and Diabetic Men

Effects of Glucagon on Lipolysis and Ketogenesis in Normal and Diabetic Men

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