Effects of glucagon on adenosine 3′,5′-monophosphate and guanosine 3′,5′-monophosphate in human plasma and urine

Broadus, Arthur E.; Kaminsky, Neil I.; Northcutt, Robert C.; Hardman, Joel G.; Sutherland, Earl W.; Liddle, Grant W.

doi:10.1172/jci106442

Cited by 197 publications

(90 citation statements)

References 39 publications

(39 reference statements)

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“…The doses of glucagon used in these studies, however, were far in excess of the dose used in the present study. In an attempt to determine whether low-dose glucagon infusion stimulates adrenal catecholamine release, Broadus and co-workers infused glucagon at 100 ng/kg/ min, twice the level of the present study, yet noted no change in blood pressure, pulse, nor half-hourly urinary catecholamines (55).…”

Section: Discussioncontrasting

confidence: 45%

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

Liljenquist¹,

Bomboy²,

Lewis³

et al. 1974

J. Clin. Invest.

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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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Section: Discussioncontrasting

confidence: 45%

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

Liljenquist¹,

Bomboy²,

Lewis³

et al. 1974

J. Clin. Invest.

Self Cite

138

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“…These patients have a diminished excretion of cyclic AMP in urine in response to PTH stimulation [9,17]. Broadus et al [2] have speculated on an active renal tubular secretion of cyclic AMP. Thus, patients with pseudohypoparathyroidism, as well as the neonate, need to be investigated in relation to such hypotheses as deficient transport of cyclic AMP.…”

Section: Discussionmentioning

confidence: 99%

“…Activation of adenyl cyclase results in increased cyclic AMP in renal parenchyma [16,18] and increased cyclic AMP excretion in urine [1,2,4,8]. Full term newborn infants have been shown to have a diminished responsiveness to PTH infusions and a developmental increase in responsiveness during the first few days of life [11].…”

Section: Introductionmentioning

confidence: 99%

The Effect of Parathyroid Hormone on Rabbit Renal Cortex Adenyl Cyclase during Development

Linarelli

Bobik

1973

Pediatr Res

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ExtractRenal cortex from fetal and neonatal rabbits (from 4-5 days preterm to 4 days of age) shows results comparable with maternal renal cortex during in vitro stimulation of the 2,200 X g pellet with parathyroid hormone (PTH) at 20 /ug/ml. Incubation with sodium fluoride (10 HIM), a nonspecific potent stimulator of adenyl cyclase, resulted in comparable increases in both the fetal and the maternal renal cortex. Glucagon, prostaglandin Ei, and vasopressin, all at 20 jug/ml, stimulate adenyl cyclase to a lesser extent than PTH. Homogenates of full term neonatal rabbits and maternal renal cortex show comparable phosphodiesterase enzyme levels with or without 0.04 M imidazole. These data show that in fetal and early neonatal renal cortex there is no developmental adenyl cyclase responsiveness to PTH. Similarly, phosphodiesterase is present equally in term and maternal rabbit renal cortex. Speculation

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“…(1), and that certain hormones can greatly alter the concentration of these cyclic nucleotides in plasma and urine (2)(3)(4)(5)(6)(7)(8). For example, cAMP levels in plasma and urine can be increased by the administration of parathyroid hormone (PTH) (3), glucagon (4), or epinephrine (4)(5)(6), and infusions of calcium (2) and norepinephrine (5,6) are each capable of elevating plasma and urinary cGMP. It is therefore possible that determinations of the level of these cyclic nucleotides in plasma and urine could be of considerable value in the investigation and diagnosis of human disease states.…”

mentioning

confidence: 99%

Sources of Cyclic Nucleotides in Plasma

Wehmann¹,

Blonde²,

Steiner³

1974

J. Clin. Invest.

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A B S T R A C T In order to determine the sites of net production and removal of the cyclic nucleotides in plasma, various blood vessels were catheterized in 17 anesthetized dogs and arterial and venous concentrations of adenosine 3',5'-monophosphate (cAMP) and guanosine 3',5'-monophosphate (cGMTP) were measured by radioimmunoassay.Aortic cAMP was 30±2 nM (mean±SE) and cGMP was 13+1 nM. There were no significant differences for either cyclic nucleotide between the concentration in the aorta and that in the inferior vena cava, coronary sinus, hepatic vein, and femoral vein. The concentration of cAMP in renal venous plasma was 25% lower than in aortic plasma, and renal venous cGMP was 51% lower than in the aorta. The pulmonary arterial concentrations of cAMP and cGMP were slightly lower than in the aorta. The concentration of cGMP in the superior mesenteric vein plasma was 83% greater than in aortic plasma; the concentration of cAMP in this vessel was only 16% greater than that in the aorta. Superior vena cava concentrations of both cyclic nucleotides were slightly greater than arterial concentrations.The results suggest that: (a) the kidneys are a major site of removal of both cyclic nucleotides from plasma. (b) The lungs may be a site of net addition of both cyclic nucleotides to plasma. (c) The small in-

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Effects of glucagon on adenosine 3′,5′-monophosphate and guanosine 3′,5′-monophosphate in human plasma and urine

Cited by 197 publications

References 39 publications

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

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

The Effect of Parathyroid Hormone on Rabbit Renal Cortex Adenyl Cyclase during Development

Sources of Cyclic Nucleotides in Plasma

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