Immunoassay of 6-Hydroxymelatonin Sulfate in Human Plasma and Urine: Abolition of the Urinary 24-Hour Rhythm with Atenolol*

Arendt, Joséphine; Bojkowski, C.; Franey, Christine; Wright, John W.; Marks, Vincent

doi:10.1210/jcem-60-6-1166

Cited by 327 publications

(138 citation statements)

References 18 publications

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“…Twenty-four hour output of 6-s-melatonin was measured in coded urine samples by laboratory personnel who were blind to study condition. A modification of the radioimmunoassay procedure of Arendt et al (1985) was used, utilizing reagents that were supplied by CID Tech Research Inc. (Mississauga, Ontario, Canada). Using an 125 I-labeled tracer, the assay has a sensitivity of 4 pg/ml (for urine diluted 1:250) and intraassay and interassay coefficients of variability of 8 and 10%, respectively.…”

Section: Methodsmentioning

confidence: 99%

Noradrenergic Function and Clinical Outcome in Antidepressant Pharmacotherapy

Miller

Ekstrom

Mason

et al. 2001

Neuropsychopharmacology

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Controversy remains regarding the role of noradrenergic systems in determining clinical response to antidepressant pharmacotherapy. Pineal gland production of melatonin can serve as a physiologic index of noradrenergic function. The aim of this study was to examine the effects of antidepressant treatment on 24-hour urinary excretion of the principle metabolite of melatonin, 6-sulfatoxymelatonin in treatment responders and nonresponders. Twenty-four outpatients meeting DSM-III-R criteria for MajorThe introduction of effective antidepressant pharmacotherapies in the 1950s revolutionized the treatment of mood disorders. However, despite several decades of research, the mechanisms of action of antidepressants remain unclear. Elucidation of these mechanisms is of considerable clinical, as well as scientific, importance. Although the majority of patients respond to treatment, a substantial minority do not, and insights regarding the necessary psychobiologic components of treatment response could help predict, and perhaps prevent, some cases of treatment failure.Early observations focused attention on the role of norepinephrine (NE) in determining antidepressant response. All of the original antidepressants, including the tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs), enhance noradrenergic neurotransmission, either directly or via active metabolites. Based on these observations, early theories of antidepressant action proposed that clinical response is related to increased noradrenergic activity in the brain (Schildkraut 1969). Later studies found that most antidepressants, including those with minimal direct biochemical effects on NE, can influence noradrenergic systems. For example, lithium, electroconvulsive therapy, the dopamine reuptake inhibitor bupropion, and the serotonin (5-HT) reuptake inhibitor zimelidine all decrease "whole-body norepinephrine turnover"; that 24 , NO . 6 is, the 24-hour excretion of NE and its major metabolites (Linnoila et al. 1983;Rudorfer et al. 1984;. Central NE turnover, as measured by cerebrospinal fluid concentrations of the NE metabolite 3-methoxy-4-hydroxy-phenylglycol (MHPG), is also reduced by a variety of antidepressants, including the 5-HT specific reuptake inhibitor zimelidine (Potter et al. 1985). Based on these observations, it seems that increased noradrenergic function is an integral component of antidepressant treatments.On the other hand, a wide variety of antidepressants, including tricyclic NE and 5-HT reuptake inhibitors, monoamine oxidase inhibitors, and repeated electroconvulsive shock, down-regulate the density of ␤ -adrenergic receptor ( ␤ AR) ligand-binding sites in limbic brain regions, including the cerebral cortex and the hippocampus (Vetulani and Sulser 1975;Banerjee et al. 1977;Sugrue 1983). Furthermore, nearly all antidepressants diminish the ability of ␤ ARs to stimulate adenylate cyclase-mediated cAMP production in these regions (Vetulani and Sulser 1975;Charney et al. 1981), and the time course for these receptor changes ...

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Section: Methodsmentioning

confidence: 99%

Noradrenergic Function and Clinical Outcome in Antidepressant Pharmacotherapy

Miller

Ekstrom

Mason

et al. 2001

Neuropsychopharmacology

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“…The interassay coefficients of variation were less than 5% for these assays. Plasma immunoreactive insulin (Hampton & Withey 1993) and aMT6s (Arendt et al 1985, modified by Aldous & Arendt 1988) were measured using in-house RIAs. The interassay coefficients of variation were less than 10% for these assays.…”

Section: Assay Proceduresmentioning

confidence: 99%

Postprandial hormone and metabolic responses amongst shift workers in Antarctica

Lund¹,

Arendt²,

Hampton³

et al. 2001

Journal of Endocrinology

180

120

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The circadian rhythms of many night-shift workers are maladapted to their imposed behavioural schedule, and this factor may be implicated in the increased occurrence of cardiovascular disease (CVD) reported in shift workers. One way in which CVD risk could be mediated is through inappropriate hormonal and metabolic responses to meals. This study investigated the responses to standard meals at different circadian times in a group of night-shift workers on a British Antarctic Survey station at Halley Bay (75 S) in Antarctica.Twelve healthy subjects (ten men and two women) were recruited. Their postprandial hormone and metabolic responses to an identical mixed test meal of 3330 kJ were measured on three occasions: (i) during daytime on a normal working day, (ii) during night-time at the beginning of a period of night-shift work, and (iii) during the daytime on return from nightworking to daytime working. Venous blood was taken for 9 h after the meal for the measurement of glucose, insulin, triacylglycerol (TAG) and non-esterified fatty acids. Urine was collected 4-hourly (longer during sleep) on each test day for assessment of the circadian phase via 6-sulphatoxymelatonin (aMT6s) assay.During normal daytime working, aMT6s acrophase was delayed (7·7 1·0 h (...)) compared with that previously found in temperate zones in a comparable age-group. During the night shift a further delay was evident (11·8 1·9 h) and subjects' acrophases remained delayed 2 days after return to daytime working (12·4 1·8 h). Integrated postprandial glucose, insulin and TAG responses were significantly elevated during the night shift compared with normal daytime working. Two days after their return to daytime working, subjects' postprandial glucose and insulin responses had returned to pre-shift levels; however, integrated TAG levels remained significantly elevated.These results are very similar to those previously found in simulated night-shift conditions; it is the first time such changes have been reported in real shift workers in field conditions. They provide evidence that the abnormal metabolic responses to meals taken at night during unadapted night shifts are due, at least in part, to a relative insulin resistance, which could contribute to the documented cardiovascular morbidity associated with shift work. When applied to the 20% of the UK workforce currently employed on shift work, these findings have major significance from an occupational health perspective.

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“…The interassay coefficients of variation were less than 5% for these assays. Plasma immunoreactive insulin (Hampton & Withey 1993), proinsulin (Hampton et al 1988), C-peptide (Hampton 1983), glucose-dependent insulinotropic polypeptide (GIP) (Morgan et al 1978) and aMT6 s (Arendt et al 1985, modified as described by Aldhous & Arendt 1988) were all measured using in-house RIAs. The interassay coefficients of variation were less than 10% for these assays.…”

Section: Assay Proceduresmentioning

confidence: 99%

Altered postprandial hormone and metabolic responses in a simulated shift work environment

Ribeiro¹,

Hampton²,

Morgan³

et al. 1998

Journal of Endocrinology

138

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The circadian rhythms of most night shift workers do not adapt fully to the imposed behavioural schedule, and this factor is considered to be responsible for many of the reported health problems. One way in which such disturbances might be mediated is through inappropriate hormonal and metabolic responses to meals, on the night shift.Twelve healthy subjects (four males and eight females) were studied on three occasions at the same clock time (1330 h), but at different body clock times, after consuming test meals, first in their normal environment, secondly after a forced 9 h phase advance (body clock time approximately 2230 h) and then again 2 days later in the normal environment. They were given a low-fat pre-meal at 0800 h, then a test meal at 1330 h with blood sampling for the following 9 h. Parameters measured included plasma glucose, non-esterified fatty acids (NEFAs), triacylglycerol (TAG), insulin, C-peptide, proinsulin and glucosedependent insulinotropic polypeptide, and urinary 6-sulphatoxymelatonin.In contrast with a previous study with a high-fat premeal, postprandial glucose and insulin responses were not affected by the phase shift. However, basal plasma NEFAs were lower immediately after the phase shift (P<0·05). Incremental (difference from basal) TAG responses were significantly higher (P<0·05) immediately after the phase shift compared with before. Two-day post-phase shift responses showed partial reversion to baseline values.This study suggests that it takes at least 2 days to adapt to eating meals on a simulated night shift, and that the nutritional content of the pre-meals consumed can have a marked effect on postprandial responses during a simulated phase shift. Such findings may provide a partial explanation for the increased occurrence of cardiovascular disease reported in shift workers.

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Immunoassay of 6-Hydroxymelatonin Sulfate in Human Plasma and Urine: Abolition of the Urinary 24-Hour Rhythm with Atenolol*

Cited by 327 publications

References 18 publications

Noradrenergic Function and Clinical Outcome in Antidepressant Pharmacotherapy

Noradrenergic Function and Clinical Outcome in Antidepressant Pharmacotherapy

Postprandial hormone and metabolic responses amongst shift workers in Antarctica

Altered postprandial hormone and metabolic responses in a simulated shift work environment

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