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A. G. WATTS
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G. FINK
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We have investigated the effects of constant light on the patterns of LH release in long-term ovariectomized rats. Some animals were implanted with a silicone elastomer capsule containing oestradiol-17β. Plasma samples in anaesthetized animals were taken from the external jugular vein and in conscious animals from an indwelling intra-atrial catheter. The pulsatile release of LH that occurred in animals not treated with oestrogen was unaffected by constant light or the steroid anaesthetic alphaxalone plus alphadolone acetate (Althesin), but was abolished by sodium pentobarbitone. However, the diurnal release of LH produced by increasing the concentrations of plasma oestradiol in conscious animals was blocked by constant light. Thus, these two rhythms of LH release are controlled by different neural pathways; the one concerned with diurnal LH release being suppressed by exposure to constant light.

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A. M. Horn
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A. G. Watts
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ABSTRACT

The aim of this study was to determine the effect of 5-hydroxytryptamine (5-HT) uptake blockade on 5-HT turnover by measuring the concentrations of 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) in brain with the aid of high performance liquid chromatography and electrochemical detection. The indoleamines were measured in the anterior hypothalamus (AH), posterior hypothalamus (PH) and raphe nuclei 30 min after the i.v. injection of either alaproclate (30 mg/kg) or zimelidine (20 mg/kg). The effect of alaproclate was studied in male rats, pro-oestrous female rats, rats ovariectomized and injected s.c. with 20 μg oestradiol benzoate (OB) on dioestrus and at 12.00 h of the next day (presumptive pro-oestrus) with 2 mg progesterone (model 1) and rats ovariectomized 3–4 weeks before an s.c. injection of 20 μg OB followed 72 h later by an s.c. injection of 2 mg progesterone (model 2). Alaproclate caused a significant decrease in the 5-HIAA/5-HT ratio in the AH and PH of the brain of male rats, in the PH and raphe nuclei in pro-oestrous rats and model 1, and in the raphe nuclei alone in model 2. Zimelidine had no effect on the 5-HIAA/5-HT ratio in any area in model 2. In male rats the injection of parachlorophenylalanine produced a marked reduction in the brain concentrations of 5-HT and 5-HIAA, but the 5-HIAA/5-HT ratio was unchanged by a subsequent injection of alaproclate. None of the pharmacological agents affected significantly the brain concentrations of noradrenaline, dopamine or dihydroxyphenylacetic acid.

These results together with the data in the preceding paper show that in female rats changes in LH and prolactin secretion produced by alaproclate may reflect changes in central 5-HT turnover.

J. Endocr. (1985) 104, 407–413

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ALISON SPEIGHT
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RACHEL POPKIN
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A. G. WATTS
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G. FINK
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We have investigated the mechanism by which oestradiol-17β augments pituitary responsiveness to luteinizing hormone releasing factor (LH-RF). Adult rats were ovariectomized on the morning of dioestrus and implanted with either an empty silicone elastomer capsule or a capsule containing oestradiol-17β. Twelve hours later the LH response, tested by injecting 50 ng LH-RF/100 g i.v., was significantly greater in animals implanted with an oestradiol capsule compared with that in animals implanted with an empty capsule. The effect of oestradiol was blocked by sodium pentobarbitone administered 4 h before the test, and this block was overcome by infusing LH-RF during the 4 h period at doses which by themselves were not sufficient to evoke a large release of LH. We also measured LH-RF in pituitary stalk blood collected under Althesin anaesthesia between 4–6 and 12–13 h after ovariectomy and capsule implantation. The concentration of LH-RF in stalk plasma fell between these two collection periods in animals implanted with empty but not with oestradiol-filled capsules. The concentrations of LH-RF in stalk plasma, although relatively low, were significantly higher in animals bearing an oestradiol-containing capsule than the concentrations in peripheral plasma from similarly treated animals, and, by comparison with the LH-RF concentrations in peripheral plasma from animals infused with LH-RF, were sufficiently high to increase significantly the responsiveness of the pituitary gland. These data show that as well as acting directly on the pituitary gonadotrophs, oestradiol-17β increases the responsiveness of the anterior pituitary gland by a mechanism that involves the release and the priming effect of LH-RF.

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A. G. Watts
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W. J. Sheward
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D. Whale
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G. Fink
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ABSTRACT

To investigate the role of suprachiasmatic efferent connections in the expression of diurnal hormone rhythms, the efferent pathway from the suprachiasmatic nucleus (the putative circadian generator in the rat) to the sub-paraventricular zone (the main terminal area of suprachiasmatic efferents) was disrupted using bilateral horizontal knife cuts in ovariectomized oestrogen-treated rats. The position of the knife cut was assessed by observing its effect on vasoactive intestinal polypeptide immunoreactivity (a marker for suprachiasmatic efferents into the sub-paraventricular zone). The size of both the diurnal plasma LH and prolactin surges was markedly and consistently reduced over the 3-week period following the lesion in animals with a total deafferentation of the sub-paraventricular zone, compared with sham-operated animals or lesioned animals with an intact sub-paraventricular zone. When lesioned animals were grouped according to the presence or absence of damage to the preoptic area, no significant differences were found in the sizes of the plasma hormone surges. When similar knife cuts were given to animals whose activity cycles were observed, no significant effects were noted in the ability of the animals to synchronize to a light/dark regime or to free-run in constant light conditions. These results suggest that the suprachiasmatic nucleus influences the diurnal surges of plasma LH and prolactin in oestrogen-treated ovariectomized rats, initially by an interaction with the sub-paraventricular zone, and not by a direct influence on gonadotrophin-releasing hormone neurones or other more rostral structures.

Journal of Endocrinology (1989) 122, 593–604

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P. J. HEALD
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K. A. ROOKLEDGE
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B. E. FURNIVAL
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G. D. WATTS
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SUMMARY

The luteinizing hormone (LH) content of the anterior pituitary of the domestic fowl has been determined at different times during the interval between successive clutches of eggs. The LH content remained constant for 12–14 hr. after the ovulation of the last egg of the sequence, decreased 16 hr. before ovulation, rose again to a peak 12 hr. before ovulation and decreased to lower levels 4 and 8 hr. before the ovulation itself, at which point levels had risen to the normal values. These changes are discussed in relation to the lighting sequence and times of oviposition. It is suggested that the decreased levels 4–8 hr. before ovulation represents the release of ovulatory LH.

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P. J. HEALD
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K. A. ROOKLEDGE
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B. E. FURNIVAL
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G. D. WATTS
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SUMMARY

Groups of laying mature domestic fowl were injected i.m. with varying doses of either oestradiol benzoate, testosterone propionate or progesterone and were killed at random intervals throughout the day without reference to any specific point in the ovulatory cycle. Luteinizing hormone (LH) was assayed in the anterior pituitaries of each group. It was shown that oestradiol in doses calculated to be equal to or above the physiological level, increased pituitary LH without necessarily affecting the laying cycle. Testosterone had no significant effect on pituitary LH, while progesterone significantly increased pituitary LH at doses which had no apparent effect upon ovulation. Doses effective in the laying hen had little or no effect on the pituitary content of LH in immature birds. The results in the laying hen are in harmony with the concept previously proposed, by which changes in the levels of circulating plasma oestrogens may regulate the ovulatory pattern of the fowl by inhibiting release of pituitary LH.

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Anna G Holmes Diabetes and Metabolism Division, School of Medical Sciences, St Vincent's Institute and Department of Medicine, CSIRO Molecular and Health Technologies, Department of Physiology, Cellular and Molecular Metabolism Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia

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Jose L Mesa Diabetes and Metabolism Division, School of Medical Sciences, St Vincent's Institute and Department of Medicine, CSIRO Molecular and Health Technologies, Department of Physiology, Cellular and Molecular Metabolism Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia

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Bronwyn A Neill Diabetes and Metabolism Division, School of Medical Sciences, St Vincent's Institute and Department of Medicine, CSIRO Molecular and Health Technologies, Department of Physiology, Cellular and Molecular Metabolism Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia
Diabetes and Metabolism Division, School of Medical Sciences, St Vincent's Institute and Department of Medicine, CSIRO Molecular and Health Technologies, Department of Physiology, Cellular and Molecular Metabolism Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia

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Jason Chung Diabetes and Metabolism Division, School of Medical Sciences, St Vincent's Institute and Department of Medicine, CSIRO Molecular and Health Technologies, Department of Physiology, Cellular and Molecular Metabolism Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia

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Andrew L Carey Diabetes and Metabolism Division, School of Medical Sciences, St Vincent's Institute and Department of Medicine, CSIRO Molecular and Health Technologies, Department of Physiology, Cellular and Molecular Metabolism Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia

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Gregory R Steinberg Diabetes and Metabolism Division, School of Medical Sciences, St Vincent's Institute and Department of Medicine, CSIRO Molecular and Health Technologies, Department of Physiology, Cellular and Molecular Metabolism Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia

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Bruce E Kemp Diabetes and Metabolism Division, School of Medical Sciences, St Vincent's Institute and Department of Medicine, CSIRO Molecular and Health Technologies, Department of Physiology, Cellular and Molecular Metabolism Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia
Diabetes and Metabolism Division, School of Medical Sciences, St Vincent's Institute and Department of Medicine, CSIRO Molecular and Health Technologies, Department of Physiology, Cellular and Molecular Metabolism Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia

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Robert J Southgate Diabetes and Metabolism Division, School of Medical Sciences, St Vincent's Institute and Department of Medicine, CSIRO Molecular and Health Technologies, Department of Physiology, Cellular and Molecular Metabolism Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia

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Graeme I Lancaster Diabetes and Metabolism Division, School of Medical Sciences, St Vincent's Institute and Department of Medicine, CSIRO Molecular and Health Technologies, Department of Physiology, Cellular and Molecular Metabolism Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia

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Clinton R Bruce Diabetes and Metabolism Division, School of Medical Sciences, St Vincent's Institute and Department of Medicine, CSIRO Molecular and Health Technologies, Department of Physiology, Cellular and Molecular Metabolism Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia

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Matthew J Watt Diabetes and Metabolism Division, School of Medical Sciences, St Vincent's Institute and Department of Medicine, CSIRO Molecular and Health Technologies, Department of Physiology, Cellular and Molecular Metabolism Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia

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Mark A Febbraio Diabetes and Metabolism Division, School of Medical Sciences, St Vincent's Institute and Department of Medicine, CSIRO Molecular and Health Technologies, Department of Physiology, Cellular and Molecular Metabolism Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Road Central, Melbourne, Victoria 8008, Australia

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Chronic elevations in interleukin (IL)-6 have been associated with insulin resistance, but acute IL-6 administration can enhance insulin sensitivity. Our aim was to exogenously administer IL-6 to rats to elicit either chronic or repeated acute elevations in systemic IL-6. We hypothesized that a continuous elevation of IL-6 would inhibit glucose tolerance and insulin sensitivity while acute intermittent elevations would improve it. Male Wistar rats were treated for 14d with recombinant human IL-6 (2.4 μg/day) or saline administered either by miniosmotic pump (continuous IL-6) or via twice-daily injection (intermittent IL-6). Glucose and insulin tolerance tests were performed following 14-d treatment and 24 h later rats were administered a bolus of insulin (150 mU/g) or saline intraperitoneally. Approximately, 10 min after insulin injection soleus, gastrocnemius and liver were excised and rapidly frozen in liquid nitrogen for subsequent metabolic measures. Irrespective of the mode of delivery, IL-6 treatment increased basal insulin sensitivity, as measured by the homeostatic model assessment of insulin resistance, and enhanced glucose clearance during an i.p. glucose tolerance test. IL-6 increased circulating fatty acids, but did not increase triglyceride accumulation in either skeletal muscle or liver, while it increased the protein expression of both PPARα and UCP2 in skeletal muscle, suggesting that IL-6 can enhance fat oxidation via mitochondrial uncoupling. These data demonstrate that, irrespective of the mode of delivery, IL-6 administration over 2 weeks enhances glucose tolerance. Our results do not support the notion that prolonged chronically elevated IL-6 impairs insulin action in vivo.

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