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J. F. SMITH
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T. J. ROBINSON
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SUMMARY

Progesterone levels were determined in the ovarian and jugular vein plasma and the corpus luteum of 68 cyclic Merino ewes (controls) and of 32 ewes which had been treated with intravaginal sponges containing a synthetic progestagen (Cronolone, Searle). The weight and diameter of the corpus luteum and the rate of flow of the ovarian vein blood were also recorded. No corrections for procedural losses were made.

The control ewes showed highly significant (P < 0·001) cyclic changes in the progesterone contents of the ovarian vein plasma and the corpus luteum, and in the mass of the corpus luteum. There were positive correlations (P < 0·001) between ovarian vein plasma progesterone concentration and the weight (r = 0·651), diameter (r = 0·692), total progesterone content (r = 0·775) and progesterone concentration (r = 0·574) of the corpus luteum.

Cyclic changes in the progesterone content of the jugular vein failed to attain significance (0·1 < P < 0·2) but the levels were positively correlated with those in the ovarian vein (r = 0·465, P < 0·001) and with weight (r = 0·432, P < 0·001) and diameter (r = 0·303, P < 0·05) of the corpus luteum.

The Cronolone-treated ewes showed cyclic changes in luteal function similar to those in controls, with the exception of animals treated on the day of oestrus. In ewes in which ovulation was not suppressed, the duration of activity of the corpus luteum, as measured by progesterone concentration in ovarian vein plasma, and concentration and content in the corpus luteum was significantly reduced. By the 12th day of the cycle the corpus luteum had almost completely regressed both morphologically and functionally.

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J. F. SMITH
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T. J. ROBINSON
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SUMMARY

The levels of free oestrogen (oestrone and oestradiol-17β) in plasma in the ovarian vein were determined in three groups, each of 27 ewes, at nine intervals at about the time of oestrus. One group had a normal oestrus while the other two had been treated for 16 days with intravaginal sponges containing either 10 or 30 mg of a synthetic progestagen (Cronolone, Searle).

In untreated ewes, the mean level (corrected) of oestradiol-17β in plasma from the active ovary rose from 25·3 ng/100 ml at −48 h to a peak of 91·6 ng/100 ml at 0 h (onset of oestrus) and then fell. There was evidence of biphasic production. The mean level of oestrone was relatively high (13·0 ng/100 ml) at −48 h; it fell to 2·0 ng/100 ml between −36 and −24 h and then rose again to 9·4 ng/100 ml at + 12 h. There was no significant change, with time, in the plasma levels of either oestrogen from the non-active ovary. The total amounts of oestradiol-17β and of oestrone produced from both ovaries at an oestrous period were estimated to average 9·7 and 2·4 μg.

In treated ewes, a similar pattern of production of oestradiol-17β was shown by the ewes treated with 30 mg Cronolone. That of ewes treated with 10 mg differed (P < 0·01). Peak level was reached at an earlier stage, relative to the onset of oestrus, and it declined more rapidly, the total amount of oestrogen produced (oestrone + oestradiol-17β) was less (10 mg Cronolone, 8·6 μg; 30 mg Cronolone, 12·1 μg; normal oestrus, 12·1 μg), and there was no biphasic production.

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T. J. HAYDEN
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S. V. SMITH
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The response of. prolactin receptor and lactose synthetase to suppression of plasma concentrations of prolactin was examined in normal and occluded (teat-sealed) mammary glands of Sprague–Dawley rats. Rats, with mammary glands unilaterally occluded, were given bromocriptine (2·5 mg/kg per 12 h) between days 5 and 8 post partum. Bromocriptine reduced plasma prolactin concentrations from 460·4±120·8 (mean ±s.e.m.) to 2·56 ± 0·89 ng/ml within 12 h whilst concentrations in control rats were 553·4± 110·25 ng/ml. Lactose synthetase activity declined rapidly, within 24 h, in occluded glands of both groups but was maintained for 24 h in normal glands of bromocriptine-treated rats and decreased thereafter. Prolactin receptors also declined significantly within 24 h in occluded glands. Desaturation of the prolactin receptor by bromocriptine treatment in vivo was compared with desaturation by exposure of membranes to MgCl2 in vitro. Both treatments enhanced prolactin binding but the increase after treatment with MgCl2 may have been partly artefactual since there was a selective loss of protein from the membranes. These results indicate that the prolactin receptor in rat mammary gland may be maintained after acute suppression of prolactin secretion.

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T. A. Parkening
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T. J. Collins
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E. R. Smith
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Plasma levels of LH were measured in young sexually mature (2- to 5-month-old) and aged (13- to 20-month-old) female C57BL/6 mice, Syrian hamsters and Wistar rats using a radioimmunoassay (RIA) and a radioreceptor assay (RRA). There were no statistically significant differences when comparing data from the two assays when examining young oestrous and dioestrous mice. Aged oestrous and dioestrous mice exhibited significantly higher levels of LH as measured by RIA than by RRA. Levels of LH analysed by RIA were also higher in aged mice compared with those in younger mice. Comparing LH concentrations with the two types of assays in younger dioestrous and aged anoestrous hamsters produced similar results. In contrast, aged pseudopregnant rats exhibited significantly lower levels of plasma LH than younger dioestrous females and there were no differences in RIA and RRA values. There were also no differences when comparing data from the two assays in younger rats. The mean (± s.e.m.) RRA: RIA ratios of 0·96 ± 0·05 (oestrous) and 0·96 ± 0·04 (dioestrous) for younger mice and 0·92 ± 0·08 for younger hamsters were significantly higher than the ratios of 0·66 ± 0·72± 0·05 and 0·71 ± 0·05 respectively of their aged counterparts. The mean RRA: RIA ratios in the two age groups of rats were almost identical (0·79 ± 0·05 and 0·80 ± 0·10). These studies suggested that a portion of the higher LH levels detectable by RIA in some aged female rodents results from qualitative changes in the LH molecule.

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Campbell J L Harter School of Human Sciences, The University of Western Australia, Perth, Western Australia, Australia

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Georgia S Kavanagh School of Human Sciences, The University of Western Australia, Perth, Western Australia, Australia

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Jeremy T Smith School of Human Sciences, The University of Western Australia, Perth, Western Australia, Australia

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Kisspeptin is a neuropeptide with a critical role in the function of the hypothalamic–pituitary–gonadal (HPG) axis. Kisspeptin is produced by two major populations of neurons located in the hypothalamus, the rostral periventricular region of the third ventricle (RP3V) and arcuate nucleus (ARC). These neurons project to and activate gonadotrophin-releasing hormone (GnRH) neurons (acting via the kisspeptin receptor, Kiss1r) in the hypothalamus and stimulate the secretion of GnRH. Gonadal sex steroids stimulate kisspeptin neurons in the RP3V, but inhibit kisspeptin neurons in the ARC, which is the underlying mechanism for positive- and negative feedback respectively, and it is now commonly accepted that the ARC kisspeptin neurons act as the GnRH pulse generator. Due to kisspeptin’s profound effect on the HPG axis, a focus of recent research has been on afferent inputs to kisspeptin neurons and one specific area of interest has been energy balance, which is thought to facilitate effects such as suppressing fertility in those with under- or severe over-nutrition. Alternatively, evidence is building for a direct role for kisspeptin in regulating energy balance and metabolism. Kiss1r-knockout (KO) mice exhibit increased adiposity and reduced energy expenditure. Although the mechanisms underlying these observations are currently unknown, Kiss1r is expressed in adipose tissue and potentially brown adipose tissue (BAT) and Kiss1rKO mice exhibit reduced energy expenditure. Recent studies are now looking at the effects of kisspeptin signalling on behaviour, with clinical evidence emerging of kisspeptin affecting sexual behaviour, further investigation of potential neuronal pathways are warranted.

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J Turinsky
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A Damrau-Abney
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J S Elmendorf
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T R Smith
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Abstract

Preincubation of rat soleus muscle with 1 and 10 μm monensin for 2 h increased the subsequent basal 2-deoxyglucose uptake by muscle 76 and 121% respectively. Under the same conditions, monensin decreased the insulin-stimulated (1 mU/ml) 2-deoxyglucose uptake by 29 and 37% respectively. The monensin-induced augmentation of basal 2-deoxyglucose uptake was inhibited 92% by cytochalasin B suggesting that the uptake is mediated by glucose transporters. Monensin did not increase the cellular accumulation of l-glucose in muscle indicating that it does not affect the cell membrane integrity. Neither the stimulatory effect of monensin on basal 2-deoxyglucose uptake nor the opposite, inhibitory action of monensin on the insulin-stimulated 2-deoxyglucose uptake were influenced by the removal of Ca2+ from the medium or by dantrolene, an inhibitor of Ca2+ release from the sarcoplasmic reticulum, suggesting that the actions of monensin are not mediated by calcium. Monensin had no effect on muscle ATP concentration. The monensin-induced augmentation of basal 2-deoxyglucose uptake was neither associated with stimulation of muscle phosphatidylinositol 3-kinase activity nor inhibited by wortmannin, demonstrating that the increase in basal 2-deoxyglucose uptake is not mediated by activation of phosphatidylinositol 3-kinase. The inhibition of insulin-stimulated 2-deoxyglucose uptake by monensin was associated with a 31% decrease in the abundance of insulin receptors in muscles, a 64% decrease in the insulin-induced autophosphorylation of the insulin receptor β-subunit, and a 44% reduction of the insulin-stimulated phosphatidylinositol 3-kinase activity. Addition of monensin into the phosphatidylinositol 3-kinase reaction had no effect on the activity of the enzyme, demonstrating that the inhibition in monensin-treated muscles is indirect and occurs upstream of phosphatidylinositol 3-kinase. It is concluded that monensin has a dual effect on 2-deoxyglucose uptake by skeletal muscle: it stimulates basal uptake but inhibits the insulin-stimulated uptake. The primary cause of the latter, inhibitory effect of monensin is at the level of the insulin receptor.

Journal of Endocrinology (1997) 154, 85–93

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C. J. LOVELL-SMITH
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J. G. T. SNEYD
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SUMMARY

Isolated fat cells from young New Zealand obese mice (NZO/Bl) showed an impaired rate of glycerol release in response to isoprenaline. Old animals showed an increased rate of glycerol release.

The impaired lipolysis in young animals may be caused by failure of the adenosine 3′,5′-cyclic monophosphate level to rise normally when isolated fat cells are treated with isoprenaline. It is proposed that the impaired lipolysis in young NZO/Bl mice is important in the development of obesity.

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I. D. SMITH
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J. M. BASSETT
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T. WILLIAMS
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Progesterone levels in the peripheral blood of non-pregnant mares have been measured by Short (1959); progesterone was detectable only when there was a fully developed corpus luteum present in the ovaries. On the other hand, Short (1964) has shown that progesterone secretion into the ovarian vein, negligible at oestrus, increases very significantly within the first 24–36 hr. after ovulation. More sensitive methods for the measurement of progesterone concentration in peripheral plasma have since been developed. Peripheral plasma progesterone concentrations have been measured throughout the menstrual cycle of women (Neill, Johansson, Datta & Knobil, 1967a) and monkeys (Neill, Johansson & Knobil, 1967b) and throughout the oestrous cycle of the ewe (Thorburn, Bassett & Smith, 1969) by competitive protein-binding techniques and in cows, pigs and sheep by gas—liquid chromatography (Stabenfeldt, Ewing, Patton & McDonald, 1969). The present study using a protein-binding assay method was undertaken in an attempt to demonstrate

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Jeremy T Smith School of Anatomy and Human Biology, The University of Western Australia, 35 Stirling Hwy Crawley, Perth, Western Australia 6009, Australia

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Peter J Mark School of Anatomy and Human Biology, The University of Western Australia, 35 Stirling Hwy Crawley, Perth, Western Australia 6009, Australia

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Brendan J Waddell School of Anatomy and Human Biology, The University of Western Australia, 35 Stirling Hwy Crawley, Perth, Western Australia 6009, Australia

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Leptin’s actions are mediated via the long form of its receptor, Ob-Rb, but access to this receptor on target cells is also influenced by truncated leptin receptor isoforms Ob-Ra and Ob-Re. Plasma leptin binding activity is primarily attributed to Ob-Re, which can restrict leptin passage to extravascular tissue. In this study we investigated whether plasma leptin binding activity changes from fetal to adult life in male and female rats, and whether tissue expression of Ob-Re mRNA changes during development. Plasma leptin binding activity was low in the fetus and prepubertal rats but then increased in male rats by more than three-fold from pre- to post-puberty and by a further two-fold by 7 months of age. A more modest increase in plasma leptin binding activity was observed in females such that a clear sex difference became evident after puberty. There was also a reduction in hypothalamic Ob-Rb protein content between puberty and adult life in female rats. Combined with the higher levels of plasma leptin binding activity, this change in hypothalamic Ob-Rb expression is likely to lead to a more leptin-resistant state in aging females. To assess possible sources of circulating leptin binding activity, Ob-Re mRNA expression was measured by quantitative RT-PCR in several tissues from male rats soon after puberty and at 7 months of age. All tissues examined (testis, epididymis, adrenal, liver, adipose and spleen) expressed Ob-Re mRNA, and there was a dramatic, age-related increase in expression (> 300-fold) in the spleen. These data show that, in addition to the developmental increase in hypothalamic Ob-Rb expression previously reported, plasma leptin binding activity increases several fold from fetal to adult life in the rat. This suggests that the actions of leptin depend not only on its synthesis in adipose tissue and Ob-Rb expression in target cells, but also on factors that regulate tissue expression of Ob-Re and thus leptin transport within plasma.

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MARGARET H. ABEL
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S. K. SMITH
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D. T. BAIRD
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Concentrations of prostaglandin F (PGF) and prostaglandin E (PGE) were measured in endometrium from 18 women with ectopic pregnancies. In the nine pregnancies not associated with vaginal bleeding or an intra-uterine contraceptive device (IUCD; intact ectopics), concentrations of PGF (12·8 ± 7·4 (s.e.m.) ng/g) and PGE (4·7 ± 3·0 ng/g) were similar to those in decidua from nine intra-uterine pregnancies of comparable gestational age (14·4 ± 4·4 and 8·2 ± 2·2 ng/g respectively). In both ectopic and intra-uterine pregnancies concentrations of prostaglandins were significantly lower than those found in endometrium throughout the normal menstrual cycle (P < 0·01). In nine ectopic pregnancies with associated vaginal bleeding and/or an IUCD, concentrations of PGF and PGE were significantly higher than in the intact group (P < 0·05), although the concentration of PGF remained significantly lower than levels in normal secretory endometrium (P < 0·05).

These results suggested that suppression of endometrial synthesis of prostaglandin during early pregnancy may be mediated systemically rather than through a local action of the conceptus.

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