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ABSTRACT

Insulin, glucose, lactate and alpha-amino acid nitrogen concentrations were measured in the plasma of ewes and their hypophysectomized fetal lambs during intravenous infusions of GH, prolactin or saline into the fetus in utero. Prolactin and saline had no effect on mother or fetus. Infusion of GH at 1·2 mg/kg per day for 2 days or at 0·4 mg/kg per day for 4 days caused a sustained twofold increase in the level of insulin and a smaller, but sustained, increase in the level of glucose in fetal plasma. We suggest that GH antagonizes the action of insulin in the fetus. Glucose supplies to the fetal brain and placenta may be protected by such antagonism of insulin use during glucose shortage.

J. Endocr. (1985) 105, 379–382

Abstract

The existence of extrapancreatic islets in the duodenal mucosa of the adult rat has been established by morphological studies and the development of these islets has been followed from the early embryonic stage to neonatal and adult life. Like the pancreatic islets, glucagon cells were the first to appear at day 12 of gestation. However, in contrast to the pancreatic islets, insulin was not detected in the extrapancreatic islets until birth. At this stage, the different endocrine cells assume their classical topography, insulin cells being surrounded by non-insulin endocrine cells. In addition, the behaviour of these extrapancreatic islets in diabetic conditions was evaluated on streptozotocin-induced diabetic rats as well as on spontaneous BB Wistar diabetic rats. In both conditions, the extrapancreatic islets were found in the duodenal mucosa but were mainly composed of glucagon cells, the insulin cells having disappeared. These results demonstrate that the extrapancreatic islets are a common normal feature of the rat duodenal mucosa. They appear during fetal development, are present in different strains of rats and behave similarly to the pancreatic islets under spontaneous or chemically induced diabetic conditions. Although their exact role remains to be established, they probably react to local hyperglycaemic environment due to intestinal absorption.

Journal of Endocrinology (1997) 153, 73–80

ABSTRACT

Fetal lambs were hypophysectomized and, after 8 days of recovery, given infusions of GH, prolactin, thyroxine and insulin with glucose. Hypophysectomy caused no consistent reduction in fetal plasma somatomedin-like activity. Fetal infusions of GH or prolactin caused no consistent change in plasma somatomedin-like activity. It was concluded that fetal somatomedin-like activity is not GH dependent. After hypophysectomy fetal lambs showed no reduction in body weight or length at term.

J. Endocr. (1985) 104, 193–199

Gross deformities appeared in Xenopus laevis maintained for about 2 yr. under laboratory conditions on a diet containing no live food. Radiographs of the affected animals revealed defective calcification of the skeleton. All animals bred in the colony were defective, and only the original adults taken from the wild had normal bones. A description of the different types of skeleton found, and later produced experimentally, is given. An analysis of the conditions under which the defects became manifest showed X. laevis to be very susceptible to lack of vitamin D. Calcification in this species is greatly affected by the nature of the basal food. Normal bones are formed when the toads are fed on a diet of rabbit liver (or ox liver) supplemented with cod-liver oil and calcium. Horse liver is toxic, causing a depression of growth and a failure of calcification even with the supplements. With guinea-pig muscle a far larger supplement of vitamin D is required to prevent the development of general calcium deficiency and to permit normal bone formation. The failure of calcification is identified as rickets with osteoporosis and its relation to these diseases in other species is discussed.

Abstract

Central catecholaminergic neurones projecting to specific hypothalamic structures are involved in stimulating and inhibiting the activity of the GnRH-containing neurosecretory neurones. Both testosterone and elevated circulating prolactin (PRL) levels inhibit postcastration LH release. Three groups of adult male rats were orchidectomized and adrenalectomized, received corticosterone replacement and were: (i) administered purified ovine PRL (oPRL; 2400 μg/s.c. injection) or (ii) its diluent, polyvinylpyrrolidone (PVP), every 12 h, or (iii) received physiological testosterone replacement for 2 days. At 0, 2 and 6 days postcastration, norepinephrine (NE), epinephrine (E) and dopamine (DA) turnover were estimated by the α-methyl-p-tyrosine method in three micro-dissected hypothalamic structures: the diagonal band of Broca at the level of the organum vasculosum of the lamina terminalis (DBB(ovlt)), the medial preoptic nucleus (MPN) and the median eminence (ME). In control (PVP-treated) rats, serum LH concentrations increased eightfold at 2 and 6 days postcastration and this rise was prevented by testosterone. oPRL treatment transiently suppressed LH secretion at 2 but not 6 days postcastration. Castration significantly decreased basal rat PRL (rPRL) levels at 2 and 6 days and testosterone administration partially prevented this effect.

NE turnover in the ME and E turnover in the MPN increased markedly at 2 and 6 days postcastration, and testosterone replacement for 2 days prevented these increases. Thus, noradrenergic neurones innervating the ME and adrenergic neurones innvervating the MPN may drive postcastration LH secretion by providing stimulatory afferent input to the GnRH neurones. It was striking to observe that oPRL blocked the increases in both ME NE and MPN E turnover at 2 but not 6 days postcastration. Hence, oPRL may transiently suppress LH release by an inhibitory action on these NE and E neurones.

DA turnover in the DBB(ovlt) was significantly decreased by 6 days postcastration. Testosterone-treated (2 days postcastration) and oPRL-treated (2 and 6 days postcastration) rats exhibited turnover values indistinguishable from day 0 controls. Hence, the A₁₄ dopaminergic neurones, which synapse on GnRH neurones in the rostral preoptic area and may exert an inhibitory effect on them, are positively regulated by PRL and perhaps by testosterone as well.

Autoregulatory feedback suppression of endogenous rPRL secretion by oPRL was observed both 2 and 6 days postcastration. In contrast to the A₁₄ dopaminergic neurones, turnover in the A₁₂ tuberoinfundibular dopaminergic (TIDA) neurones innervating the ME increased significantly by 6 days postcastration in control rats while oPRL administration further increased ME DA turnover at both 2 and 6 days. Hence, autofeedback regulation of rPRL secretion persists through at least 6 days of oPRL exposure temporally associated with markedly increased turnover in the TIDA neurones. In summary, our results support the hypothesis that the inhibitory effect of PRL on postcastration LH release is mediated by suppression of the activity of NE neurones innervating the ME and E neurones terminating in the MPN which, with time, become refractory to continued PRL exposure.

Journal of Endocrinology (1996) 148, 291–301

SUMMARY

A double antibody radioimmunoassay for canine luteinizing hormone (LH) was devised. The assay can measure immunoreactive LH in the peripheral plasma of the normal male and female dog. An increase in hormone concentration was found on the 2nd day of oestrus in the female. Ovariectomy raised plasma concentrations of the hormone to levels greater than those observed during oestrus. The administration of LH-releasing factor induced a rapid increase in the plasma concentrations of LH.

For the study of their various physiological and chemical properties, protein hormones in urine have usually been purified by adsorption or precipitation (Heller & Chandler, 1942; Bradbury, Brown & Brown, 1949; Johnsen, 1955; Albert, 1955; Butt, 1958; Loraine & Brown, 1959). Methods using kaolin adsorption followed by acetone precipitation have been widely used for the extraction of urinary gonadotrophins (HPG). However, for the immunochemical and biological characterization of isolated gonadotrophins, the kaolin-acetone method presents some potential drawbacks. Adsorption of the active constituents may be incomplete, and elution at the required high pH (11·5) as well as treatment with acetone may cause denaturation. Hobson & Wide (1964) have reported a decrease in the ratio of immunological properties to biological activity during the kaolin-acetone concentration of human chorionic gonadotrophin (HCG). In an attempt to minimize these difficulties, we have used ultrafiltration for the isolation of HPG. The results have been compared with