D-mannose is an essential monosaccharide constituent of glycoproteins and glycolipids. However, it is unknown how plasma mannose is supplied. The aim of this study was to explore the source of plasma mannose. Oral administration of glucose resulted in a significant decrease of plasma mannose concentration after 20 min in fasted normal rats. However, in fasted type 2 diabetes model rats, plasma mannose concentrations that were higher compared with normal rats did not change after the administration of glucose. When insulin was administered intravenously to fed rats, it took longer for plasma mannose concentrations to decrease significantly in diabetic rats than in normal rats (20 and 5 min, respectively). Intravenous administration of epinephrine to fed normal rats increased the plasma mannose concentration, but this effect was negated by fasting or by administration of a glycogen phosphorylase inhibitor. Epinephrine increased mannose output from the perfused liver of fed rats, but this effect was negated in the presence of a glucose-6-phosphatase inhibitor. Epinephrine also increased the hepatic levels of hexose 6-phosphates, including mannose 6-phosphate. When either lactate alone or lactate plus alanine were administered as gluconeogenic substrates to fasted rats, the concentration of plasma mannose did not increase. When lactate was used to perfuse the liver of fasted rats, a decrease, rather than an increase, in mannose output was observed. These findings indicate that hepatic glycogen is a source of plasma mannose.
The rate of secretion of 17-oxosteroids by the testes of anaesthetized dogs in vivo was used as an index of LH secretion. Intracarotid injection of luteinizing hormone releasing hormone (LH-RH, 1, 5 or 10 microgram/kg body wt) resulted in an increase in the testicular 17-oxosteroid secretion which was roughly proportional to the dose administered and which reached a maximum 60 min after the injection. Testicular output of 17-oxosteroids was unaffected by administration of melatonin (10 or 100 microgram/kg body wt) into the carotid artery. When LH-RH (5 microgram/kg) was injected into the carotid artery 3 h after intracarotid injection of melatonin (10 or 100 microgram/kg), the testicular response to LH-RH was considerably diminished. Pretreatment with melatonin (100 microgram/kg) did not alter the testicular response to human chorionic gonadotrophin (20 i.u./kg body wt) given i.v. Is is concluded that melatonin may act directly on the anterior pituitary gland in dogs to inhibit the LH-RH-induced release of LH.
The concentrations of 17-oxosteroids in the spermatic venous blood of anaesthetized dogs were used as an index of LH release to assess the effects of arginine-vasotocin on the response of the canine pituitary gland to exogenous luteinizing hormone releasing hormone (LH-RH). When injected into the carotid artery, arginine-vasotocin (1.0 microgram/kg body wt) caused no significant alterations in the testicular output of 17-oxosteroids. The administration of LH-RH (5 microgram/kg body wt, a standard dose) into the carotid artery produced typical stimulation of testicular 17-oxosteroid secretion. Administration of arginine-vasotocin (0.01, 0.1 or 1.0 microgram/kg body wt) into the carotid artery 3 h before the administration of a standard dose of LH-RH inhibited the testicular secretion of 17-oxosteroids normally induced by LH-RH. However, pretreatment with arginine-vasotocin (1.0 microgram/kg body wt) did not affect the testicular response to i.v. administration of human chorionic gonadotrophin (5 i.u./kg body wt). These results indicate that in the dog, arginine-vasotocin inhibits the LH-RH-induced release of LH by acting acting directly on the anterior pituitary gland.
The effect of prostaglandin E2 (PGE2) on the secretion of adrenaline and noradrenaline by the adrenal gland and the interaction between PGE2 and acetylcholine in the adrenal medulla were examined in anaesthetized dogs. In splanchnicotomized dogs, i.v. injection of PGE2 failed to induce any secretion of catecholamines from the adrenal gland, whereas administration of PGE2 into the lumboadrenal artery resulted in a slight, approximately dose-dependent increase in catecholamine secretion within 2 min of the injection. This effect of PGE2 was unaffected by i.v. administration of atropine. Intravenous administration of acetylcholine 1 min after the administration of PGE2 into the lumboadrenal artery of splanchnicotomized atropine-treated dogs had a markedly greater effect on adrenal catecholamine secretion; the resultant output was about twice that evoked by acetylcholine in the absence of PGE2. The effect was more than additive, since the response to acetylcholine was at least one order of magnitude greater than that to PGE2. This indicates that PGE2 and acetycholine may act synergistically in the adrenal medulla.
Melatonin has been found to inhibit the response of neonatal rat pituitary tissue to luteinizing hormone releasing hormone (LH-RH) in vitro (Martin & Klein, 1976;Martin, Engel & Klein, 1977). This inhibitory effect of melatonin has been observed previously in the pituitary gland of mature male dogs in vivo (Yamashita, Mieno, Shimizu & Yamashita, 1978), but it is not known whether the inhibition is manifested in immature animals. The response of the pituitary gland of the immature male dog to exogenous LH-RH has therefore been investigated ; the rate of secretion of 17-oxosteroids by the testis in vivo was used as an index of LH release (Yamashita, 1966). Melatonin (Sigma Chemical Co.; 100 µg/kg body weight dissolved in 0-5 ml 1-6% ethanol-isotonic saline solution) was administered into the left carotid artery of immature male dogs (approximately 2-4 months old, 1-9-4-5 kg) under pentobarbitone (25 mg/kg body weight, administered i.v.) anaesthesia in acute experiments of 4 h duration using methods described previously (Yamashita et al. 1978); control dogs received vehicle only. At the same time, the left spermatic vein was cannulated (Yamashita, 1966). Three hours after the administration of melatonin, LH-RH (Protein Research Foundation; 5 or 10 µg/kg body weight in 0-5 ml 0-9% saline) was injected into the left carotid artery for 15 s. In other experiments, human chorionic gonadotrophin (HCG; CG-10, Sigma Chemical Co.; 20 i.u./kg body weight) was administered i.v. instead of LH-RH. At intervals, the entire blood flow (about 8 ml) through the left spermatic vein was collected for 8-12 min periods and the concentrations of 17-oxosteroids in samples of plasma (3 ml) were measured (Gardner, 1953;Yamashita, 1966). With the micro-Zimmermann reaction used here, the lower limit of detectability of 17-oxosteroids in a 3 ml sample of plasma was 30 ng. The rate of secretion of 17-oxosteroids by one testis was expressed as ng kg body weight-1 min-1, calculated from the concentration of 17-oxosteroids (ng/ml) in spermatic venous plasma and the rate of flow of spermatic venous plasma (ml kg body weight-1 min-1). Student's r-test was used for statistical comparisons and a value of < 005 was regarded as significant.In the control (vehicle-treated) animals, intracarotid injection of LH-RH (5 or 10 µg/kg body weight) resulted in a slight but definite increase in the testicular output of 17-oxo¬ steroids (Table 1) and the response was greater after administration of the higher dose of hormone. When either dose of LH-RH was given to animals pretreated with 100 µg melatonin/kg body weight, a decrease in the testicular responsiveness to LH-RH was observed; the increase in the secretion of 17-oxosteroids after treatment with LH-RH was smaller than that recorded in control animals not pretreated with melatonin (Table 1). The testicular responses to HCG (20 i.u./kg body weight) were of almost the same magnitude in untreated and melatonin-treated animals (Table 1).These results show that in immature, as in mature dogs, melatonin inhibits ...
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