Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The administration of monosodium-L-glutamate (MSG) during the neonatal period is known to result in central nervous system lesions in the arcuate nucleus of the hypothalamus and the retina. Rodents so treated exhibit behavioral deficts and endocrinopathies including obesity, hypogonadism, hypothyroidism, pituitary atrophy, tail automutilation and diminished locomotor activity. Assessment of endocrine status revealed normal serum levels of glucagon, thyroid-stimulating hormone and luteinizing hormone, and diminished levels of thyroid hormones and growth hormone in MSG-treated rats. Prolactin levels were elevated in the glutamate-treated male rats. Within the brain hypothalamic levels of thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, and somatostatin were unchanged. Measurement of neurotransmitters and neurotransmitter-related enzymes in individual hypothalamic nuclei derived from MSG-treated rats revealed normal levels of norepinephrine, serotonin and glutamic acid decarboxylase, but reduced levels of choline acetyltransferase and dopamine in the arcuate nucleus and median eminence. Histochemical methods for visualization of dopamine and acetylcholinesterase in the mediobasal hypothalamus confirmed these findings. The MSG-treated animals exhibited a normal diurnal rhythm of pineal serotonin N-acetyltransferase activity. These data indicate that the MSG-induced endocrine deficiency syndrome results at least partly from destruction of cholinergic and dopamingeric tuberoinfundibular systems in the hypothalamus.
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PMID:Models of neuroendocrine regulation: use of monosodium glutamate as an investigational tool. 3 35

A case of pseudohypoparathyroidism has been investigated. Indirect evidence allows to eliminate a defect of renal 1 alpha-hydroxylase as the determining factor of this condition. Similarly, the increased size of the mean surface area of the cross-section of periosteocytic lacunae, as determined on decalcified sections of bone obtained by transiliac biopsy, shows the osteocytes to be sensitive to the endogenous PTH, discarding cAMP response to PTH in bone as a prerequisite for PTH action on bone. The authors conclude from these data and from previous experiments that the defect of parathyroid function in this condition probably relates to the existence of an abnormal PTH molecule and/or metabolism and/or interaction with the receptors sites. The endocrine function was studied as well. Prediabetes was demonstrated, as well as primary latent hypothyroidism (TRH test). Prolactin release could not be stimulated by TRH, levodopa, metoclopramide, chlorpromazine and insulin hypoglycemia. The latter produced a normal release of ACTH (as ascertained by plasma cortisol levels) and GH, and possibly a sluggish response of glucagon and gastrin. There was a deficiency of urinary concentration upon restriction of fluid intake. This was only partially corrected by ADH administration.
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PMID:[Physio-pathology of pseudohypoparathyroidism (author's transl)]. 22 97

Somatostatine is the hypothalamic factor which inhibits the secretion of growth hormone. The administration of a synthetic form decreased growth hormone levels by 50 to 75% in 5 acromegalic patients. The action is rapid but the effect is not prolonged. Prolactin was reduced in only case with galactorrhea. Thyreostimulin, as well as gastrin, are unaffected. Plasma insulin levels, and to a lesser extent those of glucagon, are decreased by somatostatine which causes no variation in either cortisol or blood glucose. Somatostatine, by correcting the pathological secretion of hormone, opens the way to medical treatment of acromegaly.
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PMID:[The effects of somatostatin in acromegaly]. 77 91

Plasma concentrations of glucose, insulin, glucagon, cortisol, growth hormone and prolactin were measured repeatedly in ten females undergoing abdominal hysterectomy during general anaesthesia. In addition to general anaesthesia five of the patients had continuous epidural analgesia effective for the first 26 postoperative hours. Plasma glucose was elevated during surgery and postoperatively, but not in patients having epidural analgesia. Insulin was low and unchanged in both groups. Glucagon was unchanged and similar in both groups. Cortisol was lower during surgery in the epidural group, but not postoperatively. Growth hormone increased during surgery in four of five patients receiving general anaesthesia alone, but no changes were observed in the epidural group. Prolactin was greatly elevated in all patients immediately after induction of anaesthesia and then fell rapidly during surgery, similarly in both groups. It is concluded that epidural analgesia can inhibit the hyperglycaemic response to surgical stress, but this effect cannot be uniformly correlated to changes in peripheral plasma levels of insulin, glucagon, cortisol, growth hormone or prolactin.
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PMID:Effect of epidural analgesia on the glycoregulatory endocrine response to surgery. 126 58

There is a great variation in body weight loss during lactation among primiparous sows fed a standard diet that is adjusted based on the number of piglets nursed and the maintenance requirements. Energy and protein catabolism is more pronounced during the first 1 to 3 weeks of lactation and sows with low weight loss recover earlier from their negative energy balance during lactation than sows with high weight loss. Using continuous blood collection a decrease in plasma levels of oxytocin, prolactin, and insulin, and an increase in plasma levels and no of LH pulses during lactation were demonstrated. Prolactin levels gradually increased in response to each suckling while only 40-50% of recorded sucklings induced a significant rise in plasma oxytocin. Following a 24-h fast during lactation, levels of prolactin were very low but increased rapidly after refeeding. Even plasma levels of insulin and glucose decreased to very low levels during fasting, but the release of LH was similar before and after refeeding. Weaning resulted in decrease in plasma levels of prolactin and increase in plasma levels and no. of LH pulses. Plasma levels of cortisol showed a diurnal pattern of change which disappeared on the day of weaning. In response to weaning plasma levels of glucagon and gastrin decreased, whereas insulin and somatostatin increased. At weaning sows with low weight loss during lactation had higher plasma insulin and lower plasma cortisol levels than sows with high weight loss, but no differences in levels or no. of LH pulses were observed between the two groups of sows.
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PMID:Metabolic and reproductive hormones during lactation and the post-weaning period in sows. 134 70

To determine lactational and glucogenic responses to increased prolactin concentrations, five lactating dairy goats were used in a crossover design. Prolactin at .85 mg/h or placebo was infused on each of 8 consecutive d via jugular catheter for 14 h initiated 30 min after the a.m. milking. To examine the effect of treatments on glucose metabolism, goats were given a single isotope injection of [6-3H]glucose 2 h after initiation of treatment infusion on the final day of the treatment period. Milk yield and milk protein percentage were not affected by prolactin infusion; however, milk fat and SNF percentage were significantly decreased. No differences in dry matter intake and digestibility of the diet were observed. Prolactin increased plasma prolactin and decreased plasma glucagon concentrations, but did not affect plasma insulin or glucose concentrations. Although glucose pool size per kilogram of BW was significantly lower in the prolactin-treated group than in the control group, no difference in glucose turnover rate was observed.
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PMID:Effect of prolactin infusion on lactation, glucose kinetics, and pancreatic hormones in lactating goats. 209 64

The neuropeptides Substance P, beta-Endorphin, Prolactin, Cholecystokinin, and Glucagon were investigated by means of Sternbergers PAP technique in the neuroepithelium of the Maculae utriculi and sacculi of the labyrinth of newborn guinea pigs. This brief report will show the localization of some neuropeptides in the neuroepithelium of the Maculae utriculi and sacculi. We could not find information about similar studies on this topic in the literature. In connection with investigations of the sensory apparatus of the inner ear we have recently presented neuropeptides evidence for the presence of certain peptides in the Ggl. spirale and the hair cells of the organ of Corti. With this paper we continue to report on neuropeptides in the labyrinth of the juvenile guinea pig as revealed by immunohistochemistry (Nowak et al., in press).
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PMID:Neuropeptides in macula utriculi and macula sacculi of guinea pig labyrinth. An immunohistochemical study. 242 38

In addition to direct toxic effects on endocrine organs chronic alcohol intake affects regulation of endocrine systems by disturbed liver function. As a result in patients with alcohol-induced liver cirrhosis gonadal axis is characterized by low total and free testosterone, elevated estradiol. LH, FSH, and sexual hormone binding globulin and an enhanced conversion of testosterone to estradiol. Prolactin also is found to be elevated. The thyrotropic axis is characterised by low T3- und T4- as well as elevated rT3-values and normal TSH. STH is elevated, while somatomedin C is decreased. The corticotropic axis may show an abolished circadian rhythm, a negative Dexamethasone-test, low transcortin and elevated free cortisol levels. The disturbance of the calcitropic axis leads to osteoporosis and osteomalacia, due to intestinal hyperparathyroidism and vitamin D malnutrition. In 50% of chronic alcoholics there are elevated insulin and glucagon values and a pathological glucose tolerance test.
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PMID:[Alcohol and endocrinologic homeostasis]. 306 42

A single acute IV injection (1 microgram/kg) of the synthetic replicate of Somatocrinin (GRF) in 40 children with growth hormone (GH) deficiency induces a marked plasma GH increase, although heterogeneous. Clinical tolerance is excellent. Compared to Propranolol + Glucagon (P + G), GRF induces a better GH response. It also discriminates better idiopathic GH deficiency (n = 13), where mean GH peak = 6.5 ng/ml (3.3 after P + G) from GH deficiency secondary to a brain tumor (n = 24) where mean GH peak = 15.5 ng/ml (5.0 after P + G) GRF induces a slight Prolactin (Prl) increase, more obvious when basal Prl is elevated. However there is no correlation between GH and Prl responses to GRF even with basal hyperprolactinemia. GH response to GRF seems to slowly decrease after radiation therapy. GRF is a new potent, well tolerated secretagogue of GH and improves the diagnostic quality of the etiology of GH deficiency.
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PMID:[Somatocrinin and children in 1984. Application to the etiological diagnosis of somatotropin deficiencies]. 392 94

The endocrine profile of FK 33-824, 0.5 mg i.m., was determined in comparison with placebo or pretreatment with naloxone, 4 mg i.v., in 14 healthy men. Prolactin (PRL), growth hormone (GH), ACTH, cortisol, gonadotropins (LH, FSH), thyrotropin (TSH), thyroxine (T4), triiodothyronine (T3), insulin and glucagon were measured and free water clearance was calculated from urine volumes and osmolar clearances. FK 33-824 increased PRL and GH (p less than 0.001). ACTH was below assay sensitivity but cortisol was significantly lowered (p less than 0.001). Free water clearance was enhanced (p less than 0.01) and the remaining parameters were unchanged. Naloxone alone had no hormonal effect but abolished the increase in PRL and GH following injection of FK 33-824 without modifying the decrease in plasma cortisol or the increase in free water clearance following the same treatment. The results indicate that the effect of FK 33-824 on PRL and GH release is mediated by opiate receptors. Other mechanisms or naloxone nonsensitive receptors may be implicated in the effects recorded on cortisol and FWC.
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PMID:Endocrine effect of a methionine-enkephalin derivative (FK 33-824) in man. 626 6


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