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)

A hypotensive, gut-contracting peptide neurotensin (NT), recently isolated from bovine hypothalami, has been found to produce hyperglycemia within minutes after iv injection into anesthetized rats. The dose-response relationship (deltaglucose, 15 min after injection) was linear over the range 30-200 pmol/100 g BW. NT did not alter the disappearance rate of [14C]glucose from plasma during the development of the hyperglycemia. However, the peptide caused a fall in liver glycogen (52 +/- 6.5 to 41 +/- 3.3 mg/g) and a 7-fold increase in the activity of the 5'-AMP independent form of liver glycogen phosphorylase. Activation of liver glycogen phosphorylase did not occur in vitro under conditions found suitable for demonstrating the effectiveness of glucagon, suggesting the possible involvement of an intermediary substanc(s) in vivo. Acute adrenalectomy did not prevent the response. Hypophysectomized rats (4 days post-operative) were less sensitive to NT, perhaps as a consequence of their diminished liver glycogen levels (normal, 52 +/- 6.5 mg/g; hypophysectomized, 23 +/- 1.8 mg/g); however, the presence of the pituitary was not essential for this response. NT was also effective in rats with hereditary diabetes insipidus (Brattleboro strain). At the time intervals sampled, radioimmunoassayable plasma levels of growth hormone, glucagon, and insulin were not significantly changed after injection of NT into normal rats. Pretreatment of rats with reserpine (7 mg/kg), morphine sulfate (10 mg/kg), propranolol (5mg/kg), or phenoxybenzamine (10 mg/kg) did not prevent the response. These findings characterize the action of NT on liver glycogen metabolism and blood glucose levels, but a physiological role for NT in this regard remains to be demonstrated.
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PMID:Hyperglycemic effect of neurotensin, a hypothalamic peptide. 82 91

The effects of glucagon on water and electrolyte transport in the kidney were investigated on hormone-deprived rats, i.e. thyroparathyroidectomized diabetes insipidus Brattleboro rats infused with somatostatin. Glucagon consistently inhibited the reabsorption of water and Na+, Cl-, K+ and Ca2+ along the proximal tubule accessible to micropuncture, leaving the reabsorption of inorganic phosphate (Pi) untouched. In the loop, besides its previously described stimulatory effects on Na+, Cl-, K+, Ca2+ and Mg2+ reabsorption, glucagon strongly inhibited Pi reabsorption, very probably in the proximal straight tubule. These effects resulted in a significant phosphaturia and considerable reductions of Mg2+ and Ca2+ excretions. The effects of glucagon at both the whole kidney and the nephron levels are very similar to those previously described for calcitonin. In the absence of an adenylate cyclase system sensitive to glucagon and calcitonin in the rat proximal tubule, and from the analogy of their physiological effects with those elicited by parathyroid hormone, it is suggested that glucagon and calcitonin exert their inhibitory effects on Na and Pi reabsorption in the proximal tubule through another pathway, which could be the phosphoinositide regulatory cascade.
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PMID:Glucagon inhibits water and NaCl transports in the proximal convoluted tubule of the rat kidney. 177 68

The medullary thick ascending limb (MAL), but not the medullary collecting tubule (MCT), has been shown to have an impaired adenylate cyclase (AC) responsiveness to ADH and a selective hypoplasia in Brattleboro diabetes insipidus (DI) rats. Since chronic ADH administration has been found to increase epithelium volume and basolateral membrane surface area in MAL but not in MCT, we investigated whether chronic ADH infusion would affect the hormone-sensitive AC and the Na-K-ATPase activity--two markers of the basolateral membrane--in single micro-dissected portions of thick ascending limb and collecting tubule in DI rats. Results indicate that 1. in MAL of ADH-treated rats, AC responses to in vitro AVP and glucagon and Na-K-ATPase activity increased to the same extent as did epithelium volume (60-80%); 2. changes in the other segments were independent of any morphological alteration. In the cortical thick ascending limb, AVP and glucagon-sensitive AC decreased by 30-40% whereas Na-K-ATPase activity did not change. In the collecting tubule, AC response to in vitro AVP was not altered by ADH-treatment but glucagon-sensitive AC dropped by 50% and Na-K-ATPase activity doubled, independently of any variation in plasma aldosterone and glucagon levels. These results show that, in the MAL, the ADH-induced variations in enzyme activity are a reflection of the enlargement of the basolateral membrane surface area. Further studies are needed to clarify the origin of enzymatic alterations in the other segments.
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PMID:Influence of chronic ADH treatment on adenylate cyclase and ATPase activity in distal nephron segments of diabetes insipidus Brattleboro rats. 299 94

We describe five patients with Wolfram syndrome (diabetes insipidus, diabetes mellitus, optic atrophy and deafness). Three of the patients appear to have had very gradual onset of diabetes mellitus at an early age yet all patients when tested for C-peptide response to glucagon were severely deficient. All patients are registered blind from primary optic atrophy, two have severe hearing difficulties and three high tone sensorineural hearing loss on audiometry. Four patients have cranial diabetes insipidus which in two cases is partial and of gradual onset and was attributed to poor control of the diabetes mellitus. In one case treatment of the insipidus relieved enuresis. All five patients have evidence of dilatation of the urinary tract and one patient is managed in the long-term by self-catheterisation which has resulted in one episode of bacteraemia. One patient has marked testicular atrophy and investigation reveals this to be due to primary hypogonadism and not to hypothalamic-pituitary dysfunction. One female patient had her menarche delayed until the age of 19 years but has subsequently had the only successful pregnancy in a patient with this syndrome of which we are aware.
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PMID:Wolfram (DIDMOAD) syndrome: a complex long-term problem in management. 308 28

Previous studies from this laboratory have demonstrated that vasopressin stimulates K, Mg, Ca, Cl, and Na reabsorption by the thick ascending limb of Henle's loop (TALH) of the rat kidney. Micropuncture of superficial nephrons and clearance experiments were performed to determine whether desensitization of the TALH to vasopressin may be demonstrated in vivo and whether such desensitization is specific for the effects of vasopressin (i.e., homologous) or also alters the response to the other hormones acting on the same pool of adenylate cyclase in this nephron segment. Brattleboro rats, with hereditary hypothalamic diabetes insipidus (DI), were given i.m. injections of 1-desamino-8-D-arginine-vasopressin (des-1-amino-[DArg8]VP (herein designated dDAVP); 2 micrograms/day) for 3 days. The effects of maximal physiological doses of arginine-8-vasopressin ([Arg8]VP (herein designated AVP); 20 pg/min per 100 g of body weight) were studied 2 days after the cessation of treatment, when the animals had returned to DI. The K, Mg, Ca, and, to a lesser extent, Cl and Na concentrations in the fluid leaving the TALH of superficial nephrons were higher in dDAVP-treated than in untreated rats given similar amounts of AVP during the experiments. A 50-60% desensitization of the TALH to AVP was still apparent 2 days after stopping the dDAVP injections. Desensitization is homologous, as judged from normal responses to physiological doses of glucagon and calcitonin, two hormones acting on the same cyclase pool as AVP in the rat TALH. The AVP-dependent increase of urine osmolality, however, indicated that its effects on the permeability to water of the collecting duct were scarcely affected in dDAVP-treated rats. It is concluded that (i) AVP induces homologous desensitization in the rat TALH and (ii) the TALH can be markedly desensitized to AVP when the collecting duct response to this hormone is poorly affected or even fully maintained.
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PMID:Desensitization of rat renal thick ascending limb cells to vasopressin. 335 89

Clearance experiments were performed to characterize the sensitivity to vasopressin of the thick ascending limbs and collecting duct system of the rat kidney. The response of the thick ascending limbs was evaluated by measuring the Mg2+ excretion rate in the urine, since the [arginine-8] vasopressin-mediated effects on Mg2+ excretion are the direct result of a stimulation of Mg2+ reabsorption in this nephron segment, and the response of the collecting ducts was evaluated by changes in urine flow. To avoid the effects of parathyroid hormone, glucagon, and calcitonin, which stimulate Mg2+ reabsorption in the thick ascending limb and distal tubule, and of calcitonin, which increases the permeability of the cortical collecting ducts to water, experiments were performed on Brattleboro D. I. rats (with hereditary diabetes insipidus, due to a lack of [Arg8]vasopressin) acutely deprived of endogenous parathyroid hormone, calcitonin, and glucagon. Vasopressin infused at rates up to 5 pg/min did not reduce the Mg2+ fractional excretion rate, whereas at 5 pg/min water excretion was decreased by 50%. The half-maximal reduction of Mg2+ excretion occurred at vasopressin infusion rates 4-6 times higher than those necessary to diminish the water excretion rate to the same extent. We conclude that in vivo, two segments involved in the production of concentrated urine have different sensitivities to vasopressin and that this difference in sensitivity is very similar for the biological response in vivo and the adenylate cyclase activation in vitro. We suggest that both the magnitude and the nature of the effects of [Arg8]vasopressin on the kidney may vary according to the required antidiuretic response.
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PMID:Sensitivities of rat kidney thick ascending limbs and collecting ducts to vasopressin in vivo. 345 86

The stress response in humans commonly includes elevations in plasma concentrations of glucocorticoids, catecholamines, glucagon, growth hormone, aldosterone, and renin, resulting in alterations in the metabolism of glucose and other energy substrates, and in increased sodium and water retention. In severe illness, triiodothyronine and sometimes thyroxine are decreased without evidence of clinical hypothyroidism. Antidiuretic hormone may be elevated in bacterial meningitis and other central nervous system disorders, as well as in acute asthma, chronic ventilator therapy, pneumothorax, atelectasis, and postoperatively. Increased ADH concentration can lead to significant hypoosmolality and hyponatremia with adverse effects on the patient. In the setting of severe intracerebral insults, ADH may be inappropriately low, resulting in diabetes insipidus. Insulin concentrations may be inappropriately low for serum glucose concentration, or insulin may have diminished receptor responsiveness in seriously stressed patients. Either situation leads to hyperglycemia. Disturbances in calcium, phosphorus, and magnesium homeostasis may occur relatively frequently in the critically ill patient in response to therapeutic interventions, or illness-induced altered metabolism. It is not always clear when an altered metabolic or hormonal state is an appropriate response to a stress, or represents decompensation of the body's mechanisms for coping with that stress. It is important, however to recognize the common responses of the organism to severe illness, and to monitor for treatable abnormalities which occur.
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PMID:Endocrine manifestations of critical illness in the child. 354 20

The effects of 1-desamino-8-D-arginine vasopressin (dDAVP) on superficial and juxtamedullary nephrons were investigated by micropuncture in diabetes insipidus (DI) Brattleboro rats chronically treated with the peptide. The rats, acutely deprived of endogenous calcitonin, parathyroid hormone (PTH), and glucagon [hormone-deprived (HD) rats], were examined either 4 days after cessation of dDAVP treatment (HDT, control diuretic rats) or when the treatment was continued until the micropuncture experiment, during which dDAVP was also given intravenously (HDT + dDAVP, experimental nondiuretic rats). In the presence of dDAVP, the reabsorption of Cl, Na, Mg, and Ca by the superficial loop of Henle was significantly increased, as previously observed in HD-untreated rats during acute infusion of dDAVP. The effects on the superficial distal tubule were also similar. The effects on K, however, were different both in the loop and in the distal tubule. At the bend of the juxtamedullary nephrons, the treatment alone (HDT rats) increased fractional delivery (FD%) of Na and Cl, whereas FD% of Mg, Ca, K, and P was unaltered. In HDT + dDAVP rats, FD% of H2O, Cl, Na, and Ca was significantly lower than in HDT rats, and FD% of K, Mg, and P did not differ significantly. In conclusion, in the presence of dDAVP, the FD% of H2O, Na, and Cl at the bend of the long-loop nephrons decreases, in accordance with our previous hypothesis that water removal along the rat descending limb increases outward NaCl diffusion along this segment.
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PMID:NaCl and Ca delivery at the bend of rat deep nephrons decreases during antidiuresis. 359 53

Two adult patients with unilateral hypoplastic optic nerves, absent septa pellucida and hypopituitarism are described. Patient 1, aged 20, presented with diabetes insipidus due to partial vasopressin deficiency. Patients 2, aged 29, presented with focal epilepsy. Both had short stature. They showed absent growth hormone (GH) response to insulin-hypoglycaemia or glucagon, but responded to 100 micrograms growth hormone releasing factor (GRF-44) with a rise in circulating GH, suggesting a hypothalamic defect in GH release though a co-existing pituitary defect cannot be excluded. Other hypothalamic-pituitary functions were normal. These two patients probably represent the milder form of the clinical spectrum of septo-optic dysplasia which, with the extensive use of CT brain scans, will be increasingly encountered by physicians attending adult patients.
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PMID:Hypothalamic defects in two adult patients with septo-optic dysplasia. 375 51

10 patients, aged 4-17 years, were investigated in order to study the influence of tumors of the pineal area on the hypothalamic endocrine function. Immunoreactive growth hormone (GH) failed to increase sufficiently in 9 patients after insulin induced hypoglycemia (IIH) and in seven patients after propranolol-glucagon (PG). Secondary adrenocortical insufficiency was present in four patients. Three of these patients showed biochemically hypothalamic hypothyroidism with elevated basal prolactin levels, hypogonadotropic hypogonadism and neurohumoral diabetes insipidus. The study shows that hypothalamic dysfunction in patients with tumors of the pineal area is at least as frequent as in patients with suprasellar tumors and that diabetes insipidus may be present before any surgical or radiological treatment.
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PMID:Hypothalamic function in patients with tumors of the pineal area. 715 55


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