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 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

We have seen a case of "diabetic non-ketotic hyperosmolar coma" with ketosis. An 84-year-old man was brought into the hospital in a deeply comatous and dehydrated state. The initial blood glucose level was 1252 mg/dl with plasma osmolarity of 435 mOsm/l, but no ketonuria was detected by the nitroprusside method (Ketostix). However, the plasma 3-hydroxybutyrate (3-OHBA) level was 5 mM in a newly developed bedside film test. The serum ketone bodies were later found to be 5.56 and 0.82 mmol/l for 3-OHBA and acetoacetate (AcAc), respectively. A marked increase in glucagon, cortisol and ADH with renal dysfunction (creatinine 5.0 mg/dl) were noted. An abnormal electrocardiogram, occular convergence and chorea like movement disappeared after correction of metabolic disturbances. The moderate level of IRI (14 microU/ml) on admission and a good response to glucagon 2 months after admission also indicate that the present case is a typical hyperosmolar non-ketotic coma. Because of a preferential increase in 3-OHBA, ketonuria seemed to be absent in the regular nitroprusside test. Marked dehydration is thought to cause renal dysfunction, and the increase in ADH may have helped to prevent further aggravation of ketoacidosis. We propose to change the term hyperosmolar non-ketotic coma (HNC) to diabetic hyperosmolar coma (DHC), because sometimes patients with hyperosmolar non-ketotic diabetic coma are ketotic, as seen in the present case. Determination of 3-OHBA or individual ketone bodies in blood is important and essential for the differential diagnosis of diabetic coma. The diagnosis of either ketoacidotic or hyperosmolar coma should be made depending on the major expression of ketoacidosis or hyperglycemic hyperosmolarity.
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PMID:A case of diabetic non-ketotic hyperosmolar coma with an increase with plasma 3-hydroxybutyrate. 184 65

After burn trauma, a very marked endocrine response occurs. Almost all the known hormones take part in it. Their response influences very much the postburn metabolic changes and participates in the integration of the body's response with the nervous and immune systems. In this review, mainly the changes in various hormone levels are described, as well as the possible role of the acute phase response after burn trauma, and the communications between the endocrine and immune systems, the cells of the latter are able to respond to various hormonal stimuli and to secrete various hormones themselves. Some of the hormones are very sensitive indicators of the burn stress, e.g., the T3 levels (very low), testosterone in males (very low), dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) (very low), ADH, catecholamines, renin and angiotensin II, cortisol (high), 17-beta-estradiol in males (usually elevated). Other hormones are usually elevated, but not always (ACTH, aldosterone, prolactin, glucagon, immunoreactive insulin, beta-endorphin, rT3, 11-beta-hydroxyandrostenedione), but there are hormones that are unually low (T4, FSH, androstenedione, progesterone--the latter especially in females). Calcitonin, parathyroid hormone, growth hormone are sometimes elevated, as well as LH (measured with RIA methods). TSH is usually normal, the biologically measured LH was reported to be low. The levels of the sensitive indicators of burn stress may be used to evaluate the effect of treatment: if the burn patient is properly treated, the indicators may become earlier normal.
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PMID:Endocrine changes after burn trauma--a review. 251 73

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

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 aging kidney suffers reduction both in mass and in glomerular filtration rate. These changes may be totally or partially due to atherosclerosis and hypertension, which reduce renal blood flow. Superimposed on these processes, and perhaps responsible for primary loss of renal mass irrespective of renal vascular disease, is glomerular damage and involution that is a consequence of adaptive increases in glomerular perfusion pressure that occurs as the number of nephrons decline with age. The data available at this time do not allow us to distinguish between these two potential mechanisms of renal senescence. The decline in GFR is in turn responsible for reduced renal acidification and the reduced renal clearance of drugs that are normally removed by the kidney. Certain renal functions, however, are depressed to a greater extent than is GFR. Both the ability to maximally dilute the urine and to maximally concentrate it are controlled by serum ADH concentrations and by the action of that hormone on the collecting duct. Aged rats do not maximally secrete ADH under conditions of dehydration and the effect of ADH on the kidney is also attenuated. Elderly humans also cannot maximally suppress ADH secretion when serum osmolality is reduced. Likewise, the renin-angiotensin-aldosterone axis is poorly responsive to volume depletion in aging subjects. As a result, elderly individuals cannot maximally retain sodium under conditions of plasma volume contraction out of proportion to reduction in GFR. The kidney is the site of vitamin D1 hydroxylation. Hydroxylation of vitamin D is reduced out of proportion to any reduction in GFR in the rat. There are no data as yet available on the effect of aging and the production of erythropoietin, a principal regulator of red blood cell mass. Neither are there data available on changes that might occur with advancing age in the ability of the aging kidney to metabolize various hormones, such as parathyroid hormone, glucagon, and insulin. The mechanisms and the full biochemical and physiologic consequences of renal senescence remain to be fully elucidated.
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PMID:The aging kidney. 391

To elucidate the ectopic hormonal pattern in patients with small cell carcinoma of the lung, plasma ACTH, serum calcitonin, serum gastrin, plasma glucagon, serum insulin, plasma secretin, plasma VIP, serum growth hormone, serum hCG/LH, the total of serum hCG and hCG-beta-subunit,serum alpha-subunit, serum human placental lactogen, urine ADH, urine 5-HIAA, urine VMA, urine HVA, and urine hCG-LH were measured prior to therapy in 75 patients. Twenty-two patients (29%) had elevated plasma ACTH, and 18 of these had concomitant increased values of corticosteroid in a 24-hour urine sample. Forty-eight patients (64%) were found to have elevated serum calcitonin, and one-third of the patients were diagnosed as having the ectopic ADH syndrome. Serum gastrin concentrations were increased in 20% of the patients, but the elevations were marginal in almost all cases. None of the remaining substances was found to be significantly elevated. Concentrations of plasma ACTH, serum calcitonin, and urine ADH were not found to be correlated with the stage of the disease, and no correlation of these substances with the histological subtypes of small cell carcinoma was disclosed.
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PMID:Hormonal polypeptides and amine metabolites in small cell carcinoma of the lung, with special reference to stage and subtypes. 624 82

The effects of Tramadol-N2O-anaesthesia on the per- and postoperative change in blood concentrations of cortisol, prolactin, thyroxine, triiodothyronine, cyclic AMP, glucagon, antidiuretic hormone, PTH-peptide (44-68), glucose, lactate, pyruvate and free fatty acids (FFA) were investigated in connection with elective orthopaedic surgery. Anaesthesia in man with Tramadol and nitrous oxide were found to be associated with a significant elevation of plasma cortisol and plasma prolactin in man. However, cortisol secretion during anaesthesia is associated with an inhibition in T4-T3 conversion. No significant alterations in plasma glucagon concentrations were observed. Generally, surgical trauma induced a significant increase in plasma cyclic AMP with intraoperative levels between 26.4 and 34.3 pmol/ml. At the end of surgery a significant fall in plasma PTH-peptide (44-68) occurred. There was also a significant change in plasma ADH levels following induction of anaesthesia. During surgery we found plasma ADH levels up to 56 pg/ml. In addition stress and surgical trauma increased blood glucose and FFA while plasma pyruvate and plasma lactate nearly remained unchanged. The data would suggest that the non-specific stress response attributed to anaesthesia may in fact be reflecting a response to relatively light anaesthesia.
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PMID:[Endocrine reaction pattern in the course of a one-phase tramadol-N2O combination anesthesia]. 629 29

The effects of glucagon and PTH on renal tubular electrolyte handling were studied in anesthetized, thyroparathyroidectomized Brattleboro rats infused with somatostatin. Fractional excretion of Ca and Mg was significantly lower during infusion of both hormones. Micropunctures of same nephrons localized the bulk of the increase in reabsorption in Henle's loop, where both hormones significantly enhanced the reabsorptive capacities for Ca, Mg, and K. Beyond the early distal tubule, Ca and Mg reabsorption was significantly greater during glucagon infusion and Ca reabsorption was significantly greater during PTH infusion. Cyclic adenosine monophosphate at a plasma concentration of 10(-6) M did not reproduce the effects of either glucagon or PTH. These results are similar to the findings reported for the effects of ADH and calcitonin on Ca, Mg, and K tubular handling, but different as far as Na and Cl are concerned, since their loop reabsorption was not significantly altered by glucagon and PTH. The data obtained here for glucagon and PTH, together with those for ADH and calcitonin, support the hypothesis that these four hormones exert similar effects in the thick ascending limb.
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PMID:PTH-like glucagon stimulation of Ca and Mg reabsorption in Henle's loop of the rat. 669 22

The effects of physiological doses of human calcitonin (HCT) on renal excretion and tubular transport of water and electrolytes were investigated in hormone-deprived rats, i.e., homozygous DI Brattleboro rats with reduced levels of circulating glucagon, parathyroid hormone, and thyrocalcitonin, as these hormones are believed, together with ADH, to stimulate the same cells of the thick ascending limb. The experimental design was similar to the one used in a preceding study aimed at determining the effects of ADH in hormone-deprived rats [C. de Rouffignac et al. Am. J. Physiol. 244 (Renal Fluid Electrolyte Physiol. 13): F156-F164, 1983]. In the present experiments, HCT consistently increased the reabsorption of Mg, Ca, and K and, to a lesser extent, Na and Cl in the loop of Henle, but phosphate transport did not rise. The urinary excretion rate of Mg and Ca fell significantly. These data are very similar to the findings obtained with ADH on hormone-deprived rats. It is concluded that, in vivo, administration of HCT 1) stimulates reabsorption of Na, Cl, Mg, Ca, and K by the thick ascending limb, and 2) consistently enhances Mg and Ca reabsorption by the whole kidney by enhancing reabsorption in the loop of Henle. The similarity of the physiological responses elicited by ADH and calcitonin on the thick ascending limb supports the hypothesis of multiple hormonal control of electrolyte transport by the thick ascending limb.
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PMID:ADH-like effects of calcitonin on electrolyte transport by Henle's loop of rat kidney. 669 23


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