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 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

The effects of vasoactive intestinal polypeptide (VIP) on several enzymes of glycogen metabolism in rat hepatocytes were compared with those of glucagon and of vasopressin (ADH). VIP caused phosphorylase activation and glycogenolysis in hepatocytes from fed rats. In hepatocytes from fasted rats incubated with glucose, lactate, and pyruvate, VIP inhibited net glycogen deposition, inactivated glycogen synthase, and activated phosphorylase. VIP was about 100-fold less potent than glucagon and 1,000-fold less potent than ADH in causing activation of phosphorylase. The ability of VIP to activate phosphorylase was not altered by chelation of the calcium in the medium. The half maximal effective doses of VIP for both phosphorylase activation and stimulation of glycogenolysis were 10-30 nM. Treatment with VIP, ADH, or glucagon did not decrease phosphorylase phosphatase activity. Each of these hormones, however, lengthened the lag time before synthase phosphatase activity was expressed in vitro. Other gut hormones tested did not affect hepatocyte glycogen metabolism. These results do not support the concept of physiologic control of hepatic glycogen metabolism by VIP or by other gut hormones.
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PMID:Effect of vasoactive intestinal polypeptide on glycogen metabolism in rat hepatocytes. 680 98

The effects of 1-desamino-8-D-arginine vasopressin (dDAVP) on renal excretion and tubular transport of water and electrolytes were investigated in homozygous DI Brattleboro rats. To ascertain these effects on the loop of Henle, circulating glucagon, parathyroid hormone, and thyrocalcitonin were reduced before the experiments, as these hormones are believed to stimulate the same cells of the thick ascending limb as ADH. dDAVP did not alter either glomerular or proximal tubular functions. In the loop, it consistently raised reabsorption of Mg, Ca, K, and, to a lesser extent, Na and Cl, but phosphate transport was not affected. dDAVP lowered the urinary excretion rates for Mg, Ca, K, Cl, and total solutes. For Mg, this reduction was independent of the drop in the urinary flow rate following dDAVP administration but was significantly correlated to this drop in the case of Ca, K, Cl, and total solutes. Na and P excretions were not altered by dDAVP. It is concluded that, in vivo, administration of ADH 1) stimulates reabsorption of Na, Cl, Mg, Ca, and K by the thick ascending limb, 2) consistently enhances Mg reabsorption by the whole kidney by enhancing reabsorption in the loop of Henle, and 3) at maximal antidiuresis, raises Ca, K, Cl, and total solute reabsorption, probably because of the drop in tubular flow rates in the distal parts of the nephron consequent to the hormone administration.
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PMID:Stimulation by antidiuretic hormone of electrolyte tubular reabsorption in rat kidney. 682 79

Ethanol suppressed, in a dose-related manner, glucose-induced insulin (IRI) release and thus delayed the disappearance of glucose from the blood of rats. Pretreatment with pyrazole, an alcohol dehydrogenase inhibitor, exacerbated the effect of ethanol on IRI release, glucose tolerance and glucagon (IRG) release. These results suggest that ethanol produces glucose intolerance by inhibiting glucose-induced IRI release and by augmenting IRG release. Moreover, these findings indicate that ethanol does not have to be metabolized completely in order to produce these effects.
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PMID:Acute pretreatment with pyrazole and ethanol: effects on glucose-induced changes in insulin and glucagon. 699 53

This article describes some of the alterations that occur in the neuroendocrine system during sepsis. With a goal of better management of the patient with sepsis, an overview of the endocrine system, its hormones, and its close relationship to the nervous system is presented. The importance of hormone target cell receptor coupling, specific mechanisms of action that result in physiological changes, and regulation of hormone secretion are detailed. The roles and effects of catecholamines, glucagon, cortisol, and growth hormone are explored. Sick euthyroid syndrome, alterations in ADH, the renin-angiotensin-aldosterone axis, and PTH secretion are also examined.
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PMID:Hormonal response in sepsis. 794 87

Previous studies indicate that catecholamines play an important role in mediating the glucose metabolic response to endotoxin. Because acute ethanol (EtOH) intoxication impairs this response, the present study was initiated to ascertain whether EtOH attenuates the lipopolysaccharide response by decreasing the increment in plasma catecholamines after endotoxin or by decreasing the responsiveness of rats to epinephrine. All studies were performed on chronically catheterized fasted rats infused intravenously with either EtOH or an equal volume of saline. In the first series of experiments, intravenous administration of Escherichia coli endotoxin increased, to the same extent, the plasma concentrations of epinephrine and norepinephrine in both saline- and EtOH-infused rats. In the second study, rats were infused with [3-3H]glucose to assess whole body glucose metabolism and the ability of EtOH to alter the glucose metabolic response to epinephrine. The exogenous infusion of a maximally stimulating dose of epinephrine (1 microgram.min-1.kg-1) into saline-infused control animals for 3 h produced a marked hyperglycemia that resulted from a sustained increase in the rate of hepatic glucose production and a reduction in the metabolic clearance rate for glucose. EtOH infusion did not prevent the epinephrine-induced hyperglycemia but blunted the stimulatory effect of epinephrine on glucose production. The differences in glucose metabolism between saline- and EtOH-treated rats could not be explained by changes in plasma insulin or glucagon concentrations. Furthermore, the ability of EtOH to impair the epinephrine-induced increase in glucose production was still evident in rats treated with 4-methylpyrazole, an inhibitor of alcohol dehydrogenase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epinephrine-induced changes in hepatic glucose production after ethanol. 802 15

To investigate pancreatic endocrine function in brain-dead patients, an intravenous glucose tolerance test (i.v. GTT) was performed in 8 brain-dead subjects maintained using the combined administration of vasopressin (ADH) and catecholamines during the first 3 days following the onset of brain death. Ten healthy adults served as control subjects. Although plasma glucose concentrations markedly increased and exceeded 300 mg/dl in most subjects just after the onset of brain death, they decreased to less than 200 mg/dl in most subjects after 24 h. The early insulin release also was significantly lower in brain dead subjects compared to controls (p < 0.01). The late insulin release was not decreased compared to controls but rather increased, which was accompanied by decreased glucose disappearance rate. The early insulin release recovered rapidly during the first 3 days following brain death without significant changes in the plasma hormone concentrations such as epinephrine, human growth hormone, thyroid-stimulating hormone, triiodothyronine, thyroxine, cortisol, and glucagon. The early insulin release and the plasma glucose concentration just before i.v. GTT was negatively correlated (R = -0.55, p < 0.05). We suggest awaiting recovery from hyperglycemia and early insulin release provides a reasonable approach to transplantation of the pancreas.
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PMID:Transient suppression of pancreatic endocrine function in patients following brain death. 865 94

The body's general response to serious thermal injury is characterized by increased vascular permeability immediately after injury and subsequent hypovolemic shock. Skeleto-muscular proteolysis, lipolysis, gluconeogenesis, increased metabolic rate, and a severe systemic inflammatory response induced by local infections or surgical procedures. The increased vascular permeability is mediated by histamine and numerous vasoactive substances, including serotonin, bradykinin, prostaglandins, leukotrienes, and platelet activating factor. Hyper-metabolism is mediated by hormones such as catecholamines, glucagon, and particularly cortisol. In addition, among the putative mediators of the metabolic response to injury, attention has recently been focused on cytokines and lipid mediators which are mainly produced by activated reticuloendothelial cells. Cytokines such as interleukin-1, interleukin-6 and tumor necrosis factor and cortisol responses are interrelated, since cytokines activate the hypothalamo-adrenal axis. The cytokine storm seen in burn patients may be associated with depression of the immune system and with susceptibility to infection. Thermal injury can also lead to activation of the renin-angiotensin-aldosterone system, increased ADH production, and production of atrial natriuretic polypeptide to maintain the circulatory volume. Burn wound infections or surgical procedures can produce and perpetuate a mediator-induced systemic inflammatory response that may lead to multiple organ failure. Serum levels of interleukin-6 are very sensitive to surgical stress, and may be a useful indicator of the general condition of severely burned patients.
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PMID:[Pathophysiologic changes in patients with severe burns: role of hormones and chemical mediators]. 954 40

Many birds switch seasonally or during ontogeny between diets of varying protein content. In mammals, high-protein diets induce hypertrophy of the kidney in general and of the thick ascending limbs (TAL) in particular, along with increases in glomerular filtration rate (GFR) and urine flow. A hypothesis to explain these phenomena is that the TAL become increasingly sensitive to peptide hormones (glucagon and antidiuretic hormone [ADH]) released in response to protein feeding; the consequent enhancement of ion reabsorption dilutes urine reaching the macula densa, thereby suppressing tubulo-glomerular feedback (TGF) and causing a rise in GFR. Avian kidneys possess most of the elements involved in this mechanism, including loops of Henle with TAL, sensitivity of TAL to ADH (arginine vasotocin [AVT] in birds), and the elements of TGF. We therefore hypothesized that switching from a low-protein to a high-protein diet would induce responses in birds similar to those found in mammals. We tested this hypothesis by feeding house sparrows, Passer domesticus, isocaloric diets containing either 8% or 30% protein. Birds on high-protein food had larger renal medullae, both in mass and in TAL diameter, but no increase in whole-kidney mass. Urine flow was approximately doubled on high-protein food, but there was no change in GFR. We were not able to detect an increased sensitivity of AVT-induced adenylyl cyclase activity in TAL from high-protein animals, and responsiveness to glucagon was higher in TAL from birds eating low-protein food. We are unable to conclude that a suppression of TGF is responsible for the rise in urine flow in birds eating high-protein foods, and the mechanisms behind the medullary hypertrophy and the diuresis remain to be fully explored.
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PMID:Renal response to dietary protein in the house sparrow Passer domesticus. 1133 19

Ethanol has profound acute effects on hepatic metabolism. While many of these effects are mediated via the redox imbalance that accompanies hepatic ethanol oxidation via the alcohol dehydrogenase (ADH) pathway, there is increasing evidence that ethanol also perturbs hepatic metabolism via its modulation of cyclic AMP-mediated signalling pathways. This paper examines the effects of ethanol on glucagon-stimulated protein phosphorylation using SDS-PAGE to analyse the 32P-labelling of cytosolic peptides in isolated rat hepatocytes pre-equilibrated with 32PO4(3-). We show that ethanol has biphasic effects on glucagon-stimulated protein phosphorylation. At a low concentration (50 mM), ethanol decreased the phosphorylation of certain peptides, whereas at higher concentrations (100-200 mM) it increased the 32P-labelling of all of the eleven glucagon-stimulated cytosolic peptides. The non-metabolizable alcohol 2-methylpyrazole-2-ol had no effects on glucagon-stimulated protein phosphorylation. The ADH inhibitor 4-methylpyrazole at 150 mM ethanol concentration abolished the potentiating effect of ethanol on the glucagon-stimulated phosphorylation of most peptides. In conclusion, the results indicate that ethanol alters glucagon-receptor-dependent protein phosphorylation in isolated hepatocytes via a complex mechanism that is partially dependent on ethanol oxidation via ADH.
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PMID:Effects of ethanol on glucagon-stimulated protein phosphorylation in isolated hepatocytes. 1464 35


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