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 influence of salt adaptation on specific adenylate cyclase activity (measured by conversion of [alpha-32p]-ATP into [alpha-32p]-cAMP) was investigated in gill plasma membranes of rainbow trout (Salmo gairdneri) adapted to various salinities (deionized water, DW; fresh water, FW; 3/4 sea water, 3/4 SW; sea water, SW) and in sea water adapted-mullet (Mugil sp.). Basal activity declined by a factor of 2 in trout with increasing external salinity (pmoles cAMP/mg protein/10 min: 530 in DW, 440 in FW, 340 in 3/4 SW; 250 in SW) and was very low in SW adapted-mullet: 35. The Km for ATP was similar (0.5 mM) in both FW adapted- and SW adapted- trout in either the absence (basal activity) or in the presence of stimulating agents (isoproterenol; NaF) while the Vm varied. Analysis of stimulation ratios with respect to basal levels of the enzyme showed that hormones (glucagon, VIP) and pharmacological substances (isoproterenol, NaF) display a greater potency in high salt than in low salt adapted- fish gills. In contrast, salt adaptation did not have any effect on the regulation of adenylate cyclase by PGE1. These results are interpreted in relation to the general process of osmoregulation.
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PMID:Adenylate cyclase activity in fish gills in relation to salt adaptation. 311 May 22

A high glomerular filtration rate (GFR) is often found early in insulin-dependent diabetes mellitus (IDDM). It has been suggested that high circulating glucose, glucagon, and GH levels could play a role in this increase in GFR. On the other hand, patients with IDDM in poor metabolic control also have high circulating ketone body levels. This study was undertaken to determine whether exogenous D,L-3-hydroxybutyric acid at two infusion rates (40 and 30 mumol kg-1 min-1) for 180 min altered renal plasma flow (RPF), GFR, and the excretion rate of total protein, beta 2-microglobulin, and albumin in 11 normal (N) subjects and 11 IDDM patients in whom euglycemia was achieved and maintained using the insulin-glucose clamp technique. RPF and GFR were measured by a priming-continuous infusion of [125I]hippurate and [51Cr]EDTA, respectively. The 40 mumol kg-1 min-1 D,L-3-hydroxybutyric acid infusion increased RPF and GFR in both N and IDDM subjects. Mean RPF increased from 588 +/- 78 (+/- SD) to 706 +/- 129 mL min-1 1.73 m-2 in N and from 671 +/- 101 to 781 +/- 99 in IDDM. GFR increased from 121 +/- 11 to 151 +/- 15 ml min-1 1.73 m-2 in N and from 136 +/- 11 to 191 +/- 16 in IDDM. The filtration fraction also was significantly higher in IDDM than in N during the D,L-3-hydroxybutyric acid infusion. The 30 mumol kg-1 min-1 D,L-3-hydroxybutyric acid infusion increased RPF and GFR to a somewhat lesser extent in both groups. D,L-3-hydroxybutyric acid infusions increased the tubular reabsorption rate of ketone bodies and sodium. The increase in tubular sodium reabsorption rate was correlated significantly to that in the tubular ketone body reabsorption rate. A significant decrease in urinary pH was found during the D,L-3-hydroxybutyric acid infusion. D,L-3-Hydroxybutyrate sodium salt (30 mumol kg-1 min-1) also was infused in 5 of the 11 diabetic patients. A similar increase in GFR and RPF occurred. Both total protein and beta 2-microglobulin, but not albumin, excretion rates increased during D,L-3-hydroxybutyric acid (40 mumol kg-1 min-1) infusion in N and IDDM subjects. D,L-3-Hydroxybutyric acid infusion did not change plasma glucagon, GH, or renin activity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Glomerular filtration rate is increased in man by the infusion of both D,L-3-hydroxybutyric acid and sodium D,L-3-hydroxybutyrate. 329 5

Both glucagon and prostaglandin F2 alpha have been shown to stimulate a chloride-rich choleresis in dogs. This study was performed to ascertain the interrelationship between glucagon and prostaglandin F2 alpha in stimulating bile flow. The experiments were performed using dogs with chronic biliary and gastric fistulas. Initially, the effects of prostaglandin F2 alpha on serum glucagon levels were evaluated. Glucagon administration increased bile volume and chloride secretion as did prostaglandin F2 alpha. Serum glucagon levels during prostaglandin F2 alpha administration were increased significantly over baseline values. During prostaglandin F2 alpha administration, the increase in serum glucagon concentration correlated well with the increase in hepatic bile flow. Administration of somatostatin, a hormone known to inhibit glucagon release, prevented the choleresis produced by prostaglandin F2 alpha while simultaneously eliminating the hyperglucagonemia. Subsequently, the effects of glucagon on bile prostaglandin F secretion and the effect of prostaglandin synthetase inhibition on glucagon choleresis were evaluated. Bile prostaglandin F secretion increased from control values of 101 +/- 27 pg per min (mean +/- S.D.) during bile salt infusion alone to 1,498 +/- 1,086 pg per min during the administration of 1 microgram kg-1 hr-1 glucagon. The prostaglandin synthetase inhibitor, indomethacin, significantly decreased the choleresis, the increased bile chloride secretion and the increased bile prostaglandin F secretion produced by glucagon. The results of this study indicate that prostaglandin F2 alpha-stimulated bile flow is primarily the result of glucagon release and suggest that prostaglandin F2 alpha may be involved in glucagon secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The relationship between glucagon and prostaglandin F in stimulating canine hepatic bile flow. 345 73

Pharmacologic doses of glucagon affect canine bile secretion by increasing bile flow while simultaneously decreasing biliary cholesterol output. The present study was performed to determine if physiologic doses of glucagon reduce biliary cholesterol output. Awake dogs received both intravenous 1% sodium taurocholate (50 ml/hr) to stabilize bile flow and somatostatin (12 micrograms/kg/hr) to suppress endogenous pancreatic hormone release. Suppression was documented by significant decreases in portal plasma glucagon and insulin levels. During experimental trials, dogs received, in addition, glucagon (5 ng/kg/min) infused via a splenic vein catheter. Bile flow significantly decreased during the initial hour of somatostatin infusion but increased significantly only in experimental trials during subsequent glucagon infusion. Biliary cholesterol output showed no change during control studies (N = 9), but decreased significantly during glucagon infusion studies (N = 11). Biliary phospholipids and bile salts failed to show any changes during glucagon infusion. These data demonstrate that glucagon at physiologic levels influences both the volume and cholesterol content of bile and suggest the mechanism of decreasing cholesterol output must be independent of pathways for influencing bile salt or phospholipid secretion.
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PMID:Glucagon lowers canine biliary cholesterol output at physiologic doses. 351 1

We investigated by micropuncture the effects of glucagon and parathyroid hormone (PTH) on thin limbs of juxtamedullary nephrons of rats with reduced plasma concentration of endogenous glucagon, PTH, antidiuretic hormone (ADH) and calcitonin, all four hormones enhancing the adenylate-cyclase activity in the thick ascending limbs and the distal nephron. Such a hormonal depletion suppresses the corticomedullary concentration gradient, making favourable conditions for studying the influence of these hormones on the renal concentrating mechanism. Administration of glucagon (4.4 ng/min-1) or PTH (5 mU/min-1) to these hormone-deprived rats elicited the expected decrease in urinary Mg and Ca fractional excretion without modifying either fractional or absolute excretion of water. At the tip of the loop, glucagon enhanced the loop fluid osmolality by 20%, but left the delivery of water unchanged. The Na and Cl concentrations increased significantly with the osmolality, resulting in a positive correlation between the fractional delivery of either ion and the loop fluid osmolality. PTH increased the fraction of filtered phosphate delivered to the thin limbs, as expected, but, in contrast to glucagon, did not alter either the Na, Cl, or total solute fractional deliveries. The Mg, Ca and K deliveries were unaffected by glucagon and PTH. In conclusion, glucagon, which activates the cyclase system of both the medullary and cortical portion of the thick ascending limb, enhances the delivery of salt to the tip of the loop by net sodium chloride addition to the descending limb. PTH which activates the adenyl-cyclase system only in the cortical thick ascending limb cannot enhance such NaCl delivery. NaCl, when added, might therefore originate from the medullary thick ascending limb.
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PMID:Effects of glucagon and PTH on the loop of Henle of rat juxtamedullary nephrons. 371 66

Recent studies showed that taurine, a sulphonic amino acid, could decrease blood pressure and increase sympathoadrenal tone in DoCA-salt-treated hypertensive rats. To determine whether taurine exerts its antihypertensive action in man in a similar fashion, we studied the effect of oral administration of taurine (6 g for 7 days) on blood pressure and plasma catecholamines in 19 young patients with borderline hypertension in a double-blind, placebo-controlled fashion. Systolic blood pressure in the 10 patients who were treated with taurine decreased by 9.0 +/- 2.9 mm Hg (mean +/- SE; p less than .05 by paired t test), compared with a 2.7 +/- 2.3 mm Hg decrease (NS) in the nine patients treated with placebo and diastolic blood pressure in the taurine-treated patients decreased by 4.1 +/- 1.7 mm Hg (p less than .05) compared with 1.2 +/- 3.0 mm Hg (NS) in the placebo-treated subjects. In the patients receiving taurine plasma epinephrine (E) decreased significantly, with a negligible decrease in plasma norepinephrine (NE). The effect of taurine on plasma catecholamines and the response of plasma E after the stimulation with glucagon was also studied in 12 borderline hypertensive and nine age-matched normotensive subjects. Basal plasma E was significantly higher in borderline hypertensive than in normal subjects, but basal plasma NE did not differ in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of increased adrenomedullary activity and taurine in young patients with borderline hypertension. 381 64

Exogenous glucagon administration is associated with stimulation of hepatic bile flow. The physiologic role that glucagon plays in the control of hepatic bile flow remains indeterminant. The purpose of this study was to evaluate amino acid administration, a stimulus of endogenous glucagon release, on canine hepatic bile flow. The experiments were performed utilizing cholecystectomized dogs with chronic biliary fistulas. The enterohepatic circulation of bile salts was artificially maintained by intravenous bile salt administration. Intravenous L-arginine stimulated endogenous glucagon release and hepatic bile secretion. Intravenous amino acid administration produced significant increases in hepatic bile flow and plasma glucagon and was significantly more potent than intravenous arginine. Intravenous amino acid administration produced small but significant increases in serum insulin but did not significantly change plasma concentrations of cholecystokinin. The results of this study suggest that endogenous glucagon secretion produces a choleresis and supports a role for glucagon in the physiologic control of canine hepatic bile flow.
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PMID:Effect of stimulation of endogenous glucagon secretion by amino acid administration on canine hepatic bile flow. 382 81

1. Intracellular recordings of membrane potential were made from superficial cells of isolated mouse liver segments superfused with physiological salt solutions.2. The mean resting cell membrane potential was -39.4 mV.3. Glucagon caused a dose-dependent membrane hyperpolarization which was detectable at 10(-9)M and maximal (7 mV) at 10(-7)M. The hyperpolarization started within half a minute after exposure to glucagon. Secretion (2 x 10(-7)M) had no effect on the membrane potential.4. Adrenaline (10(-6)M) and isoprenaline (10(-6)M) also caused membrane hyperpolarization (4-6 mV). The effect of isoprenaline, but not that of adrenaline, was blocked by propranolol (5 x 10(-6)M).5. Dibutyryl adenosine 3',5'-monophosphate (10(-3)M) caused a membrane hyperpolarization of 4-8 mV.6. In the absence of extracellular K or the presence of Strophanthin-G (10(-3)M) the resting potential was decreased and the response to glucagon reduced. During exposure to a solution containing 20 mM-K the resting potential was slightly enhanced and the amplitude of the glucagon-induced hyperpolarization reduced compared with control conditions.7. It is concluded that the effect of glucagon on the membrane potential is due to an interaction with specific membrane receptors probably leading to activation of the membrane-bound adenyl cyclase. It is probable that the hyperpolarization is mediated by cyclic AMP. The hyperpolarization induced by glucagon is dependent on a normal function of the membrane Na-K pump.
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PMID:The effect of glucagon on the liver cell membrane potential. 436 92

It has been suggested that glucagon-like immunoreactivity (GLI) of gastrointestinal tissues might, like pancreatic glucagon, have calcium-lowering activity. Studies were designed, therefore, to determine if calcium absorption was associated with GLI release from the gut. The intraduodenal administration of 4.5 mmoles of calcium chloride per kg of body weight to conscious dogs was associated with a prompt rise in plasma GLI from a base line of 2.2 ng/ml (SEM +/-0.2) to a peak of 4.3 ng/ml (SEM +/-0.3) at 45 and 60 min, in association with a rise of plasma calcium from 8.6 to 10.4 mg/100 ml. Neither pancreatic glucagon, insulin, nor glucose changed. Smaller calcium loads had progressively diminishing effects on GLI release. Calcium lactate also appeared to stimulate effectively GLI release. Both magnesium chloride and sodium chloride given intraduodenally were associated with a significant though modest increase in GLI. To determine if stimulation of GLI release by substances other than calcium would lower serum calcium, glucose was administered intraduodenally. Despite a marked increase in GLI, plasma calcium fell only 9%, a decline which could be entirely accounted for by hemodilution. Although the physiologic significance of this demonstration that the absorption of calcium salts is associated with GLI release is open to serious question, the findings are not incompatible with the concept that glucagon-like polypeptides are released from the gut during the absorption of certain salts, possibly to alert appropriate homeostatic regulators so as to avoid major changes in electrolyte concentration after the ingestion of large salt loads.
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PMID:The effect of calcium and other salts upon the release of glucagon-like immunoreactivity from the gut. 501 13

The role of insulin in control of bile secretion is uncertain. To study the mechanism of choleresis produced by large doses of insulin, bile was collected through modified Thomas cannulas from dogs anesthetized with pentobarbital. Animals received pipenzolate methylbromide, sodium taurocholate, and [14C]erythritol. After bile flow had stabilized three animals received infusions of insulin at 2, 4, 13, 26, 35, and 70 mU . kg-1 . min-1 for 40 min each. Bile and [14C]erythritol clearance increased (P less than 0.005), but bile salt output remained constant, suggesting that the choleresis was mainly due to enhanced bile salt-independent canalicular flow. Plasma insulin and glucagon levels also rose when insulin was infused. To exclude the possible effects of glucagon three additional animals received somatostatin (800 ng . kg-1 . min-1) along with infusions of insulin. Bile flow and [14C]erythritol clearance again increased significantly, but glucagon levels remained low, suggesting that the effects on bile flow were due to insulin alone. To determine whether physiological doses of insulin altered bile flow dogs were anesthetized with pentobarbital and received pipenzolate methylbromide, taurocholate, [14C]erythritol, and somatostatin (800 ng . kg-1 . min-1). Insulin (0.2 and 0.8 mU . kg-1 . min-1) was infused through the portal vein for 1 h each. Bile flow and [14C]erythritol clearance increased with insulin (0.8 mU . kg-1 . min-1; P less than 0.02), suggesting that the choleresis may have been due to bile salt-independent canalicular flow. Plasma insulin rose to physiological postprandial levels. These studies demonstrate that pharmacological and physiological levels of insulin administered to dogs produce a significant choleresis. Thus insulin may play an important role in the regulation of bile secretion.
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PMID:Pharmacological and physiological doses of insulin and determinants of bile flow in dogs. 613 50


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