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)

1. Adipocytes isolated from rats 6--9 days after adrenalectomy had significantly increased sensitivity to insulin action against noradrenaline-stimulated lipolysis. In the presence of adenosine deaminase there was no significant difference in insulin sensitivity between cells from adrenalectomized and sham-operated rats. 2. Adipocytes from adrenalectomized rats had decreased lipolytic responses to all concentrations of noradrenaline and glucagon tested and a decreased lipolytic response to low but not high concentrations of corticotropin. There was no difference in lipolytic response to theophylline after adrenalectomy. Adenosine deaminase corrected the differences in response to noradrenaline and glucagon resulting from adrenalectomy. 3. In the presence of adenosine deaminase rates of lipolysis, after stimulation by high concentrations of noradrenaline, glucagon, corticotropin or theophylline, were the same in cells from adrenalectomized or sham-operated rats. 4. These findings and previously reported effects of adenosine and adrenalectomy on adipocyte function are discussed. It is proposed that changes in adipocyte hormone responsiveness after adrenalectomy may result from changes in adenosine metabolism or release.
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PMID:Alterations in response of rat white adipocytes to insulin, noradrenaline, corticotropin and glucagon after adrenalectomy. Correction of these changes by adenosine deaminase. 21 18

The hyperfiltration action of atrial natriuretic factor (ANF) and glucagon is accompanied by an elevation of adenosine in urine. We employed adenosine deaminase to evaluate the role of intrarenal adenosine in glomerular hyperfiltration induced by those hormones. Administration of ANF (2 micrograms/kg/min) resulted in an increase in the glomerular filtration rate (GFR): 1.99 vs. 3.01 ml/min (p less than 0.02) which was associated with a rise of adenosine excretion 87 vs. 151 pmol/min. Similarly, infusion of glucagon (2 micrograms/kg/min) raised the GFR from 1.86 to 2.67 ml/min (p less than 0.02) and adenosine excretion from 105 to 178 pmol/min (p less than 0.02). Adenosine deaminase treatment (2 U x kg/min) did not change the basal GFR and renal plasma flow but decreased plasma adenosine level 0.64 vs. 0.18 microM (p less than 0.001) and its excretion: 93 vs. 13 pmol/min (p less than 0.01). In adenosine deaminase treated rats ANF dramatically increased the GFR from 2.09 to 4.18 ml/min (p less than 0.001) and fractional filtration from 0.29 to 0.57, and the increase persisted throughout infusion of ANF. Similarly, adenosine deaminase treatment potentiated and prolonged the effect of glucagon on the GFR. These data indicate that depletion in renal adenosine does not decrease the GFR and that adenosine is present at inhibitory concentrations only during hormonal stimulation of glomerular filtration. It is concluded that renal endogenous adenosine functions do restrain hyperfiltration induced by ANF or glucagon.
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PMID:Intrarenal adenosine prevents hyperfiltration induced by atrial natriuretic factor. 213 65

Effects of adenosine deaminase and glucagon on insulin-stimulated 2-deoxyglucose uptake by rat adipocytes are reported. (1) Adenosine deaminase (10 micrograms/ml) caused a rightward shift in the dose-response curve for the stimulation by insulin of 2-deoxyglucose uptake, but the enzyme did not alter either the basal or the maximally insulin-stimulated uptake rate. (2) In adipocytes obtained from 24 h-starved rats, glucagon inhibited the effect of insulin on 2-deoxyglucose uptake in the presence (but not in the absence) of adenosine deaminase. Basal uptake rates were unaffected. (3) Glucagon inhibited insulin-stimulated 2-deoxyglucose uptake to a greater extent in cells isolated from starved rats than in cells from fed rats. (4) Adipocytes isolated from fed and from starved rats did not differ in their capacity for degradation of 125I-labelled glucagon. The results suggest that adenosine and glucagon are regulators of insulin action in adipose tissue.
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PMID:Glucagon inhibition of insulin-stimulated 2-deoxyglucose uptake by rat adipocytes in the presence of adenosine deaminase. 634 92

During winter, hibernating animals rely on their lipid stores for survival. In vitro lipolytic activity of isolated adipocytes from gonadal and subcutaneous white adipose tissue (WAT) was studied in captive alpine marmots (Marmota marmota) at two different times of their yearly cycle. During the summer, when marmots were eating, adipocyte responsiveness and sensitivity to isoprenaline and noradrenaline were higher in gonadal than in subcutaneous WAT. During hibernation, when marmots were spontaneously fasting. both the response and sensitivity to catecholamines decreased in gonadal WAT to the level of subcutaneous WAT. A similar pattern of response was also observed when lipolysis was stimulated with glucagon but the lipolytic rate was three times lower than with catecholamines. Adenosine deaminase (ADA) had a marked stimulatory effect on lipolysis, especially during the 'feeding' period, suggesting that adenosine may be a potent lipolytic modulator in marmot adipocytes. It is concluded that in marmots, lipolysis could be differentially regulated between fat depots during the annual cycle possibly to optimize either the building-up or the use of fat reserves.
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PMID:Regional variation of white adipocyte lipolysis during the annual cycle of the alpine marmot. 1053 Aug 94