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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied the effects of two modulations--streptozotocin-induced diabetes in vivo, and the presence of the carboxylic proton ionophore monensin in vitro--on the degradation of 3H-asialoorosomucoid ligand in isolated rat hepatocytes. The ligand was internalized by means of a synchronous wave procedure. Diabetes was associated with a marked decrease in the amount of total degraded radioactive ligand compared to that in normal cells (3.6% and 37.3% of internalized ligand respectively, at 60 min), together with increased secretion of degradation products into the incubation medium (87% and 46.3% of the total degraded ligand was secreted by diabetic and normal cells, respectively). Monensin induced similar effects in normal cells, but had no apparent effect in diabetic cells.
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PMID:Effect of monensin and diabetes on asialoglycoprotein degradation in rat hepatocytes. 151 81

The In-R1-G9 cell line is one of the clones derived from the In-111-R1 hamster insulinoma cell line and produces glucagon. The secretory responses of In-R1-G9 cells were further examined to characterize the nature of the cells. Vincristine had no effect on glucagon secretion and colchicine enhanced glucagon secretion slightly after a short incubation. Two calmodulin inhibitors, trifluoperazine and chlorpromazine, did not affect glucagon secretion. Monensin at 10(-8) M suppressed glucagon secretion by 50%. Secretion of glucagon was calcium-dependent. The addition of A23187 to the incubation medium resulted in a 180% increase over control for 1 h and calcium deprivation from the medium suppressed glucagon secretion markedly. Theophylline, a phosphodiesterase inhibitor, caused a 230% increase in glucagon secretion. An experiment using cycloheximide suggested that newly synthesized glucagon appears in the medium at 30 min. This cell line should be useful for various experiments in many fields of research.
Diabetes Res Clin Pract 1988 Feb 19
PMID:Characterization of secretory responses of a glucagon-producing In-R1-G9 cell line. 283 60

We studied the effect of alloxan-induced diabetes on Na+ pump activity in isolated rabbit bladder strips. In addition, the effects of diabetes and the Na+ pump inhibitor ouabain on contractions induced by carbachol (CCh) and KCl were studied. In bladder strips from diabetic rabbits, ouabain-sensitive 86Rb+ uptake (a measure of Na+ pump activity) was approximately 50% less compared with strips from normal bladder. Diabetes also reduced the maximum contractions induced by CCh and KCl. Treatment of bladder strips with ouabain alone caused an acute concentration-dependent increase in tone. In contrast, longer incubation with ouabain inhibited CCh- and KCl-induced contractions in normal and diabetic bladders. Furthermore, differences in agonist-mediated contractions observed between normal and diabetic bladders were abolished in the presence of the maximally effective concentration of ouabain (10 microM). The ability of CCh to cause contraction in normal and diabetic rabbit bladders was also significantly inhibited by the Na+ ionophore monensin but not by the Ca2+ ionophore A-23187 or by depolarization with KCl. Monensin also inhibited KCl-induced contractions in normal bladder strips. These results indicate that 1) Na+ pump activity is an important modulator of bladder smooth muscle tone, 2) diabetes diminishes Na+ pump activity and inhibits agonist-induced contractions in bladder, and 3) an increase in intracellular Na+ concentration, secondary to inhibition of bladder smooth muscle Na+ pump activity, is associated with reduced responsiveness to contractile agonists. Diminished Na+ pump activity in diabetes may, in part, contribute to the development of bladder cystopathy.
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PMID:Altered contractility of urinary bladder in diabetic rabbits: relationship to reduced Na+ pump activity. 899 7