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Aim To investigate the effects of dopamine(DA)on insulin secretion from rat islets and the possible mechanism.Methods Pancreatic islets were obtained from the pancreatic of male SD rats by collagenase P digestion and histopaque-1077 density gradient separation.Insulin secretion experiment was used to observe the change of insulin release after DA treatments.As to study the potential mechanisms of the effects of DA,patch-clamp experiment and calcuim image technique were applied to test the depolarization-evoked Ca2+ currents,action potential duration and intracellular Ca2+ concentration.Results In 2.8 mmol·L-1 glucose,DA had no effect on insulin secretion;in 16.7 mmol·L-1 glucose,dopamine inhibited insulin secretion in a dose-dependent manner.DA inhibited the inward calcium current,shorten the action potential duration,and reduced the intracellular Ca2+ concentration.Conclusion DA inhibits insulin secretion maybe by decreasing the inward calcium current leading to shorten the action potential duration and reduce the intracellular Ca2+ concentration.
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Aim To observe the effects of glucose-stim-ulated insulin secretion ( GSIS ) on rat islets after S1 P treatments and the underlying molecular mechanisms. Methods Collagenase P and Histopaque 1077 were used to digest and isolate rat pancreatic islets, and Dispase II was used to digest pancreatic islet to obtain pancreatic cells. Insulin secretions were measured after S1P (0~20 μmol·L-1 ) treatment under low glucose ( LG, 2. 8 mmol·L-1 ) and high glucose ( HG, 16. 7 mmol·L-1 ) conditions. Patch-clamp recordings were applied to monitor voltage-dependent potassium chan-nel currents (Kv currents) after S1P treatment. Calci-um image technique was used to measure the changes of intracellular Ca2+ concentration after S1P ( 0 ~20μmol·L-1 ) treatments. Results HG group signifi-cantly increased insulin secretion compared to LG group ( P0. 05 ) . S1 P increased insulin secretion significantly in a dose-dependent man-ner under HG condition ( P<0. 01 ) . Kv currents ofβcells were inhibited significantly after S1 P treatment ( P<0. 01 ) . S1 P increased the concentrations of in-tracellular Ca2+ in a dose-dependent manner under HG condition( P <0. 01) . Conclusion S1P may pro-mote GSIS by inhibiting Kv currents and increasing the level of intracellular Ca2+.
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Aim To study the insulinotropic effects of Efaroxan and the underlying mechanism in rat βcells. Methods Pancreatic islets were isolated by college-nase p digestion.Radioimmunoassay was used to meas-ure insulin secretion and cAMP level in rat pancreatic islets.Results Efaroxan only potentiated insulin se-cretion at high glucose concentrations(8.3,1 1 .1 mmol ·L -1 )but not at low glucose concentrations.KU1 4R,an antagonist of Efaroxan,remarkably inhibited Efarox-an-potentiated insulin secretion;and similarly,KU1 4R significantly inhibited forskolin-induced and IBMX-in-duced insulin secretion.cAMP measurement showed that forskolin and IBMX significantly increased cAMP levels,but Efaroxan and KU1 4R had no effects on cAMP content in pancreatic islets.Conclusion The mechanism of Efaroxan-potentiated insulin secretion is related to downstream of cAMP signaling pathway, KU1 4R antagonized the downstream of cAMP signaling leading to its inhibitory effects on Efaroxan,forskolin and IBMX-induced insulin secretion.
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leptin-induced VSMCs proliferation as well as expression of PCNA and OB-R at both mRNA and protein levels. The maximum effect was at 100 μmol/L(P<0.01).
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Objective: To explore the effects of thiazolidinediones pioglitazone on the mRNA expressions of adiponectin and its receptor in human adipocytes.Methods: We obtained omental adipose tissue biopsies from patients undergoing elective open-abdominal surgery,performed primary culture and differentiation induction of the human preadipocytes,treated them with pioglitazone at different concentrations,and detected the mRNA expressions of adiponectin and its receptor in them by RT-PCR.Results: The mRNA expressions of adiponectin and its receptor were higher in the pioglitazone groups than in the non-pioglitazone control.Conclusion: Pioglitazone promotes the mRNA expressions of adiponectin and its receptor in human adipocytes.