Association between angiotensinogen gene M235T polymorphism and mitral valve prolapse syndrome in Taiwan Chinese

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Title:	Association between angiotensinogen gene M235T polymorphism and mitral valve prolapse syndrome in Taiwan Chinese
Authors:	Chou, HT;Hung, JS;Chen, YT;Shi, YR;Tsai, FJ
Contributors:	附設醫院內科部心臟科;China Med Coll Hosp, Dept Med, Div Cardiol, Taichung 404, Taiwan;China Med Coll Hosp, Dept Pediat Med Res & Med Genet, Taichung 404, Taiwan
Date:	2002
Issue Date:	2010-09-24 14:19:21 (UTC+8)
Publisher:	I C R PUBLISHERS
Abstract:	The effect of beta-endorphin on plasma glucose levels was investigated in streptozotocin-induced diabetic rats (STZ-diabetic rats). A dose-dependent lowering of plasma glucose was observed in the fasting STZ-diabetic rat fifteen minutes after intravenous injection of beta-endorphin. The plasma glucose-lowering effect of beta-endorphin was abolished by pretreatment with naloxone or naloxonazine at doses sufficient to block opioid p-receptors. Also, unlike wild-type diabetic mice, beta-endorphin failed to induce its plasma glucose-lowering effect in the opioid beta-receptor knock-out diabetic mice. In isolated soleus muscle, beta-endorphin enhanced the uptake of radioactive glucose in a concentration-dependent manner. Stimulatory effects of beta-enclorphin on glycogen synthesis were also seen in hepatocytes isolated from STZ-diabetic rats. The blockade of these actions by naloxone and naloxonazine indicated the mediation of opioid beta-receptors. In the presence of U73312, the specific inhibitor of phospholipase C (PLC), the uptake of radioactive glucose into isolated soleus muscle induced by beta-endorphin was reduced in a concentration-dependent manner, but it was not affected by U73343, the negative control of U73312. Moreover, chelerythrine and GF 109203X diminished the stimulatory action of P-endorphin on the uptake of radioactive glucose at a concentration sufficient to inhibit protein kinase C (PKC). The data obtained suggest that activating opioid p-receptors by beta-endorphin may increase glucose utilization in peripheral tissues via the PLC-PKC pathway to lower plasma glucose in diabetic rats lacking insulin.
Relation:	JOURNAL OF HEART VALVE DISEASE 11(6):830-836
Appears in Collections:	[China Medical University Hospital] Jurnal articles

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