Effects of Glycyrrhetic Acid (GE) on Some Gluconeogenic Enzymes, Lipoprotein Lipase and Peroxisome Proliferator-Activated Receptors Alpha and Gamma

Hui Ping Yaw, S. Ton, K. A. Kadir, Tee Yee Tan, Y. W. Teo, Michael Yohanes
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引用次数: 11

Abstract

The aim of this study was to examine the role of glycyrrhetic acid (GE) as a potential compound in the amelio- ration of metabolic syndrome. Rats given intraperitoneal injection of GE were sacrificed after 24 hours. Blood was col- lected for the determination of glucose, insulin and lipid profiles; while tissues were used for 11� -HSD1, gluconeogenic enzymes activities, PPAR-� /-� and LPL expression by RT-PCR. Intraperitoneal injection of 50mg/kg GE to normal rats significantly lowered blood glucose while insulin level and HOMA-IR showed no significant changes. H6PDH activities increased in the liver, kidney, subcutaneous and visceral adipose tissues and quadriceps femoris but decreased in the ab- dominal muscle. PEPCK activities were significantly reduced in the kidney and decreased in the liver but showed an in- crease in the subcutaneous and visceral adipose tissues. G6Pase activities were found to be reduced in both the liver and kidney. 11� -HSD1 activities increased in the liver but decreased in all other tissues. There were improvements in lipid profiles in GE-treated rats. Up-regulation of LPL activity was seen in all tissues except quadriceps femoris. PPAR-� ex- pression was up-regulated in the liver, heart and abdominal muscle while down-regulated in the kidney and quadriceps femoris but were undetectable in the subcutaneous and visceral adipose tissues. PPAR-� expression was up-regulated in all tissues except the kidney. GE prevented hyperglycaemia and improved lipid profiles possibly through 11� -HSD1 inhi- bition instead of via PPAR agonism.
甘草次酸(GE)对某些糖异生酶、脂蛋白脂肪酶和过氧化物酶体增殖物激活受体α和γ的影响
本研究的目的是研究甘草酸(GE)作为一种潜在的化合物在代谢综合征的治疗中的作用。腹腔注射GE大鼠24小时后处死。取血测定血糖、胰岛素和血脂;RT-PCR检测组织中11′- hsd1、糖异生酶活性、PPAR- /-和LPL的表达。正常大鼠腹腔注射50mg/kg GE可显著降低血糖,而胰岛素水平和HOMA-IR无明显变化。H6PDH活性在肝脏、肾脏、皮下和内脏脂肪组织以及股四头肌中升高,而在腹肌中降低。PEPCK活性在肾脏和肝脏中显著降低,但在皮下和内脏脂肪组织中呈上升趋势。肝脏和肾脏的G6Pase活性均降低。11 α -HSD1活性在肝脏中升高,而在其他组织中降低。ge处理大鼠的脂质谱有改善。LPL活性在除股四头肌外的所有组织中均出现上调。PPAR-在肝脏、心脏和腹肌中表达上调,而在肾脏和股四头肌中表达下调,但在皮下和内脏脂肪组织中未检测到。PPAR- 2在除肾脏外的所有组织中表达上调。GE预防高血糖和改善脂质谱可能是通过11 α - hsd1抑制而不是通过PPAR激动作用。
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