糖原分解

大鼠脱水时糖原分解的调节

Regulation of Liver Glycogenolysis During Dehydration in Rat

2型糖尿病大鼠骨骼肌组织中抑制糖酵解的基因、促进肌糖原分解及肝糖异生的基因表达上调；

Genes of inhibiting glycolysis , accelerating glycogenolysis and gluconeogenesis were up-regulated in type 2 diabetic rats .

利用大鼠肝细胞激素诱导磷酸化酶α激活，来研究不同激素对cAMP和Ca~（2+）依赖的糖原分解途径的调节。

CAMP and Ca2 + - dependent glycogenolytic pathways are regulated by different hormones involved in the activation of glycogen phosphorylase in isolated rat hepatocytes .

血小板活化因子（PAF）在肝脏中主要表现为增加肝脏血管阻力及糖原分解两大作用，同时还可介导超氧化物的释放、花生四烯酸的代谢、细胞因子的生成等。

Increasing hepatic vascular resistance and glycogenolysis are two principal effects induced by platelet-activating factor ( PAF ) in the liver .

NO-1886抑制糖尿病兔肝糖原分解和肝脏脂肪病变的实验研究

Liver Glycogenolysis and Fat Pathological Changes Suppressed By NO - 1886 in Diabetic Rabbits

结论：Art引起血吸虫PPa活力的增加，使虫的糖原分解，并抑制LDH使虫糖酵解的终产物乳酸明显减少。

CONCLUSION : In schistosomes , the increase in the activity of AMP-independent PPa induced by Art may enhance the decomposition of glycogen and the inhibition of LDH by Art could reduce the formalin of lactate .

结论NO-1886不仅可改善脂质代谢紊乱，而且可降低血清葡萄糖，减少肝糖原分解和减轻肝脏脂肪病变。

Conclusion NO - 1886 improved lipid metabolic disorder and decreased plasma glucose or liver glycogenolysis and improved liver fat pathological changes .

PKA对生长、分化、特定基因的表达以及糖原分解起调节作用，其活性异常与许多疾病相关，是药物设计的潜在靶点。

PKA has regulatory roles in cell proliferation , differentiation , gene expression and glycogen metabolism . PKA is the primary potential target for therapeutic agents , since its unregulated activity has been implicated in many diseases .

激素诱导大鼠离体肝细胞糖原分解的调节

Regulation of Glycogenolysis Against Hormones in Isolated Rat Hepatocytes

结论：山楂酸具有降血糖作用，机制与其抑制肝糖原分解有关。

CONCLUSION : Maslinic acid presents anti-diabetic effect , the mechanism is probably concerned with inhibiting excessive hepatic glycogen degradation .

结果表明，只有在同时含有葡萄糖及胰岛素的灌洗液时，可阻止肝细胞内糖原分解或增加糖原的含量。

Adding glucose or insulin to the preservation solution was without effect on glycogenolysis , but a combination of added glucose plus insulin prevented glycogenolysis .

其降血糖的胰内机制是促进胰岛β细胞分泌胰岛素，抑制胰岛α细胞分泌胰高血糖素，胰外机制可能是抑制肝糖原分解和促进肝糖原合成。

Its mechanisms are stimulating the secretion of insulin from β cells and inhibiting the secretion of glucagons from α cells , and it can probably decrease the decomposition of liver glucogen and increase the synthesis of liver glucogen .

当机体进入代谢起涨期后，糖原分解殆尽，糖原合成不足，此时血糖升高主要来源于糖异生，糖摄取利用障碍也可能是原因之一。

When it gradually comes to theflowphase ( a period of high metabolism reactions ), as glycogenolysis is almost exhausted and glycogenesis becomes insufficient , the rising blood glucose mainly results from glyconeogenesis , and may also be accompanied by the inhibition of glucose utilization .

结果显示：孵化第22～28期（第3.5～5天），原始生殖腺内的原始生殖细胞（PGCs）胞质内的糖原颗粒开始分解；

The results showed that : At the stage 22 ~ 28 ( 3.5 ~ 5 ~ ( th ) hatching day ), the glycogen in the PGCs cytoplasm reduced gradually .

目的：糖原磷酸化酶（GP，E.C.2.4.1.1）是糖原分解代谢的关键酶，是肌肉收缩能量来源的重要途径。

Objective : Glycogen phosphorylase ( GP , E.C.2.4.1.1 ) is a key enzyme of glycogen catabolism . GP is composed of two identical subunits .

上述结果提示，amylin可以通过激活糖原磷酸化酶活力，加强小鼠肝细胞的糖原分解过程，促进肝细胞对葡萄糖的释放，从而对肝细胞内糖原储量及糖代谢平衡进行调节。

Amylin could enhance glycogenolysis by activating glycogen phosphorylase and thus influence glycogen metabolism .