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      Isoform-specific roles of Akt/PKB in adipocyte metabolism

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      https://www.riss.kr/link?id=E1064350

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      Major functions of adipocyte are to store energy(in the form of triacylglycerol) for use during period of caloric insufficiency. Considerable progress has been made during past few years in our understanding of insulin action on adipocyte metabolism. Here we showed that Akt/PKB, key regulatory enzyme in insulin action, plays pivotal roles in glucose homeostasis by using gene targeting strategy. Interestingly, Akt2/PKB was major responsible enzyme in regulation of glucose homeostasis among Akt1/PKB, Akt2/PKB, and Akt3/PKB. Furthermore, cells isolated from mice lacking Akt2/PKB showed less glucose uptake than that of wild type. Reduced glucose uptake was due to the defect of GLUT4 translocation to the plasma membrane in Akt2/PKB null cells. Therefore, it seems like that Akt2/PKB regulates glucose uptake through the control of GLUT4 translocation. Insulin blocks lipolysis induced by adrenergic receptor agonist. Here we also showed that Akt2/PKB controls lipolysis through the regulation of perilipin phosphorylation. Finally, fat depot size in Akt2/PKB null mice was significantly reduced. These results demonstrate that Akt2/PKB regulates adipocyte metabolim.
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      Major functions of adipocyte are to store energy(in the form of triacylglycerol) for use during period of caloric insufficiency. Considerable progress has been made during past few years in our understanding of insulin action on adipocyte metabolism. ...

      Major functions of adipocyte are to store energy(in the form of triacylglycerol) for use during period of caloric insufficiency. Considerable progress has been made during past few years in our understanding of insulin action on adipocyte metabolism. Here we showed that Akt/PKB, key regulatory enzyme in insulin action, plays pivotal roles in glucose homeostasis by using gene targeting strategy. Interestingly, Akt2/PKB was major responsible enzyme in regulation of glucose homeostasis among Akt1/PKB, Akt2/PKB, and Akt3/PKB. Furthermore, cells isolated from mice lacking Akt2/PKB showed less glucose uptake than that of wild type. Reduced glucose uptake was due to the defect of GLUT4 translocation to the plasma membrane in Akt2/PKB null cells. Therefore, it seems like that Akt2/PKB regulates glucose uptake through the control of GLUT4 translocation. Insulin blocks lipolysis induced by adrenergic receptor agonist. Here we also showed that Akt2/PKB controls lipolysis through the regulation of perilipin phosphorylation. Finally, fat depot size in Akt2/PKB null mice was significantly reduced. These results demonstrate that Akt2/PKB regulates adipocyte metabolim.

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