2017
DOI: 10.7554/elife.26896
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Distinct Akt phosphorylation states are required for insulin regulated Glut4 and Glut1-mediated glucose uptake

Abstract: Insulin, downstream of Akt activation, promotes glucose uptake into fat and muscle cells to lower postprandial blood glucose, an enforced change in cellular metabolism to maintain glucose homeostasis. This effect is mediated by the Glut4 glucose transporter. Growth factors also enhance glucose uptake to fuel an anabolic metabolism required for tissue growth and repair. This activity is predominantly mediated by the Glut1. Akt is activated by phosphorylation of its kinase and hydrophobic motif (HM) domains. We … Show more

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Cited by 132 publications
(123 citation statements)
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“…It was reported that the Warburg shift is a dominant vascular phenomenon in PAH and RV dysfunction [27]. Akt activation by phosphorylation can enhance cellular glucose uptake through the glucose transporters, Glut4 and Glut1, and can increase glycolysis in PAH [28]. In the present study, we profiled Glut4 and Glut 1 expression in different cellular fractions and found that it was increased in the membrane.…”
Section: Discussionsupporting
confidence: 50%
“…It was reported that the Warburg shift is a dominant vascular phenomenon in PAH and RV dysfunction [27]. Akt activation by phosphorylation can enhance cellular glucose uptake through the glucose transporters, Glut4 and Glut1, and can increase glycolysis in PAH [28]. In the present study, we profiled Glut4 and Glut 1 expression in different cellular fractions and found that it was increased in the membrane.…”
Section: Discussionsupporting
confidence: 50%
“…Insulin binding to insulin receptor causes activation (i.e., autophosphorylation) of this receptor leading to a phosphorylation cascade that activates IRS protein and PI3K, which in turn triggers the phosphorylation of Akt and its resulting activation. Akt, also known as protein kinase B, plays an essential role in the metabolic effects of insulin, including the increase in the translocation of glucose carriers (GLUTs; Beg, Abdullah, Thowfeik, Altorki, & McGraw, ). In particular, it has been demonstrated that GLUT4 and GLUT‐1 contribute in a relatively comparable way to the overall effect of insulin to stimulate glucose transport because knockdown of these transporters led to a marked impairment of overall insulin‐stimulated glucose transport in 3T3‐L1 (Liao et al, ).…”
Section: Resultsmentioning
confidence: 99%
“…For example, several different growth factors increase surface levels of a range of nutrient receptors and transporters, such as the transferrin receptor, amino acid transporters, and other glucose transporters like GLUT1. What has recently become clear is that adipocytes and muscle cells also possess this generic regulated recycling system in addition to the more specialized GSV exocytosis system (69). However, it has proven challenging to molecularly distinguish these systems from each other.…”
Section: The Glut4 Itinerary and Its Many Unknownsmentioning
confidence: 99%