2015
DOI: 10.1111/jdi.12369
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A novel role for the cell cycle regulatory complex cyclin D1–CDK4 in gluconeogenesis

Abstract: Dysregulation of gluconeogenesis is a key pathological feature of type 2 diabetes. However, the molecular mechanisms underlying the regulation of gluconeogenesis remain unclear. Bhalla et al. recently reported that cyclin D1 suppresses hepatic gluconeogenesis through CDK4‐dependent phosphorylation of PGC1alpha and consequent inhibition of its activity. The cyclin D1–CDK4 might thus serve as an important link between the cell cycle and control of energy metabolism through modulation of PGC1alpha activity.

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Cited by 14 publications
(9 citation statements)
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“…The previous studies showed the effect of certain antidiabetic drugs on the cell-cycle through the decrease of cyclin D1 expression [ 118 ]. Cyclin D1 is an essential link between cell-cycle and energy control metabolism [ 119 ]; this may explain why CHP was only effective in reducing cyclin D1 protein expression but not pRb and pcdc2 expression.…”
Section: Discussionmentioning
confidence: 99%
“…The previous studies showed the effect of certain antidiabetic drugs on the cell-cycle through the decrease of cyclin D1 expression [ 118 ]. Cyclin D1 is an essential link between cell-cycle and energy control metabolism [ 119 ]; this may explain why CHP was only effective in reducing cyclin D1 protein expression but not pRb and pcdc2 expression.…”
Section: Discussionmentioning
confidence: 99%
“…To the best of the authors’ knowledge, this is among very few clinical studies to investigate the role of Cyclin-D beyond oncologic disorders. A recent study of Hosooka and Ogawa [ 67 ] on cyclin D-1 clarified its relation to the physiologic and pathologic glucose metabolism. They explained that cyclin D1 is a regulator of the cell cycle that promotes the transition from G1 to S phase by activating cyclin-dependent kinase 4 (CDK4) or CDK6.…”
Section: Discussionmentioning
confidence: 99%
“…In addition to these well-known tumor suppressors, some circRNAs could also regulate tumor growth by regulating cell cycle mediators, such as Cyclin D1, a well-known regulator of the cell cycle that promotes the transition from G1 to S phase by activating CDK4 or CDK6 [96]. Xue and coworkers [97] performed a circRNA microarray to analyze the variability of circRNAs in arsenite-treated HaCaT (As-HaCaT) cells and in arsenite-transformed cells compared to normal HaCaT cells and identify cirRNAs that involved in arsenite-induced acceleration of the cell cycle.…”
Section: Introductionmentioning
confidence: 99%