mTORC1 to AMPK switching underlies β-cell metabolic plasticity during maturation and diabetes.

@article{Jaafar2019mTORC1TA,
  title={mTORC1 to AMPK switching underlies β-cell metabolic plasticity during maturation and diabetes.},
  author={Rami Jaafar and Stella Tran and Ajit N. Shah and Gao feng Sun and Mart{\'i}n Valdearcos and Piero Marchetti and Matilde Masini and Avital Swisa and Simone Giacometti and Ernesto Bernal-Mizrachi and Aleksey V Matveyenko and Matthias Hebrok and Yuval Dor and Guy A Rutter and Suneil Koliwad and Anil Bhushan},
  journal={The Journal of clinical investigation},
  year={2019},
  volume={130}
}
Pancreatic beta cells (β-cells) differentiate during fetal life, but only postnatally acquire the capacity for glucose-stimulated insulin secretion (GSIS). How this happens is not clear. In exploring what molecular mechanisms drive the maturation of β-cell function, we found that the control of cellular signaling in β-cells fundamentally switched from the nutrient sensor target of rapamycin (mTORC1) to the energy sensor 5'-adenosine monophosphate-activated protein kinase (AMPK), and that this… CONTINUE READING

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