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Opposite to AKT and mTORC1, AMPK is activated when energy supply is low and more energy is needed by the cell. Stimulus that activate AMPK are, among others, low glucose levels (fasting), physical exercise, hyppoxia and isquemia.

Low energy supply result in AMP+ADT/ATP ratio increase. This activates AMPK.

AMPK inhibits all process that consume energy and activates all processed that deliver energy for the cell. AMPK activates TSC1/TSC2 complex and, consequently, inactivates mTORC1.

Therefore, AMPK inactivates protein synthesis and activates autophagy.

AMPK inhibits FA synthesis through SREBP-1 and glucose synthesis through FOXO. Both processes are energy consuming.

To provide energy, AMPK activates FA mobilization from the adipose tissue through the activation of HSL and ATGL lipase enzymes.

AMPK also promotes FA oxydation through CPT-1 activation.

AMPK promotes glucose uptake through GLUT4 and glycolysis through the activation of glycolytic enzymes.