AMPK vs MTOR/PSX pathways?

The AMPK and mTOR/PSX pathways play differing and somewhat opposing roles in cellular processes, as explained by Andrew Huberman. During fasting, there's a reduction in phospho MTOR and PS6, which is consistent with a decrease in cellular growth activities. In contrast, fasting increases markers like AMPK and sirtuins, which are associated with cellular repair and autophagy—essentially the clearing out of cells to make way for newer, healthier cells. This differentiation indicates that mTOR and PSX are tied to cell growth while AMPK includes pathways that favor cell repair and rejuvenation. These distinctions manifest depending on whether one is in a fed or a fasted state, thus impacting cellular outcomes based on dietary behaviors 1.

Moreover, both AMPK and the mTOR pathways interact importantly in the context of longevity and cell repair mechanisms. When fasting or sustaining low blood glucose, a pathway like mTOR registers the reduced intake of key proteins, and with this lack of nutrients, it down-regulates to trigger protective and repair processes across cells. This interplay explains how the body's response to fasting involves a decrease in mTOR activity, subsequently activating repair and maintenance through processes associated with AMPK and other longevity pathways like sirtuins 2.