Reversing Muscle Fibrosis and Senescence in Older Adults: Metformin’s Revitalizing Role

An exciting new study published in Aging Cell reveals that metformin, a common diabetes drug that regulates blood sugar, can also prevent muscle atrophy and muscular fibrosis. Before I get into why this is potentially exciting news, I’d like to break down how the science behind the study.

First, metformin works by activating AMPK, which helps maintain muscle mass and function. AMPK is an enzyme that plays a key role in regulating energy metabolism in cells. It is activated when cellular energy levels are low, such as during exercise or fasting. Activation of AMPK leads to increased glucose uptake and fatty acid oxidation, which helps to maintain energy balance in cells.In addition to its role in energy metabolism, AMPK has also been shown to regulate cell growth and proliferation.

What the study found was that metformin treatment increased AMPK activity in muscle cells and prevented muscle atrophy and fibrosis in mice. The researchers also found that metformin treatment increased gene expression in mitochondrial biogenesis and function. One conclusion we can draw is that metformin may help to prevent age-related muscle loss by improving mitochondrial function. And yet another aspect of metformin was that it reduced cellular senescence and excessive collagen deposition (reducing fibrosis).  

The next important question for those of us interested in anti-aging and longevity protocols is this:

Will berberine have similar effects as metformin? 

Like metformin, berberine has been shown to activate AMPK and improve cell glucose uptake and fatty acid oxidation. Berberine has also been shown to have anti-inflammatory and antioxidant effects.Berberine and metformin have both been shown to activate AMPK and improve cell glucose uptake and fatty acid oxidation. However, the mechanisms by which they activate AMPK may be different. 

Berberine has been shown to activate AMPK by increasing the cyclic AMP (cAMP) production, which activates AMPK. Metformin, on the other hand, has been shown to activate AMPK by inhibiting complex I of the mitochondrial respiratory chain. 

Inhibiting complex I of the mitochondrial respiratory chain has been shown to improve mitochondrial function by reducing the production of reactive oxygen species (ROS) in cells. ROS are molecules produced during normal cellular metabolism and can cause damage to cells if their levels become too high. Complex I is a major source of ROS production in cells, and inhibiting its activity can reduce ROS levels and improve mitochondrial function. 

It’s important to note that AMPK itself will inhibit Complex 1 diminishing ROS. Both berberine and metformin also act as transcription factors in genes involved in mitochondrial biogenesis and function, including peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), nuclear respiratory factor 1 (NRF-1), and mitochondrial transcription factor A (TFAM).

While this use of metformin to reverse muscle fibrosis is interesting, I prefer berberine, as it will provide similar benefits.


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