Metformin has a long-standing history. It was called ‘the glucose eater’ or Glucophage by French doctor Jean Sterne.
It has a long-standing history in modern medical science. Though long ago, it was from Galega officinalis, a herbal leaf used to treat diabetes symptoms in the early days; Metformin has been recognized as a potent molecule with a crucial role in glucose metabolism.
However, recent research has uncovered that Metformin's influence extends beyond glucose control. Retrospective studies and animal experiments have revealed its potential to impact various metabolic and cellular processes associated with age-related conditions.
Notably, it has shown efficacy in reducing superoxide build-up and the inflammatory cascade, critical factors in the aging process. Metformin helps prevent early organ degeneration and aging by diminishing apoptosis and cell senescence.
Given its unique properties, Metformin has piqued the interest of gerontologists and researchers exploring interventions for the aging process. It mimics a fasting state by upregulating AMP-activated protein kinase (AMPK), a key player in nutrient-sensing pathways.
Scientists have noted that a fall in energy levels in fasting or caloric restriction swings the ratio of ATP to ADP in favor of ADP due to reduced production of ATP or increased consumption of ATP as in exercise leads to increased activity of AMPK.
Activated AMPK switches on the catabolic pathways while at the same time switching off processes that use up ATP.
Metformin replicates this mode by activating AMPK and inhibiting mTORC1. Hence Metformin induces a cellular response similar to caloric restriction, optimizing energy utilization and metabolic processes.
The relationship between nutrient sensing and aging is bidirectional. Aging impairs nutrient-sensing mechanisms and metabolic signaling, leading to dysregulated metabolic pathways and, in turn, accelerated aging.
The same impairment to nutrient sensing also leads to the decline in insulin-like signaling (IIS) pathway activity with age, resulting in insulin resistance and the metabolic syndrome of obesity, type 2 diabetes, and dyslipidemia.
Hyperglycemia resulting from insulin deficiency as type 2 diabetes leads to the formation of advanced glycation end products (AGEs), contributing to tissue damage and further accelerating aging.
In light of scientific evidence, sustained caloric restriction or fasting has been established to delay aging. Metformin taps into this function by mimicking the effects of caloric restriction through AMPK activation and mTORC1 inhibition to influence the amelioration of hyperglycemia in Type 2 diabetes.
As researchers delve deeper into the mode of action of Metformin, its potential as an anti-aging intervention becomes increasingly intriguing. A study Metformin in Life extension MILES has had scientist upbeat on this potential. Understanding its multifaceted effects on metabolic pathways and cellular processes may uncover new strategies for promoting healthy aging and extending lifespan.
Note: While the benefits of Metformin in aging are promising, it is crucial to consult with a healthcare professional before considering any interventions or changes to your medical regimen.