A familiar diabetes medicine is drawing fresh attention from cancer researchers, not because it shrinks tumours, but because it appears to trigger some of the same internal metabolic signals normally associated with vigorous physical exercise.

New research suggests that metformin, one of the most widely prescribed drugs in the world, may help support energy balance and weight control in men receiving treatment for prostate cancer, even when fatigue or illness makes regular movement difficult.

The findings come from a collaborative study led by scientists at a major US cancer centre and medical school and have been published in the peer‑reviewed journal EMBO Molecular Medicine.

“Higher levels of Lac‑Phe were linked to reduced food intake and improved weight control, two outcomes often associated with regular physical activity”

The work adds to a growing body of evidence that cancer care extends beyond attacking malignant cells. How the body handles energy, weight, and metabolic stress during treatment matters, both for quality of life and long‑term health.

Exercise has long been recognised as one of the most effective ways to protect physical and metabolic health during cancer therapy. Regular activity can stabilise body weight, improve blood sugar control, and reduce cardiovascular risk. It can also ease fatigue and support recovery once treatment ends.

Yet for many patients, especially those undergoing hormone therapy or managing advanced disease, exercise is not always possible. Tiredness, pain, muscle loss, and other side effects can make even gentle activity a challenge.

This tension has prompted an important scientific question. If exercise exerts many of its benefits through specific biological signals inside the body, could some of those signals be activated in other ways, without requiring physical exertion? The new study suggests that, at least in part, the answer may be yes.

“Metformin has been used for decades to treat type 2 diabetes and is known to influence how the body uses glucose and responds to insulin. Its effects on weight and appetite have been well documented”

At the centre of the research is a small molecule with a complex name: N‑lactoyl‑phenylalanine, known as Lac‑Phe. Despite its technical label, its role is relatively straightforward. Lac‑Phe is produced when the body is under metabolic demand. It forms when lactate, a substance that accumulates during exertion, combines with phenylalanine, one of the amino acids used to build proteins.

Scientists first became interested in Lac‑Phe several years ago when they noticed that its levels rise sharply after intense exercise. Those increases appeared alongside changes in appetite and energy use. In animal studies and early human research, higher levels of Lac‑Phe were linked to reduced food intake and improved weight control, two outcomes often associated with regular physical activity.

What intrigued researchers further was the observation that Lac‑Phe does not rise only after exercise. Elevated levels were also detected in people taking metformin, even when they were not physically active.

Metformin has been used for decades to treat type 2 diabetes and is known to influence how the body uses glucose and responds to insulin. Its effects on weight and appetite have been well documented, though the precise biological mechanisms remain an area of active investigation.

The overlap between exercise‑induced and drug‑induced increases in Lac‑Phe raised a compelling possibility for cancer care. Could a metabolic pathway normally activated by movement be triggered pharmacologically in patients whose treatments limit activity? To explore that idea, the research team focused on men with prostate cancer.

Prostate cancer provided a particularly relevant context. Many patients receive hormone‑based therapies that suppress testosterone, a key driver of tumour growth. While effective against the cancer, these treatments often disrupt normal metabolism. Weight gain, loss of muscle mass, insulin resistance, and increased cardiovascular risk are common. Fatigue is also frequent, creating a cycle in which reduced activity further worsens metabolic health.

In the study, blood samples from prostate cancer patients were analysed before and after metformin treatment. The researchers measured levels of Lac‑Phe and compared them with known benchmarks from exercise studies. They found that metformin consistently raised Lac‑Phe levels, bringing them close to those previously reported after strenuous physical activity.

Crucially, these increases occurred even though the patients were not exercising at the time the samples were taken. The effect also persisted after hormone therapy had begun, suggesting that metformin could engage this metabolic pathway despite the added strain of cancer treatment.

“The researchers stress that no pill can replace physical activity. Exercise delivers a wide range of benefits, from cardiovascular conditioning to mental health support, that no single drug can replicate”

From a clinical perspective, the signal was striking. A molecular change commonly associated with intense exercise appeared in patients whose therapies often limit their ability to move. For individuals struggling with fatigue or other treatment‑related side effects, this could be particularly meaningful.

The researchers were careful to draw clear boundaries around what the findings do and do not show. The rise in Lac‑Phe was not linked to a direct anti‑cancer effect. The metabolite did not correlate with changes in prostate‑specific antigen, or PSA, the blood marker typically used to track prostate cancer activity. In other words, Lac‑Phe does not appear to reflect tumour response to metformin.

Instead, the molecule seems to act as a marker of how the body is handling energy and metabolic stress during treatment. That distinction is important. Cancer therapy affects far more than tumours alone. How patients feel, how much weight they gain or lose, and how well their metabolism copes with prolonged stress can all influence adherence to treatment and overall wellbeing.

To ensure the findings were robust, the team looked beyond a single clinical setting. They observed similar increases in Lac‑Phe among patients receiving other metabolic interventions, suggesting that the effect is not unique to metformin. This points to Lac‑Phe as a broader signal of metabolic adaptation rather than a drug‑specific curiosity.

The study also explored how Lac‑Phe relates to other known metabolic signals. Metformin is known to raise levels of a stress‑related hormone called GDF‑15, which has been linked to reduced appetite and weight loss. Interestingly, the researchers found that Lac‑Phe and GDF‑15 did not rise in tandem. Moreover, changes in body weight were more closely associated with Lac‑Phe levels than with GDF‑15.

This separation suggests that metformin may influence weight and energy balance through multiple biological pathways. Lac‑Phe appears to play a distinct role, potentially offering a more precise window into how the drug affects metabolism in patients undergoing cancer therapy.

“For now, the message is one of cautious optimism. A familiar medicine may help activate some of the body’s natural exercise‑related signals at a time when movement is hard. It is not a replacement for physical activity, nor a new cancer treatment”

Experts involved in the research emphasised the broader implications. Metabolism underpins virtually every cellular process in the body. When treatments place the body under prolonged metabolic stress, as hormone therapy often does, even small shifts in how energy is managed can have meaningful effects over time. Identifying signals like Lac‑Phe helps researchers understand these shifts with greater clarity.

The findings also reinforce a more holistic view of cancer care. While targeting tumours remains the primary goal, supporting the whole patient is increasingly recognised as essential. Maintaining metabolic health can influence how well patients tolerate treatment, how resilient they feel, and how they recover in the months and years that follow.

Importantly, the researchers stress that no pill can replace physical activity. Exercise delivers a wide range of benefits, from cardiovascular conditioning to mental health support, that no single drug can replicate. The study does not suggest that patients should substitute medication for movement where exercise is possible.

Instead, the work offers insight into the internal biology of exercise itself. By identifying and understanding the molecular signals involved, clinicians may one day be able to better support patients who cannot be active, at least for a time. For men with prostate cancer facing long courses of hormone therapy, that support could make a tangible difference to daily life.

While further studies will be needed to confirm the findings in larger and more diverse patient groups, the work adds a new layer to the story of metformin, a drug already known for its versatility.

For now, the message is one of cautious optimism. A familiar medicine may help activate some of the body’s natural exercise‑related signals at a time when movement is hard. It is not a replacement for physical activity, nor a new cancer treatment. Always talk to your healthcare providers for medical advice.

It is, however, a reminder that small molecules can have wide‑ranging effects, and that supporting metabolic health is an integral part of modern cancer care.