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Diabetes and the heart: when muscle looks after our mitochondria

We are often told that moving protects against diabetes and heart disease. But why, exactly? Two reviews published in late September and early October 2026 provide part of the answer: muscle produces messengers that act on the mitochondria of the whole body.

Diabetes, also a story about energy

Type 2 diabetes and metabolic syndrome (a large waist, high blood pressure, high blood sugar and blood fats) affect millions of people. A review published in September 2026 in Diabetes, Metabolic Syndrome and Obesity shows that mitochondria are involved at every stage: they burn fuel less well, produce more oxidising molecules, renew themselves less, and the pancreatic cells that make insulin end up short of energy.

The authors describe a vicious circle: excess food, belly fat and inflammation damage mitochondria, and damaged mitochondria in turn worsen insulin resistance. They point out, however, that the mitochondrion is not the sole cause of diabetes, but one amplifier among others.

Muscle, an organ that talks

We think of muscle as an engine. It is also a gland. When it works, it releases messengers, myokines, which circulate in the blood and act on the liver, fat, heart and blood vessels.

A Colombian review published on 2 October 2026 in the Journal of Physiology and Biochemistry puts forward a simple idea: in cardiometabolic diseases, muscle sends "bad" messages, and this degraded profile helps wear out mitochondria. Conversely, restoring a favourable myokine profile helps mitochondria work better. Part of this work remains experimental, and trials in humans are only beginning.

What this changes in practice

Both reviews agree on one point: physical activity and weight loss are among the approaches with established benefits in humans, and they work partly through mitochondria. A muscle that works regularly multiplies its mitochondria, burns sugar better and sends better signals to the rest of the body. By contrast, approaches that target mitochondria directly are, for the most part, still at the research stage.

Key takeaways

  • In type 2 diabetes, mitochondria work less well and sustain insulin resistance.
  • Muscle releases messengers, myokines, that influence the mitochondria of the whole body.
  • Regular physical activity is one of the best-established ways to benefit from them.
  • Many mechanisms still need to be confirmed by trials in humans.

Sources

  • Saavedra JE, Gallo-Villegas J, Calderón JC. Myokines and mitochondrial function in cardiometabolic diseases. Journal of Physiology and Biochemistry, 2026. https://doi.org/10.1007/s13105-026-01233-8
  • Alghzawi HM et al. Mitochondrial dysfunction in type 2 diabetes and metabolic syndrome: mechanisms, biomarkers, and emerging therapies. Diabetes, Metabolic Syndrome and Obesity, 2026. https://doi.org/10.2147/DMSO.S627029
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