The metabolic case: insulin, obesity, liver

The strongest indication cluster, and where the human data actually lands

If MOTS-c ever becomes a medicine, the most plausible first home is metabolic disease: insulin resistance, type 2 diabetes, obesity, and fatty liver. The founding 2015 paper was a metabolic paper, the mechanism is metabolic, and a human gene variant ties MOTS-c sequence to diabetes risk. This is the indication with the deepest rationale.

It is also where you most need to separate mouse efficacy from human reality. The animal metabolic data is strong and repeated; the human data is genetics and circulating-level associations, some of them pointing in confusing directions. This unit builds the metabolic case fairly, then shows exactly where it still falls short of proof.