In nondiabetic, hyperinsulinaemic men with NAFLD, insulin suppression of VLDL‐TG secretion and particle size was lower compared to men without NAFLD (31.9% vs. 64.7%), suggesting that greater export of TG from the liver may be an early physiological response to compensate for hepatic lipid accumulation (Steiner & Lewis, 1996). Here, INS is linked to metabolic dysfunction-associated steatotic liver disease.