Simultaneously, chronic hyperinsulinemia and hyperglycemia, common features in MASLD, negatively impact bone metabolism (34), where these metabolic insults impair insulin/IGF-1 signaling to osteoblasts, thereby inhibiting bone formation, and favor adipogenic differentiation within the bone marrow niche at the expense of osteogenesis (67, 68). This evidence concerns the gene INS and metabolic dysfunction-associated steatotic liver disease.