Altogether, our results showed for the first time that TTR insufficiency, which can result from its tetrameric instability, as described in familial amyloid polyneuropathy [60], in Alzheimer’s disease [42,44] and in diabetes type I [41], can cause hepatic metabolic dysfunction, as deduced by the higher extracellular or plasma glucose levels, lower expression of influx glucose transporters, lower expression of glycolytic enzyme PKM, a higher degree of oxidative phosphorylation, and thus dysregulation in mitochondrial function (see Figure 5 for a possible interpretation of our results). Here, TTR is linked to early-onset autosomal dominant Alzheimer disease.