All these metabolites could support muscle insulin sensitivity [14], [32] since (i) muscle β-hydroxybutyrate represents a strong marker and a possible causal factor for insulin resistance, which correlates with plasma NEFA levels [59]; (ii) α-hydroxybutyrate, a marker of mitochondrial redox status, is linked to the regulation of BCAA [59] and it was recently identified as an early biomarker of insulin resistance [60]; and (iii) malonyl-CoA is the key lipogenic intermediate controlling mitochondrial activity of β-oxidation by inhibiting CPT-1 (ref. [47]; see below). The gene discussed is CPT1A; the disease is Insulin resistance.