The stimulation of VAT from the Non-Ob controls with GLP-1 (100 nM) decreased acetate production (Non-Ob: GLP-1 (0 nM), 2.40 ± 2.20 nmol/mg of VAT vs. GLP-1 (100 nM), 3.21 ± 2.37 nmol/mg of VAT; Δ −25.20%, p < 0.05), while in VAT from Ob + Pre-T2D, it increased lactate (Ob + Pre-T2D: GLP-1 (0 nM), 45.33 ± 15.61 nmol/mg of VAT vs. GLP-1 (100 nM), 65.20 ± 19.59 nmol/mg of VAT, Δ 43.83%, p < 0.01) and alanine production (Ob + Pre-T2D: GLP-1 (0 nM), 0.97 ± 0.40 nmol/mg of VAT vs. GLP-1 (100 nM), 1.29 ± 0.55 nmol/mg of VAT, Δ 32.56%, p < 0.05) (Figure 2, Table S1). The gene discussed is GLP1R; the disease is type 2 diabetes mellitus.