Introduction & Objective: Insulin resistance in obesity and type 2 diabetes (T2D) is associated with elevated plasma branched-chain amino acid (BCAA) levels. Whether insulin action on plasma BCAA and the ability of acute exercise or exercise training to alter insulin action on plasma BCAA are intact in obesity and T2D remains to be established.
Methods: In studies (STs) of persons with T2D and glucose-tolerant, obese (OB), and lean (LE) controls examined by hyperinsulinemic-euglycemic clamps (insulin infusion 40 mU/min/m2), we studied the effect of insulin for 4-h (ST1) and insulin for 2-h before and after an acute exercise (1-h, VO2max 70%) bout (ST2) and before and after exercise training for 8 weeks (ST3) on plasma BCAA using a BCAA detection kit.
Results: Insulin-stimulated glucose disposal in T2D was 30-50% lower than in OB (ST1-3) and 40-60% lower than in LE (ST1+3), and 20% lower in OB than in LE (ST1), with p<0.05. Exercise training (ST3) increased insulin-stimulated glucose disposal by 30-40% in all groups (all p<0.01). Plasma BCAA was increased in T2D compared with OB and LE (ST1+3), and in OB compared with LE (ST1), in particular, in the insulin-stimulated state (all p<0.05). In line, the ability of insulin to reduce plasma BCAA was significantly attenuated (~30%) in T2D compared with OB and LE both before (ST1+3) and after exercise training (ST3), with p<0.05. Prior acute exercise (ST2) reduced plasma BCAA (10-15%) and attenuated (20-25%) the ability of insulin to further reduce plasma BCAA in both T2D and OB (all p<0.05).
Conclusion: An impaired ability of insulin to clear BCAA from plasma in T2D and, to a lesser extent, in OB may contribute to elevated plasma BCAA and is not improved after exercise training. An acute bout of exercise lowers plasma BCAA but does not augment insulin action on plasma BCAA in T2D or OB.
P.M. Møller: None. R. Kjøbsted: None. M. Houborg Petersen: None. J.F.P. Wojtaszewski: Consultant; Pfizer Inc. Stock/Shareholder; Pfizer Inc., Novo Nordisk A/S. K. Hojlund: None.