Adiponectin is an insulin-sensitizing hormone. Obesity and type 2 diabetes (T2D) have decreased adiponectin and elevated branched-chain amino acids (BCAAs). Their relationship is poorly understood. Correlations with AAs, leucine (Leu) kinetics and insulin effects on protein anabolism were determined. Fifty-three men 42±2 years were studied: 31 lean, 10 obese, 12 obese T2D. Endogenous Leu appearance (Ra), oxidative and non-oxidative disappearance (Rd) were measured by [1-13C]-Leu infusion in 33 (19 lean, 10 obese, 4 obese T2D). Anabolism was determined by change in net Leu balance from postabsorptive to clamped hyperinsulinema (40 mU/m2/min), euglycemia (5.5 mM) and isoaminoacidemia (14 lean, 4 obese T2D). In n=53, adiponectin was inversely correlated with waist circumference (r=−0.369, p=0.007), fasting insulin (r=−0.450, p=0.001), HOMA (r=−0.441, p=0.002), BCAAs (r=−0.414, p=0.002) and glutamate (Glu) (r=−0.545, p<0.001), but none of 16 other AAs. Multivariate linear regression showed waist circumference (std beta 0.48, p<0.001) and adiponectin (std beta −0.26, p=0.036) accounted for 37% of the BCAA variance; insulin and HOMA did not contribute additively. In the n=33, it correlated negatively with oxidative Leu Rd (r=−0.403, p=0.020), BCAA and Glu, and Leu Ra (r=−0.312, but p=0.077). With n=18, it correlated with the clamp increase in net Leu balance (r=0.555, p=0.017), signifying enhanced insulin-stimulated anabolism. Controlled for fasting insulin, this lost significance; hence, protein anabolism was mainly determined by insulin sensitivity. Results are consistent with adiponectin's proposed role in: 1. regulating postabsorptive BCAAs, independent of associations with abdominal adiposity and insulin resistance, 2. suppressing BCAA catabolism.