Insulin action on heart and skeletal muscle FDG uptake in patients with hypertriglyceridemia

Abnormal heart and skeletal muscle F-18-fluorodeoxyglucose (FDG) uptake in patients with insulin resistance has been demonstrated. Although the existe nce of whole-body insulin resistance has been reported in hypertriglyceride mics, its specific role in heart and skeletal muscle FDG uptake in hypertri glyceridemics has not been clarified. Methods: We compared heart and skelet al muscle FDG uptake using PET and the whole-body glucose disposal rate (GD R) during insulin clamping in 17 hypertriglyceridemics and 12 age-matched c ontrol subjects to increase our knowledge of whole-body insulin resistance and its relationship to heart and skeletal muscle FDG uptake in hypertrigly ceridemics. Results: GDR was significantly reduced in hypertriglyceridemics compared with control subjects (4.50 +/- 1.37 mg/min/kg versus 10.0 +/- 2. 97 mg/min/kg, P = 0.00001), as were the skeletal muscle FDG K-i = (k(1) x k (3))/(k(2) + k(3)) (SFKi: 0.007 +/- 0.003 mL/min/g versus 0.018 +/- 0.01 ml /min/g, P = 0.0001) and skeletal muscle FDG uptake ([SMFU] 0.725 +/- 0.282 mg/min/100 g versus 1.86 +/- 1.06 mg/min/100 g, P = 0.00023). However, myoc ardial FDG K-i (MFKi) tended to be reduced in hypertriglyceridemics compare d with that in control subjects (0.062 +/- 0.017 mL/min/g versus 0.068 +/- 0.015 mL/min/g), but the difference was statistically insignificant (P = 0. 3532). Moreover, myocardial FDG uptake (MFU) in hypertriglyceridemics (6.47 +/- 1.72 mg/min/100 g) tended to be reduced compared with that in control subjects (6.97 +/- 1.73 mg/min/100 g), but the difference was statistically insignificant (P = 0.4485). GDR was significantly correlated with SFKi (r = 0.69, P = 0.0022), SMFU (r = 0.612, P = 0.009), MFK, (r = 0.57, P = 0.017 4) and MFU (r = 0.505, P = 0.0385) in hypertriglyceridemics. Conclusion: Bo th heart and skeletal muscle glucose utilization were related to insulin re sistance in hypertriglyceridemics. However the less severe reduction in MFU (compared with SMFU) suggests that myocardium may have a mechanism to oppo se insulin resistance in hypertriglyceridemics.