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Departments of Cardiovascular Medicine, Metabolic Diseases, Radiology and Gastroenterology, University of Tokyo, Tokyo, Japan
Correspondence: For correspondence or reprints contact: Ikuo Yokoyama, MD, Department of Cardiovascular Disease, University of Tokyo, 7-3-1 Hongoh Bunkyo-ku, Tokyo 113-8655, Japan.
ABSTRACT
Abnormal heart and skeletal muscle 18F-fluorodeoxyglucose (FDG) uptake in patients with insulin resistance has been demonstrated. Although the existence of whole-body insulin resistance has been reported in hypertriglyceridemics, its specific role in heart and skeletal muscle FDG uptake in hypertriglyceridemics has not been clarified. Methods: We compared heart and skeletal muscle FDG uptake using PET and the whole-body glucose disposal rate (GDR) during insulin clamping in 17 hypertriglyceridemics and 12 age-matched control subjects to increase our knowledge of whole-body insulin resistance and its relationship to heart and skeletal muscle FDG uptake in hypertriglyceridemics. 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 Ki, = (k1, x k3)/(k2 + k3) (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, myocardial FDG Ki (MFKi) tended to be reduced in hypertriglyceridemics compared 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), MFKi (r = 0.57, P = 0.0174) and MFU (r = 0.505, P = 0.0385) in hypertriglyceridemics. Conclusion: Both heart and skeletal muscle glucose utilization were related to insulin resistance in hypertriglyceridemics. However, the less severe reduction in MFU (compared with SMFU) suggests that myocardium may have a mechanism to oppose insulin resistance in hypertriglyceridemics.
Key Words: insulin resistance hypertriglyceridemia fluorodeoxyglucose PET heart and skeletal muscle glucose metabolism
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