Yokoyama I, Ohtake T, Momomura S, Yonekura K, Kobayakawa N, Aoyagi T, Sugiura S, Yamada N, Ohtomo K, Sasaki Y, Omata M, Yazaki Y
Department of Cardiovascular Medicine, University of Tokyo, Japan.
J Nucl Med. 1999 Jul;40(7):1116-21.
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.
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.
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.
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.
胰岛素抵抗患者心脏和骨骼肌的18F-氟脱氧葡萄糖（FDG）摄取异常已得到证实。尽管已有报道称高甘油三酯血症患者存在全身胰岛素抵抗，但其在高甘油三酯血症患者心脏和骨骼肌FDG摄取中的具体作用尚未阐明。
我们比较了17例高甘油三酯血症患者和12例年龄匹配的对照受试者在胰岛素钳夹期间使用PET测量的心脏和骨骼肌FDG摄取以及全身葡萄糖处置率（GDR），以增进我们对全身胰岛素抵抗及其与高甘油三酯血症患者心脏和骨骼肌FDG摄取关系的了解。
与对照受试者相比，高甘油三酯血症患者的GDR显著降低（4.50±1.37mg/min/kg对10.0±2.97mg/min/kg，P = 0.00001），骨骼肌FDG Ki =（k1×k3）/（k2 + k3）（SFKi：0.007±0.003mL/min/g对0.018±0.01mL/min/g，P = 0.0001）和骨骼肌FDG摄取（[SMFU] 0.725±0.282mg/min/100g对1.86±1.06mg/min/100g，P = 0.00023）也显著降低。然而，与对照受试者相比，高甘油三酯血症患者的心肌FDG Ki（MFKi）有降低趋势（0.062±0.017mL/min/g对0.068±0.015mL/min/g）但差异无统计学意义（P = 0.3532）。此外高甘油三酯血症患者的心肌FDG摄取（MFU）（6.47±1.72mg/min/100g）与对照受试者相比有降低趋势（6.97±1.73mg/min/100g）但差异无统计学意义（P = 0.4485）。在高甘油三酯血症患者中，GDR与SFKi（r = 0.69，P = 0.0022）、SMFU（r = 0.612，P = 0.009）、MFKi（r = 0.57，P = 0.0174）和MFU（r = 0.505，P = 0.0385）显著相关。
高甘油三酯血症患者心脏和骨骼肌的葡萄糖利用均与胰岛素抵抗有关。然而，MFU降低程度较轻（与SMFU相比）表明心肌可能具有抵抗高甘油三酯血症患者胰岛素抵抗的机制。
