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


CONCLUSIONS
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.
Department of Cardiovascular Medicine, University of Tokyo, Japan.
I
I
Yokoyama
T
T
Ohtake
S
S
Momomura
K
K
Yonekura
N
N
Kobayakawa
T
T
Aoyagi
S
S
Sugiura
N
N
Yamada
K
K
Ohtomo
Y
Y
Sasaki
M
M
Omata
Y
Y
Yazaki
D016022:Case-Control Studies; D005260:Female; D005462:Fluorine Radioisotopes; D019788:Fluorodeoxyglucose F18; D005947:Glucose / Q000378:metabolism; D015309:Glucose Clamp Technique; D006321:Heart / Q000000981:diagnostic imaging*; D006801:Humans; D015228:Hypertriglyceridemia / Q000000981:diagnostic imaging* / Q000378:metabolism; D007328:Insulin / Q000502:physiology*; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000000981:diagnostic imaging*; D019275:Radiopharmaceuticals; D014055:Tomography, Emission-Computed
D005462:Fluorine Radioisotopes; D007328:Insulin; D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18; D005947:Glucose