I. Yokoyama et al., Troglitazone improves whole-body insulin resistance and skeletal muscle glucose use in type II diabetic patients, J NUCL MED, 42(7), 2001, pp. 1005-1010
Citations number
33
Categorie Soggetti
Radiology ,Nuclear Medicine & Imaging","Medical Research Diagnosis & Treatment
Recently, troglitazone has emerged as an insulin sensitizer for the treatme
nt of type II diabetes. However, its effect on skeletal muscle glucose use
(SMGU) has not been studied. Methods: To investigate the effect of troglita
zone on SMGU in patients with type II diabetes, we undertook skeletal muscl
e F-18-FDG PET dynamic imaging under insulin clamping before and after admi
nistration of SMGU to 20 patients with type Ii diabetes. Data were compared
with those for 12 age-matched healthy volunteers. Results: The whole-body
glucose disposal rate (GDR) was significantly lower in patients 129.9 +/- 9
.83 mu mol/min/kg) than in control subjects (55.6 +/- 16.5 mu mol/min/kg, P
< 0.01), as was the SMGU (patients, 3.27 +/-: 2.17 mu mol/min/kg; control
subjects, 10.9 +/- 6.4 mu mol/min/kg; P < 0.01). After the therapy, GDR sig
nificantly improved in patients (29.3 +/- 14.6 mu mol/min/kg, P < 0.05), as
did SMGU (5.96 +/- 2.11 mu mol/min/kg, P < 0.05). When results for patient
s with and without hypertension were separately analyzed, a significant imp
rovement in SMGU after troglitazone was seen in both normotensive and hyper
tensive patients 9 normotensive [n = 10]: baseline, 3.67 +/- 2.89 mu mol/mi
n/kg; after therapy, 5.28 +/- 2.57 mu mol/min/kg; P < 0.05; hypertensive [n
= 10]: baseline, 2.89 +/- 1.22 mu mol/min/kg; after therapy, 4.72 +/- 1.39
mu mol/min/kg; P < 0.05). GDR in patients with and without hypertension wa
s significantly improved by troglitazone (normotensive: baseline, 17.9 +/-
10.2 mu mol/min/kg; after therapy, 31.9 +/- 15.9 mu mol/min/kg; P < 0.01; h
ypertensive: baseline, 39.6 +/- 15.1 mu mol/min/kg; after therapy, 47.7 +/-
23.8 mu mol/min/kg; P < 0.05). The plasma free fatty acid concentration du
ring insulin clamping was not changed by troglitazone (baseline, 1.1 +/- 0.
86 mEq/L; after therapy, 0.93 +/- 0.65 mEq/L; P = not significant). Conclus
ion: Troglitazone can improve whole-body insulin resistance through the imp
rovement of SMGU but not through a decline in plasma free fatty acid concen
tration in patients with type II diabetes with or without hypertension.