Comparison of effects of α-Glucosidase inhibitors and glinide drugs on endothelial dysfunction in diabetic patients with coronary artery disease.
BACKGROUND
Studies have shown that repeated post-prandial hyperglycemia may play an important role in the development of atherosclerosis by suppressing endothelial function. α-Glucosidase inhibitors (α-GIs), which reduce post-prandial hyperglycemia without stimulating insulin secretion, significantly reduce the risk of coronary artery disease (CAD), whereas glinides, which improve post-prandial hyperglycemia through post-prandial insulin secretion, do not appear to affect CAD.


RESULTS
A total of 104 diabetic patients with CAD were randomly divided into 2 groups: those treated with miglitol (M-group; n=52) and those treated with nateglinide (N-group; n=52). After 4 months' treatment, although hemoglobin A1c and 1,5-anhydroglucitol were significantly improved in both groups, only the M-group had significant reductions in insulin resistance index and triglyceride/high-density lipoprotein cholesterol (TG/HDL-C; a beneficial index for assessing the presence of small dense low-density lipoprotein, and a marker of atherogenic dyslipidemia). Furthermore, only the M-group had improvement in percentage flow-mediated dilatation (%FMD) and reactive oxygen metabolites. In the M-group, multiple regression analysis showed that improvement in TG/HDL-C, in addition to 1,5-anhydroglucitol, was an independent predictor of improvement in %FMD.


CONCLUSIONS
The ameliorating effect of α-GI on post-prandial hyperglycemia without stimulating insulin secretion may improve atherogenic dyslipidemia by reducing insulin resistance. These effects are associated with its beneficial impact on oxidative stress, consequently leading to an improvement in endothelial dysfunction.
Division of Cardiovascular Medicine, Himeji Brain and Heart Center.
Takahiro
T
Sawada
Hideyuki
H
Shiotani
Daisuke
D
Terashita
Yoshinori
Y
Nagasawa
Su-Shiku
SS
Kim
Masanobu
M
Koide
Mitsuhiro
M
Yokoyama
D017485:1-Deoxynojirimycin / Q000008:administration & dosage / Q000031:analogs & derivatives*; D000368:Aged; D000369:Aged, 80 and over; D003324:Coronary Artery Disease / Q000097:blood / Q000188:drug therapy / Q000473:pathology; D003510:Cyclohexanes / Q000008:administration & dosage*; D003925:Diabetic Angiopathies / Q000097:blood / Q000188:drug therapy / Q000473:pathology; D050171:Dyslipidemias / Q000097:blood / Q000188:drug therapy / Q000473:pathology; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000473:pathology; D004791:Enzyme Inhibitors / Q000008:administration & dosage*; D005260:Female; D065089:Glycoside Hydrolase Inhibitors; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000188:drug therapy / Q000473:pathology; D007004:Hypoglycemic Agents / Q000008:administration & dosage*; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D000077715:Nateglinide; D010649:Phenylalanine / Q000008:administration & dosage / Q000031:analogs & derivatives*
D003510:Cyclohexanes; D004791:Enzyme Inhibitors; D065089:Glycoside Hydrolase Inhibitors; D007004:Hypoglycemic Agents; D008055:Lipids; C045621:miglitol; D017485:1-Deoxynojirimycin; D000077715:Nateglinide; D010649:Phenylalanine