Miglitol suppresses the postprandial increase in interleukin 6 and enhances active glucagon-like peptide 1 secretion in viscerally obese subjects.
Visceral obesity and insulin resistance are regarded as risk factors for atherosclerosis. Epidemiologic studies have demonstrated long-term anti-atherosclerotic effects with administration of alpha-glucosidase inhibitors. Alpha-glucosidase inhibitors also have been reported to enhance glucagon-like peptide 1 (GLP-1) secretion. We compared the postprandial effects of a single administration of miglitol and acarbose on glucose and lipid metabolism, on insulin requirement, on GLP-1 secretion, and on inflammatory and endothelial markers in viscerally obese subjects. Twenty-four viscerally obese subjects with relative insulin resistance participated in this study. Subjects were given a single dose of miglitol (50 mg), acarbose (100 mg), or placebo blindly and randomly before a meal in a crossover design. The meal loads after drug administration were tested 3 times within 2 weeks. We measured glucose, insulin, lipids, lipoprotein lipase, interleukin 6, intracellular adhesion molecule 1, vascular cell adhesion molecule 1, and active GLP-1 at before and various minutes after the meal. Single administration of both alpha-glucosidase inhibitors had several beneficial effects in improving postprandial hyperglycemia and reducing postprandial insulin requirement approximately 25% of placebo without adversely affecting lipid profiles. Although lipoprotein lipase levels within 2 hours after the meal did not show differences among miglitol, acarbose, and placebo administrations, miglitol significantly suppressed the increases in triglycerides, remnant-like particle triglycerides, and remnant-like particle cholesterol compared to acarbose and placebo in the early phase. Miglitol also significantly enhanced active GLP-1 secretion to a greater extent than acarbose (P < .01) and placebo (P < .001), and significantly suppressed the postprandial increase in interleukin 6 compared to placebo (P < .01). The results point to the potential suitability of miglitol as an anti-atherosclerotic effect in viscerally obese subjects, in preference to acarbose. Further studies are needed to elucidate the long-term effects on enhanced GLP-1 secretion and anti-atherosclerosis.
Arakawa
Masayuki
M
Department of Medicine, Metabolism and Endocrinology, Juntendo University School of Medicine, Tokyo, Japan.
Ebato
Chie
C
Mita
Tomoya
T
Fujitani
Yoshio
Y
Shimizu
Tomoaki
T
Watada
Hirotaka
H
Kawamori
Ryuzo
R
Hirose
Takahisa
T
D017485:1-Deoxynojirimycin / Q000031:analogs & derivatives* / Q000627:therapeutic use; D020909:Acarbose / Q000627:therapeutic use; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D018592:Cross-Over Studies; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D005260:Female; D052216:Glucagon-Like Peptide 1 / Q000097:blood / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000008:administration & dosage / Q000097:blood / Q000627:therapeutic use; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008055:Lipids / Q000097:blood; D008071:Lipoprotein Lipase / Q000097:blood; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000188:drug therapy / Q000378:metabolism*; D019518:Postprandial Period; D016037:Single-Blind Method; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D014781:Viscera; D000093242:Interleukin-6 Inhibitors
D017485:1-Deoxynojirimycin; D020909:Acarbose; D001786:Blood Glucose; D004791:Enzyme Inhibitors; D052216:Glucagon-Like Peptide 1; D007328:Insulin; D018799:Intercellular Adhesion Molecule-1; D015850:Interleukin-6; D008055:Lipids; D008071:Lipoprotein Lipase; D019010:Vascular Cell Adhesion Molecule-1; D000093242:Interleukin-6 Inhibitors; C045621:miglitol