Miglitol increases the adiponectin level and decreases urinary albumin excretion in patients with type 2 diabetes mellitus.
Postprandial hyperglycemia is associated with increased cardiovascular mortality; therefore, lowering postprandial hyperglycemia seems crucial in type 2 diabetes mellitus. We assessed the effect of 2 different postprandial glucose-lowering agents, the alpha-glucosidase inhibitor miglitol and the meglitinide analogue mitiglinide, on metabolic profile and atherosclerosis-related markers. Glucose levels, insulin levels, lipid profile, serum adiponectin, pulse wave velocity (PWV), and urinary albumin excretion rate (AER) were assessed before and after 3 months in 28 patients with type 2 diabetes mellitus randomly allocated to either miglitol 150 mg/d or mitiglinide 30 mg/d. Both agents improved postprandial glucose levels but exhibited different patterns of insulin levels. Body mass index (BMI) tended to decrease with miglitol (P = .06), and homeostasis model assessment of insulin resistance and AER significantly decreased (P < .05 and P < .001, respectively) with miglitol; these changes were not obtained with mitiglinide. Pulse wave velocity did not change. The 3-month changes in 1,5-anhydroglucitol levels were significantly more with miglitol than with mitiglinide (P = .007). Adiponectin levels were significantly increased only with miglitol (P < .01), and the 3-month changes were significantly more with miglitol than with mitiglinide (P = .048). The significant increase in adiponectin by miglitol was inversely correlated with the ratio of the 60-minute change in blood glucose at 3 months divided by the change at baseline (r = -0.59, P = .020), which was independent of the effect of age, sex, changes in hemoglobin A(1c) and BMI, and the baseline concentration of adiponectin. The present comparative study indicated favorable effects of miglitol on BMI, homeostasis model assessment of insulin resistance, adiponectin, and AER, which are markers related to insulin resistance and atherosclerosis. Future studies are needed to elucidate the long-term effect.
Yokoyama
Hiroki
H
Jiyugaoka Medical Clinic, Internal Medicine, Obihiro 080-0848, Japan. hiroki@m2.octv.ne.jp
Kannno
Sakiko
S
Ishimura
Ikue
I
Node
Koichi
K
D017485:1-Deoxynojirimycin / Q000031:analogs & derivatives* / Q000494:pharmacology; D052242:Adiponectin / Q000097:blood*; D000419:Albuminuria / Q000150:complications*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000652:urine*; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D050112:Imino Pyranoses / Q000494:pharmacology; D008297:Male; D008875:Middle Aged
D052242:Adiponectin; D007004:Hypoglycemic Agents; D050112:Imino Pyranoses; C045621:miglitol; D017485:1-Deoxynojirimycin