Therapeutic potentials of acarbose as first-line drug in NIDDM insufficiently treated with diet alone.
OBJECTIVE
Acarbose inhibits alpha-glucosidases of the small intestine and thus delays glucose release from complex carbohydrates. Therefore, its efficacy and acceptability as a first-line drug in non-insulin-dependent diabetes mellitus (NIDDM) insufficiently treated with diet alone was tested in a randomized double-blind placebo-controlled study.


METHODS
Ninety-four NIDDM subjects, aged 43-70 yr with average body mass index of 28 kg/m2 and undergoing a pretreatment period of at least 3 mo with diet alone, were treated with 100 mg acarbose three times daily or placebo for 24 wk. The patients were recruited after a 4-wk screening period of dietary reinforcement. The inclusion limits for patients termed diet not satisfactory were fasting blood glucose (FBG) greater than or equal to 7.8 mM and/or postprandial blood glucose (BG) greater than or equal to 10 mM.


RESULTS
FBG was lowered in the acarbose group from 9.8 to 8.4 mM and in the placebo group from 10.2 to 9.6 mM after 24 wk (P = 0.007 vs. placebo). The most impressive therapeutic effect was a highly significant reduction of postprandial hyperglycemia for at least 5 h after the test meal (1-h postprandial BG with acarbose 10.4 mM and placebo 13.5 mM at 24 wk, P less than 0.001) accompanied by a significant decrease in HbA1 (acarbose 8.65%, placebo 9.32%, P = 0.003). Whereas C-peptide and fasting serum insulin were not significantly affected by acarbose, postprandial insulin increment was approximately 30% lower after 24 wk compared with placebo. Furthermore, acarbose significantly reduced 1-h postprandial triglyceride levels. After an initial phase of greater than 4 wk (when 76.6% in the acarbose group vs. 28% on placebo complained about flatulence, P less than 0.001), the drug was well accepted. At the end of the study, only 32% showed mild or moderate gastrointestinal sensations.


CONCLUSIONS
Extrapolation shows that acarbose is an efficient and acceptable drug for the treatment of NIDDM with poor metabolic control by diet alone. It has beneficial effects on postprandial hyperinsulinemia and postprandial hypertriglyceridemia.
Hanefeld
M
M
Department of Metabolic Diseases and Endocrinology, Medical Academy Carl Gustav Carus Dresden, Germany.
Fischer
S
S
Schulze
J
J
Spengler
M
M
Wargenau
M
M
Schollberg
K
K
Fücker
K
K
D020909:Acarbose; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D002096:C-Peptide / Q000097:blood; D002784:Cholesterol / Q000097:blood; D003131:Combined Modality Therapy; D003924:Diabetes Mellitus, Type 2 / Q000178:diet therapy / Q000188:drug therapy* / Q000503:physiopathology; D003927:Diet, Diabetic; D004435:Eating; D005215:Fasting; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D065089:Glycoside Hydrolase Inhibitors; D006801:Humans; D007328:Insulin / Q000097:blood; D008297:Male; D008875:Middle Aged; D014280:Triglycerides / Q000097:blood; D014312:Trisaccharides / Q000627:therapeutic use*
D020909:Acarbose; D001786:Blood Glucose; D002096:C-Peptide; D002784:Cholesterol; D006442:Glycated Hemoglobin; D065089:Glycoside Hydrolase Inhibitors; D007328:Insulin; D014280:Triglycerides; D014312:Trisaccharides