Will acarbose improve the metabolic abnormalities of insulin-resistant type 2 diabetes mellitus?

Citation
R. Scott et al., Will acarbose improve the metabolic abnormalities of insulin-resistant type 2 diabetes mellitus?, DIABET RE C, 43(3), 1999, pp. 179-185
Citations number
21
Categorie Soggetti
Endocrynology, Metabolism & Nutrition
Journal title
DIABETES RESEARCH AND CLINICAL PRACTICE
ISSN journal
01688227 → ACNP
Volume
43
Issue
3
Year of publication
1999
Pages
179 - 185
Database
ISI
SICI code
0168-8227(199903)43:3<179:WAITMA>2.0.ZU;2-M
Abstract
Individuals with type 2 diabetes mellitus (n = 105; age 36-71 years) on die t therapy alone, and with quite good glycaemic control (mean HbA(1c) simila r or equal to 7 0%) were randomized to receive acarbose (100 mg three times daily) or placebo for 16 weeks, and changes in clinical and metabolic para meters indicative of Syndrome X were monitored. Fasting levels of glucose, glycosylated haemoglobin (HbA(1c)), true insulin, proinsulin, fibrinogen an d lipids were measured four times weekly, and glucose, insulin, proinsulin and triglyceride responses to a standardized 1.6 MJ breakfast were determin ed at 0, 1 and 2 h post meal. Analysis was on an intention-to-treat basis. Fasting levels of glucose (P < 0.0001), triglycerides (P = 0.03) and HbA(1c ) (P = 0.003) were reduced by acarbose over the 16 weeks of treatment. The mean change in HbA(1c) from week 0 to 16 differed by 0.4% (P=0.003) between the two groups. Insulin (P = 0.06), proinsulin (P = 0.07) and glucose (P < 0.0001) responses to the standard meal were reduced. These data show that acarbose reduces fasting glucose and triglyceride levels, lowers HbA(1c) an d limits the glycaemic and insulin response to food in individuals with typ e 2 diabetes mellitus with Syndrome X. Pharmacological agents that improve the metabolic environment and reduce insulin resistance have the potential to limit the progression of atherogenesis associated with type 2 diabetes m ellitus. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.