title: Effects of acarbose treatment on markers of insulin sensitivity and systemic inflammation.
abstract: BACKGROUND
  This study assessed the effect of postprandial glucose reduction by acarbose on insulin sensitivity and biomarkers of systemic inflammation.
  
  
  METHODS
  This was a single-center, double-blind, randomized, placebo-controlled, crossover study <40 weeks in duration, involving 66 subjects with varying degrees of glucose tolerance. Eligible patients completed a 3-week run-in period and were randomized to receive either 100 mg of acarbose three times daily followed by placebo, or vice versa, lasting 12 weeks each with a 12-week washout between interventions. Liquid meal challenges and hyperinsulinemic-euglycemic glucose clamp were performed at weeks 0, 12, 24, and 36.
  
  
  RESULTS
  Fasting proinsulin levels and proinsulin-to-adiponectin ratios but not fasting adiponectin levels were significantly lower during acarbose versus placebo treatment. Clamp-derived insulin sensitivity index and body weight were unchanged by the intervention. Levels of fasting insulin, fasting glucose, monocyte chemoattractant protein-1, interleukin-6, and interleukin-1β were comparable between treatments. In the liquid meal challenge tests, postprandial glucose and insulin responses were significantly lower during acarbose versus placebo treatment. The effects of acarbose on the reduction of fasting proinsulin was most pronounced in subjects with impaired fasting glucose/impaired glucose tolerance (n = 24).
  
  
  CONCLUSIONS
  Reduction of the glycemic load by acarbose decreased fasting levels of proinsulin but had no effect on adiponectin and whole-body insulin sensitivity as well as biomarkers reflecting inflammation. The preventive effects of acarbose on type 2 diabetes mellitus and cardiovascular risk need further investigation and cannot be explained by changes of insulin resistance and inflammatory biomarkers.
authors.affiliation: Department of Clinical Nutrition, German Institute of Human Nutrition Potsdam, Nuthetal, Germany. rudovich@dife.de
authors.forename: Natalia N
authors.initials: NN
authors.lastname: Rudovich
authors.forename: Martin O
authors.initials: MO
authors.lastname: Weickert
authors.forename: Olga
authors.initials: O
authors.lastname: Pivovarova
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Bernigau
authors.forename: Andreas F H
authors.initials: AF
authors.lastname: Pfeiffer
mesh_terms: D020909:Acarbose / Q000627:therapeutic use*; D052242:Adiponectin / Q000097:blood; D015415:Biomarkers / Q000097:blood; D015992:Body Mass Index; D002318:Cardiovascular Diseases / Q000517:prevention & control; D018592:Cross-Over Studies; D016207:Cytokines / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000276:immunology; D004311:Double-Blind Method; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D005260:Female; D018149:Glucose Intolerance / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000276:immunology; D065089:Glycoside Hydrolase Inhibitors; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D018836:Inflammation Mediators / Q000097:blood; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D050177:Overweight / Q000150:complications; D011384:Proinsulin / Q000097:blood; D012720:Severity of Illness Index
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D015415:Biomarkers; D016207:Cytokines; D004791:Enzyme Inhibitors; D065089:Glycoside Hydrolase Inhibitors; D007004:Hypoglycemic Agents; D018836:Inflammation Mediators; D011384:Proinsulin; D020909:Acarbose