title: Combined treatment with exercise training and acarbose improves metabolic control and cardiovascular risk factor profile in subjects with mild type 2 diabetes.
abstract: OBJECTIVE
  The effect of exercise training and acarbose on glycemic control, insulin sensitivity, and phenotype was investigated in mild type 2 diabetes.
  
  
  METHODS
  Sixty-two men and women with type 2 diabetes were randomized to 12 weeks of structured exercise training with or without acarbose treatment or to acarbose alone. Glycemic control was determined by HbA(1c) (A1C), insulin sensitivity (M value) by euglycemic-hyperinsulinemic clamp, and regional fat distribution by computerized tomography and dual X-ray absorptiometry. Physical fitness was determined as maximal oxygen uptake (Vo(2max)). All investigations were performed before and after the intervention.
  
  
  RESULTS
  Forty-eight subjects completed the study. Exercise improved M value by 92% (P = 0.017) and decreased total and truncal fat (P = 0.002, 0.001) and systolic blood pressure (P = 0.01) but had no significant effect on Vo(2max) or A1C level. The combination of exercise and acarbose significantly decreased fasting plasma glucose, A1C, lipids, and diastolic blood pressure and increased Vo(2max), whereas effects on M value and body composition were comparable with that of exercise alone. Acarbose alone had no significant effect on either M value or A1C but decreased systolic (P = 0.001) and diastolic blood pressure (P = 0.001) and fasting proinsulin level (P = 0.009). Multiple regression analysis showed that addition of acarbose to exercise improved glycemic control.
  
  
  CONCLUSIONS
  In subjects with mild type 2 diabetes, exercise training improved insulin sensitivity but had no effect on glycemic control. The addition of acarbose to exercise, however, was associated with significant improvement of glycemic control and possibly cardiovascular risk factors.
authors.affiliation: Department of Molecular Medicine and Surgery, Karolinska Institutet, SE-171 76 Stockholm, Sweden. henrik.wagner@karolinska.se
authors.forename: Henrik
authors.initials: H
authors.lastname: Wagner
authors.forename: Marie
authors.initials: M
authors.lastname: Degerblad
authors.forename: Anders
authors.initials: A
authors.lastname: Thorell
authors.forename: Jonas
authors.initials: J
authors.lastname: Nygren
authors.forename: Agneta
authors.initials: A
authors.lastname: Ståhle
authors.forename: Jeanette
authors.initials: J
authors.lastname: Kuhl
authors.forename: Torkel B
authors.initials: TB
authors.lastname: Brismar
authors.forename: John
authors.initials: J
authors.lastname: Ohrvik
authors.forename: Suad
authors.initials: S
authors.lastname: Efendic
authors.forename: Peter N
authors.initials: PN
authors.lastname: Båvenholm
mesh_terms: D020909:Acarbose / Q000627:therapeutic use*; D001053:Apolipoproteins / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism*; D001794:Blood Pressure; D002318:Cardiovascular Diseases / Q000209:etiology*; D003924:Diabetes Mellitus, Type 2 / Q000628:therapy*; D015444:Exercise / Q000502:physiology*; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007333:Insulin Resistance / Q000502:physiology; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012307:Risk Factors
chemical_list: D001053:Apolipoproteins; D001786:Blood Glucose; D007004:Hypoglycemic Agents; D008055:Lipids; D017395:Plasminogen Activator Inhibitor 1; D020909:Acarbose