title: Ginseng and ginsenoside Re do not improve β-cell function or insulin sensitivity in overweight and obese subjects with impaired glucose tolerance or diabetes.
abstract: OBJECTIVE
  Ginseng and its active component, ginsenoside Re, are popular herbal products that are advocated for treatment of diabetes. The purpose of this study was to determine whether ginseng or ginsenoside Re improves β-cell function and insulin sensitivity (IS) in insulin-resistant subjects.
  
  
  METHODS
  Overweight or obese subjects (BMI = 34 ± 1 kg/m²) with impaired glucose tolerance or newly diagnosed type 2 diabetes were randomized to 30 days of treatment with ginseng root extract (8 g/day), ginsenoside Re (250-500 mg/day), or placebo. β-Cell function was assessed as the disposition index (DI) and measured by a frequently sampled oral glucose tolerance test, and IS was assessed as the relative increase in glucose disposal during a hyperinsulinemic-euglycemic clamp procedure plus stable isotope tracer infusion.
  
  
  RESULTS
  Values for DI and IS after therapy (Post) were not different from values before therapy (Pre) in the placebo (DI: Pre, 5.8 ± 0.9 × 10⁻³ and Post, 5.8 ± 0.8 × 10⁻³, P = 0.99; IS: Pre,165 ± 29% and Post, 185 ± 24%, P = 0.34), ginseng (DI: Pre, 7.7 ± 2.0 × 10⁻³ and Post, 6.0 ± 0.8 × 10⁻³, P = 0.29; IS: Pre, 171 ± 72% and Post,137 ± 59%, P = 0.88), and ginsenoside Re (DI: Pre, 7.4 ± 3.0 × 10⁻³ and Post, 5.9 ± 1.1 × 10⁻³, P = 0.50; IS: Pre, 117 ± 31% and Post, 134 ± 34%, P = 0.44) groups. Ginsenosides Re, Rb₁, and Rb₂ were not detectable in plasma after treatment with ginseng root extract or ginsenoside Re.
  
  
  CONCLUSIONS
  Oral ginseng or ginsenoside Re therapy does not improve β-cell function or IS in overweight/obese subjects with impaired glucose tolerance or newly diagnosed diabetes. Poor systemic bioavailability might be responsible for the absence of a therapeutic effect.
authors.affiliation: Center for Human Nutrition and Atkins Center of Excellence in Obesity Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
authors.forename: Dominic N
authors.initials: DN
authors.lastname: Reeds
authors.forename: Bruce W
authors.initials: BW
authors.lastname: Patterson
authors.forename: Adewole
authors.initials: A
authors.lastname: Okunade
authors.forename: John O
authors.initials: JO
authors.lastname: Holloszy
authors.forename: Kenneth S
authors.initials: KS
authors.lastname: Polonsky
authors.forename: Samuel
authors.initials: S
authors.lastname: Klein
mesh_terms: D000328:Adult; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D036145:Ginsenosides / Q000627:therapeutic use*; D015309:Glucose Clamp Technique; D018149:Glucose Intolerance / Q000188:drug therapy*; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D050417:Insulin-Secreting Cells / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000188:drug therapy* / Q000503:physiopathology; D050177:Overweight / Q000188:drug therapy* / Q000503:physiopathology; D005894:Panax; D028321:Plant Preparations / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D036145:Ginsenosides; D028321:Plant Preparations; C049864:ginsenoside Re