title: Insulin vs GLP-1 analogues in poorly controlled Type 2 diabetic subjects on oral therapy: a meta-analysis.
abstract: OBJECTIVE
  To compare insulin and GLP-1 analogues therapy on glycemic control in poorly controlled Type 2 diabetes (T2DM) subjects failing on oral therapy.
  
  
  METHODS
  The electronic database PubMed was systematically searched for randomized controlled trial (RCT) with duration >16 weeks comparing the addition of insulin therapy vs glucagon-like peptide (GLP-1) analogues in poorly controlled T2DM subjects on oral therapy.
  
  
  RESULTS
  We identified 7 RCT with 2199 patients of whom 1119 were assigned to insulin therapy and 1080 received a GLP-1 analogue. Both insulin and GLP-1 analogues were effective in lowering glycated hemoglobin (HbA(1c)) with no statistically significant difference between the mean decreases in HbA(1c). However, insulin was more effective than GLP-1 analogues in lowering the fasting plasma glucose concentration, while GLP-1 agonists were more effective in lowering the postprandial glucose concentration. Insulin therapy was associated with weight gain while GLP-1 analogues consistently caused weight loss and the difference between the mean change in body weight between the two therapies was highly statistically significant. Despite a similar decrease in HbA(1c), the risk of hypoglycemia was 35% lower (p=0.001) with GLP-1 therapy compared to insulin. Compared to insulin, GLP-1 analogues caused a significant decrease in systolic blood pressure and were associated with greater rate of gastrointestinal adverse events.
  
  
  CONCLUSIONS
  In poorly controlled T2DM subjects on oral therapy, GLP-1 analogues and insulin are equally effective in lowering the HbA(1c). However, GLP-1 analogues have additional non-glycemic benefits and lower risk of hypoglycemia. Thus, GLP-1 analogues should be considered as a treatment option in this group of diabetic individuals.
authors.affiliation: Division of Diabetes, University of Texas Health Science Center at San Antonio, TX, USA.
authors.forename: M A
authors.initials: MA
authors.lastname: Abdul-Ghani
authors.forename: K
authors.initials: K
authors.lastname: Williams
authors.forename: M
authors.initials: M
authors.lastname: Kanat
authors.forename: Y
authors.initials: Y
authors.lastname: Altuntas
authors.forename: R A
authors.initials: RA
authors.lastname: DeFronzo
mesh_terms: D000284:Administration, Oral; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy* / Q000453:epidemiology / Q000503:physiopathology; D005767:Gastrointestinal Diseases / Q000139:chemically induced / Q000453:epidemiology; D052216:Glucagon-Like Peptide 1 / Q000008:administration & dosage* / Q000009:adverse effects / Q000031:analogs & derivatives*; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage* / Q000009:adverse effects; D007328:Insulin / Q000008:administration & dosage* / Q000009:adverse effects; D008055:Lipids / Q000097:blood; D008875:Middle Aged; D016032:Randomized Controlled Trials as Topic; D017211:Treatment Failure
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D008055:Lipids; D052216:Glucagon-Like Peptide 1