title: Suppression of nocturnal fatty acid concentrations by bedtime carbohydrate supplement in type 2 diabetes: effects on insulin sensitivity, lipids, and glycemic control.
abstract: BACKGROUND
  Bedtime ingestion of slow-release carbohydrates leads to sustained nocturnal fatty acid suppression and improved glucose tolerance in type 2 diabetic patients.
  
  
  OBJECTIVE
  This study assessed the effects of 2 different doses of bedtime carbohydrate supplement (BCS) on morning glycemic control and glycated hemoglobin (Hb A(1c)) in type 2 diabetic patients. In addition, the effects of the high-dose BCS on insulin sensitivity and postprandial glucose and triacylglycerol concentrations were assessed.
  
  
  METHODS
  Two BCS doses were studied separately in 7-wk randomized, placebo-controlled, double-blind studies with either a parallel (low-dose BCS; n = 24 patients) or crossover (high-dose BCS; n = 14 patients) design. The effects of the low and high doses (0.30 and 0.55 g uncooked cornstarch/kg body wt, respectively) were compared with those of a starch-free placebo.
  
  
  RESULTS
  Compared with the starch-free placebo, the high-dose BCS ( approximately 45 g) produced enhanced nocturnal glucose (P < 0.01) and insulin (P < 0.01) concentrations as well as a 32% suppression of fatty acid concentrations (P < 0.01). Moreover, glucose tolerance (P < 0.05) and C-peptide response (P < 0.05) improved after breakfast the next morning. The low-dose BCS ( approximately 25 g) improved fasting blood glucose concentrations (P < 0.05). However, there were no improvements in insulin sensitivity, postprandial triacylglycerol concentrations, or Hb A(1c) after 7 wk.
  
  
  CONCLUSIONS
  Nocturnal fatty acid suppression by BCS improved fasting and postprandial blood glucose concentrations in type 2 diabetic patients the next morning. In contrast, no improvements in insulin sensitivity, postprandial triacylglycerol concentrations, or long-term glycemic control assessed by Hb A(1c) were seen after BCS supplementation.
authors.affiliation: Lundberg Laboratory for Diabetes Research and the Division of Clinical Nutrition, the Department of Internal Medicine, Sahlgrenska University Hospital, Göteborg University, Göteborg, Sweden. mette.axelsen@medicine.gu.se
authors.forename: M
authors.initials: M
authors.lastname: Axelsen
authors.forename: P
authors.initials: P
authors.lastname: Lönnroth
authors.forename: R A
authors.initials: RA
authors.lastname: Lenner
authors.forename: M R
authors.initials: MR
authors.lastname: Taskinen
authors.forename: U
authors.initials: U
authors.lastname: Smith
mesh_terms: D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D002096:C-Peptide / Q000097:blood; D002940:Circadian Rhythm; D018592:Cross-Over Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000378:metabolism*; D004311:Double-Blind Method; D005227:Fatty Acids / Q000097:blood*; D005260:Female; D005951:Glucose Tolerance Test; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008875:Middle Aged; D013213:Starch / Q000008:administration & dosage*; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D002096:C-Peptide; D005227:Fatty Acids; D006442:Glycated Hemoglobin; D007328:Insulin; D019344:Lactic Acid; D013213:Starch; D014280:Triglycerides