title: Increases in muscle blood flow after a mixed meal are impaired at all stages of type 2 diabetes.
abstract: OBJECTIVE
  In type 2 diabetes, although the impairment of postprandial muscle blood flow response is well established, information on the effect of this impairment on glucose uptake and lipid metabolism is controversial.
  
  
  METHODS
  Postprandial forearm blood flow responses and metabolic parameters were assessed in a cross-sectional study of subjects at various stages of insulin resistance.
  
  
  METHODS
  Eleven healthy subjects (CONTROLS), 11 first-degree relatives of type-2 diabetics (RELATIVES), 10 patients with impaired glucose tolerance (IGT), 10 diabetic patients with postprandial hyperglycaemia (DMA), and 13 diabetic patients with both fasting and postprandial hyperglycaemia (DMB).
  
  
  METHODS
  All subjects received a meal. Blood was drawn from a forearm deep vein and the radial artery at specific time-points during a period of 360 min for measurements of glucose, insulin, triglycerides and nonesterified-fatty acids. Forearm muscle blood flow was measured with strain-gauge plethysmography. Glucose uptake and ISI Index were calculated.
  
  
  RESULTS
  Peak-baseline muscle blood flow was higher in CONTROLS (3.32 ± 0.4) than in RELATIVES (0.53 ± 0.29), IGT (0.82 ± 0.2), DMA (1.44 ± 0.34), DMB (1.23 ± 0.35 ml/min/100 ml tissue), P < 0.001. Glucose uptake (AUC(0-360,) μmol/100 ml tissue) was higher in CONTROLS (1023 ± 132) than in RELATIVES (488 ± 42), IGT (458 ± 43), DMA (347 ± 63), DMB (543 ± 53), P < 0.001. ISI index, postprandial triglycerides and nonesterified-fatty acids behaved in a similar way. Peak-baseline muscle blood flow correlated positively with glucose uptake (r = 0.440, P = 0.001) and ISI index (r = 0.397, P = 0.003), and negatively with postprandial triglycerides (r = -0.434, P = 0.001) and nonesterified-fatty acids (r = -0.370, P = 0.005).
  
  
  CONCLUSIONS
  These results suggest that increase in muscle blood flow after a meal is impaired at all stages of type-2 diabetes. This defect influences glucose uptake and is associated with impaired lipid metabolism in the postprandial state.
authors.affiliation: 2nd Department of Internal Medicine, Research Institute and Diabetes Center, Attikon University Hospital, Athens University Medical School, Athens, Greece.
authors.forename: Vaia
authors.initials: V
authors.lastname: Lambadiari
authors.forename: Panayota
authors.initials: P
authors.lastname: Mitrou
authors.forename: Eirini
authors.initials: E
authors.lastname: Maratou
authors.forename: Athanassios
authors.initials: A
authors.lastname: Raptis
authors.forename: Sotirios A
authors.initials: SA
authors.lastname: Raptis
authors.forename: George
authors.initials: G
authors.lastname: Dimitriadis
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000503:physiopathology*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000503:physiopathology; D019518:Postprandial Period / Q000502:physiology*; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D014280:Triglycerides