title: Postprandial whole-body glycolysis is similar in insulin-resistant and insulin-sensitive non-diabetic humans.
abstract: OBJECTIVE
  Insulin resistance is characterised by impaired glucose utilisation when measured by a euglycaemic-hyperinsulinaemic clamp. We hypothesised that, in response to postprandial conditions, non-diabetic individuals would have similar intracellular glycolytic and oxidative glucose metabolism independent of the degree of insulin resistance.
  
  
  METHODS
  Fourteen (seven male) sedentary, insulin-sensitive participants (mean ± SD: BMI 25 ± 4 kg/m²; age 39 ± 10 years; glucose disposal rate 9.4 ± 2.1 mg [kg estimated metabolic body size]⁻¹ min⁻¹) and 14 (six male) sedentary, non-diabetic, insulin-resistant volunteers (29 ± 4 kg/m²; 34 ± 13 years; 5.3 ± 1.2 mg [kg estimated metabolic body size]⁻¹ min⁻¹) received after a 10 h fast 60 g glucose plus 15 g [6,6-²H₂]glucose. Serum glucose and insulin concentrations, plasma ²H enrichment and whole-body gas exchange were determined before glucose ingestion and hourly thereafter for 4 h. Plasma ²H₂O production is an index of glycolytic disposal. On day 2, participants received a weight-maintenance diet. On day 3, a euglycaemic-hyperinsulinaemic clamp was performed.
  
  
  RESULTS
  Insulin-resistant individuals had about a twofold higher postprandial insulin response than insulin-sensitive individuals (p = 0.003). Resting metabolic rate was similar in the two groups before (p = 0.29) and after (p = 0.33-0.99 over time) glucose ingestion, whereas a trend for blunted glucose-induced thermogenesis was observed in insulin-resistant vs insulin-sensitive individuals (p = 0.06). However, over the 4 h after the 75 g glucose ingestion, glycolytic glucose disposal was the same in insulin-sensitive and insulin-resistant individuals (36.5 ± 3.7 and 36.2 ± 6.4 mmol, respectively; p = 0.99). Similarly, whole-body carbohydrate oxidation did not differ between the groups either before or after glucose ingestion (p = 0.41).
  
  
  CONCLUSIONS
  Postprandial hyperinsulinaemia and modest hyperglycaemia overcome insulin resistance by enhancing tissue glucose uptake and intracellular glucose utilisation.
authors.affiliation: Department of Nutrition, Faculty of Medicine, University of Chile, Independencia 1027, Clasificador 7, Santiago, Chile. jgalgani@med.uchile.cl
authors.forename: J E
authors.initials: JE
authors.lastname: Galgani
authors.forename: E
authors.initials: E
authors.lastname: Ravussin
mesh_terms: D000328:Adult; D001481:Basal Metabolism; D001786:Blood Glucose / Q000032:analysis; D003903:Deuterium; D005260:Female; D005947:Glucose / Q000378:metabolism*; D015309:Glucose Clamp Technique; D006019:Glycolysis; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000378:metabolism / Q000503:physiopathology; D006946:Hyperinsulinism / Q000097:blood / Q000378:metabolism / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D010085:Oxidative Phosphorylation; D019518:Postprandial Period; D012720:Severity of Illness Index; D022722:Thermogenesis; D055815:Young Adult
chemical_list: D001786:Blood Glucose; D007328:Insulin; D003903:Deuterium; D005947:Glucose