title: Basal and insulin mediated VLDL-triglyceride kinetics in type 2 diabetic men.
abstract: OBJECTIVE
  Increased very-low-density lipoprotein triglycerides (VLDL-TG) concentration is a central feature of diabetic dyslipidemia. The objective was to compare basal and insulin mediated VLDL-TG kinetics, oxidation, and adipose tissue storage in type 2 diabetic and healthy (nondiabetic) men.
  
  
  METHODS
  Eleven type 2 diabetic and 11 healthy men, matched for BMI and age, were included. Ex vivo-labeled VLDL-TG tracers, blood and breath samples, fat biopsies, indirect calorimetry, and body composition measures were applied to determine VLDL-TG kinetics, VLDL-TG fatty acids (FA) oxidation, and storage in regional adipose tissue before and during a hyperinsulinemic euglycaemic clamp.
  
  
  RESULTS
  VLDL-TG secretion was significantly greater in diabetic compared with healthy men (basal: 86.9 [31.0] vs. 61.9 [30.0] μmol/min, P = 0.03; clamp: 60.0 [26.2] vs. 34.2 [17.9] μmol · min⁻¹, P = 0.01). The insulin mediated suppression of VLDL-TG secretion was significant in both groups. VLDL-TG clearance was lower in diabetic men (basal: 84.6 [32.7] vs. 115.4 [44.3] ml · min⁻¹, P = 0.08; clamp: 76.3 [30.6] vs. 119.0 [50.2] ml · min⁻¹, P = 0.03). During hyperinsulinemia fractional VLDL-TG FA oxidation was comparable, but in percentage of energy expenditure (EE), significantly higher in diabetic men. Basal VLDL-TG storage was similar, but significantly greater in abdominal compared with leg fat.
  
  
  CONCLUSIONS
  Increased VLDL-TG in type 2 diabetic men is caused by greater VLDL-TG secretion and less so by lower VLDL-TG clearance. The ability of hyperinsulinemia to suppress VLDL-TG secretion appears preserved. During hyperinsulinemia VLDL-TG FA oxidation is significantly increased in proportion of EE in type 2 diabetic men. Greater basal abdominal VLDL-TG storage may help explain the accumulation of upper-body fat in insulin-resistant individuals.
authors.affiliation: Department of Endocrinology and Internal Medicine, University Hospital, Aarhus, Denmark.
authors.forename: Lars P
authors.initials: LP
authors.lastname: Sørensen
authors.forename: Iben R
authors.initials: IR
authors.lastname: Andersen
authors.forename: Esben
authors.initials: E
authors.lastname: Søndergaard
authors.forename: Lars C
authors.initials: LC
authors.lastname: Gormsen
authors.forename: Ole
authors.initials: O
authors.lastname: Schmitz
authors.forename: Jens S
authors.initials: JS
authors.lastname: Christiansen
authors.forename: Søren
authors.initials: S
authors.lastname: Nielsen
mesh_terms: D000273:Adipose Tissue / Q000033:anatomy & histology; D000328:Adult; D000368:Aged; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000378:metabolism*; D002149:Energy Intake; D005227:Fatty Acids / Q000097:blood / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000097:blood / Q000627:therapeutic use*; D007553:Isotope Labeling / Q000379:methods; D008079:Lipoproteins, VLDL / Q000097:blood / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012016:Reference Values; D014280:Triglycerides / Q000097:blood / Q000378:metabolism*
chemical_list: D002784:Cholesterol; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005227:Fatty Acids; D005230:Fatty Acids, Nonesterified; D006442:Glycated Hemoglobin; D007328:Insulin; D008079:Lipoproteins, VLDL; D014280:Triglycerides; C030106:very low density lipoprotein triglyceride