title: De novo lipogenesis and cholesterol synthesis in humans with long-standing type 1 diabetes are comparable to non-diabetic individuals.
abstract: BACKGROUND
  Synthesis of lipid species, including fatty acids (FA) and cholesterol, can contribute to pathological disease. The purpose of this study was to investigate FA and cholesterol synthesis in individuals with type 1 diabetes, a group at elevated risk for vascular disease, using stable isotope analysis.
  
  
  METHODS
  Individuals with type 1 diabetes (n = 9) and age-, sex-, and BMI-matched non-diabetic subjects (n = 9) were recruited. On testing day, meals were provided to standardize food intake and elicit typical feeding responses. Blood samples were analyzed at fasting (0 and 24 h) and postprandial (2, 4, 6, and 8 hours after breakfast) time points. FA was isolated from VLDL to estimate hepatic FA synthesis, whereas free cholesterol (FC) and cholesteryl ester (CE) was isolated from plasma and VLDL to estimate whole-body and hepatic cholesterol synthesis, respectively. Lipid synthesis was measured using deuterium incorporation and isotope ratio mass spectrometry.
  
  
  RESULTS
  Fasting total hepatic lipogenesis (3.91 ± 0.90% vs. 5.30 ± 1.22%; P = 0.41) was not significantly different between diabetic and control groups, respectively, nor was synthesis of myristic (28.60 ± 4.90% vs. 26.66 ± 4.57%; P = 0.76), palmitic (12.52 ± 2.75% vs. 13.71 ± 2.64%; P = 0.65), palmitoleic (3.86 ± 0.91% vs. 4.80 ± 1.22%; P = 0.65), stearic (5.55 ± 1.04% vs. 6.96 ± 0.97%; P = 0.29), and oleic acid (1.45 ± 0.28% vs. 2.10 ± 0.51%; P = 0.21). Postprandial lipogenesis was also not different between groups (P = 0.38). Similarly, fasting synthesis of whole-body FC (8.2 ± 1.3% vs. 7.3 ± 0.8%/day; P = 0.88) and CE (1.9 ± 0.4% vs. 2.0 ± 0.3%/day; P = 0.96) and hepatic FC (8.2 ± 2.0% vs. 8.1 ± 0.8%/day; P = 0.72) was not significantly different between diabetic and control subjects.
  
  
  CONCLUSIONS
  Despite long-standing disease, lipogenesis and cholesterol synthesis was not different in individuals with type 1 diabetes compared to healthy non-diabetic humans.
authors.affiliation: Alberta Institute for Human Nutrition, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: Jennifer E
authors.initials: JE
authors.lastname: Lambert
authors.affiliation: Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: Edmond A
authors.initials: EA
authors.lastname: Ryan
authors.affiliation: Alberta Institute for Human Nutrition, University of Alberta, Edmonton, Alberta, Canada ; Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: Alan B R
authors.initials: AB
authors.lastname: Thomson
authors.affiliation: Alberta Institute for Human Nutrition, University of Alberta, Edmonton, Alberta, Canada ; Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.
authors.forename: Michael T
authors.initials: MT
authors.lastname: Clandinin
mesh_terms: D016022:Case-Control Studies; D002784:Cholesterol / Q000096:biosynthesis*; D002788:Cholesterol Esters / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000378:metabolism*; D005215:Fasting / Q000097:blood; D005227:Fatty Acids / Q000096:biosynthesis; D005260:Female; D006801:Humans; D050155:Lipogenesis; D008079:Lipoproteins, VLDL / Q000097:blood; D008099:Liver / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D019518:Postprandial Period; D014280:Triglycerides / Q000097:blood
chemical_list: D002788:Cholesterol Esters; D005227:Fatty Acids; D008079:Lipoproteins, VLDL; D014280:Triglycerides; C030106:very low density lipoprotein triglyceride; D002784:Cholesterol