title: Glucose intolerance and the amount of visceral adipose tissue contribute to an increase in circulating triglyceride concentrations in Caucasian obese females.
abstract: BACKGROUND
  Lipotoxicity is a risk factor for developing obesity-related metabolic complications, including non-alcoholic fatty liver disease, type 2 diabetes (DM2), cardiovascular disease and stroke. Yet, the mechanisms underlying the development of lipotoxicity itself remain poorly understood. Here, we investigated whether glucose intolerance aggravates lipotoxicity by evaluating the association between triglyceride (TG) concentrations and glucose tolerance status in a cross-sectional study on obese Caucasian women at risk for DM2.
  
  
  METHODS
  913 obese females unknown to have diabetes were recruited (mean age: 41.2 ± SD 12.3; median BMI: 36.2, IQR 32.9-40.2). Visceral (VAT) and subcutaneous abdominal adipose tissue volumes were quantified with computed tomography. Glucose, insulin, and triglyceride concentrations were determined in fasting state and following a 75 gram oral glucose tolerance test.
  
  
  RESULTS
  Based on fasting and 2 h post-load glucose levels, 27% of the women had impaired glucose tolerance (IGT), and 8% had newly diagnosed DM2. Fasting TG concentrations were similar between the IGT- and DM2-groups, and increased as compared to women with normal glucose tolerance (NGT). Even when adjusting for age, hip circumference and VAT, fasting TG concentrations remained elevated as compared to NGT. Mixed modelling analysis of post-load responses showed that TG concentrations declined more slowly in the DM2-group as compared to IGT and NGT. However, when adjusting for VAT the difference in decline between the glucose tolerance groups disappeared.
  
  
  CONCLUSIONS
  Glucose intolerance associates with elevated fasting TG concentrations in obese Caucasian women. We propose that glucose intolerance and increased VAT reduce lipid disposal mechanisms and may accelerate lipotoxicity.
authors.affiliation: Department of Endocrinology, Ghent University Hospital, Ghent, Belgium.
authors.forename: Margot
authors.initials: M
authors.lastname: Berings
authors.forename: Charline
authors.initials: C
authors.lastname: Wehlou
authors.forename: An
authors.initials: A
authors.lastname: Verrijken
authors.forename: Ellen
authors.initials: E
authors.lastname: Deschepper
authors.forename: Ilse
authors.initials: I
authors.lastname: Mertens
authors.forename: Jean-Marc
authors.initials: JM
authors.lastname: Kaufman
authors.forename: Luc F
authors.initials: LF
authors.lastname: Van Gaal
authors.forename: D Margriet
authors.initials: DM
authors.lastname: Ouwens
authors.forename: Johannes B
authors.initials: JB
authors.lastname: Ruige
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000000981:diagnostic imaging; D005215:Fasting / Q000097:blood; D005260:Female; D018149:Glucose Intolerance / Q000097:blood* / Q000000981:diagnostic imaging / Q000473:pathology*; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000097:blood; D050152:Intra-Abdominal Fat / Q000000981:diagnostic imaging / Q000378:metabolism*; D016014:Linear Models; D008875:Middle Aged; D009765:Obesity / Q000097:blood*; D011859:Radiography; D014280:Triglycerides / Q000097:blood*; D044465:White People
chemical_list: D001786:Blood Glucose; D007328:Insulin; D014280:Triglycerides