title: Impaired glucose tolerance is not associated with lipid intolerance.
abstract: Post-prandial (pp) hypertriglyceridaemia (HTG) has an important role in the development of atherosclerosis in Type 2 diabetes. Impaired glucose tolerance (IGT) is associated with an increased risk of atherosclerosis and increased level of fasting triglycerides (TG). The aim of this study was to analyse pp HTG and the composition of TG-rich lipoproteins in carefully selected subjects with IGT in comparison to controls with normal glucose tolerance (NGT). Fifteen men with IGT and 27 men with NGT, aged 44 to 70 yr, were examined. All study participants were non-smokers and had fasting TG <4.6 mmol/l. The subjects underwent an oral glucose tolerance test (75 g glucose) and a lipid-glucose tolerance test (LGTT; 92 g fat, 126 g carbohydrate), that allowed the assessment of lipid and glucose tolerance in one test. HbA1C, plasma glucose and lipids were measured by routine methods. Lipoprotein subfraction analysis of VLDL (VLDL1: Sf60-400 and VLDL2: Sf20-60) was conducted in a fasting state, as well as 4 hr after the LGTT using a density gradient ultracentrifugation with a subsequent compositional analysis. No significant difference was found either for fasting or pp TG, or for area under curve (AUC) -TG (12.21 +/- 4.27 mmol/l x 6 hr vs 13.95 +/- 6.74 mmol/l x 6 hr; p>0.05) between the IGT and NGT. A highly significant correlation was found between the fasting TG and the AUC-TG (r=0.925; p<0.01). To avoid bias by differences in fasting plasma TG known to affect lipid tolerance we investigated 11 matched pairs for fasting TG. Also, the matched-pairs evaluation pp TG course did not differ significantly from the IGT and NGT. No significant difference for fasting or pp levels of VLDL1 and VLDL2, or for the TG content of chylomicron, VLDL1 and VLDL2 and for the percentage of TG in VLDL1 and VLDL2 was found between the IGT and NGT group. In conclusion, IGT subjects with a similar level of fasting TG do not exhibit lipid intolerance. Our data suggest that glucose intolerance should precede lipid intolerance.
authors.affiliation: Centre of Clinical Studies-Metabolism and Endocrinology, Science and Technology Transfer GWT, Technial University Dresden, Germany.
authors.forename: E
authors.initials: E
authors.lastname: Henkel
authors.forename: Th
authors.initials: T
authors.lastname: Temelkova-Kurktschiev
authors.forename: C
authors.initials: C
authors.lastname: Koehler
authors.forename: J
authors.initials: J
authors.lastname: Pietzsch
authors.forename: W
authors.initials: W
authors.lastname: Leonhardt
authors.forename: M
authors.initials: M
authors.lastname: Hanefeld
mesh_terms: D000328:Adult; D000368:Aged; D019540:Area Under Curve; D001161:Arteriosclerosis / Q000097:blood / Q000209:etiology; D001786:Blood Glucose / Q000032:analysis; D016022:Case-Control Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D005215:Fasting; D018149:Glucose Intolerance / Q000097:blood / Q000150:complications*; D005951:Glucose Tolerance Test; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood*; D008079:Lipoproteins, VLDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D019518:Postprandial Period; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood*
chemical_list: D001786:Blood Glucose; D008079:Lipoproteins, VLDL; D014280:Triglycerides