Impaired fasting glucose vs. glucose intolerance in pre-menopausal women: distinct metabolic entities and cardiovascular disease risk?

Background: Impaired glucose tolerance (IGT) is associated with an increased cardiovascular disease risk. Less is known about cardiovascular disease risk among subjects with impaired fasting glucose (IFG) or with combined IFG and IGT.

Aims: To compare body composition, body fat distribution, plasma glucose-insulin homeostasis and plasma lipid-lipoprotein profile between pre-menopausal women having either a normal glucose tolerance (NGT), isolated IFG, isolated IGT or combined IFG and IGT.

Postprandial hyperlipidemia: another correlate of the "hypertriglyceridemic waist" phenotype in men.

Fasting hypertriglyceridemia has been reported to be predictive of an exaggerated triglyceride (TG) response to an oral fat load. Abdominal obesity has also been associated with postprandial hyperlipidemia. The objective of the present study was to quantify the contribution of abdominal obesity and fasting hypertriglyceridemia to the magnitude of postprandial lipemia.

Contribution of visceral adiposity to the exaggerated postprandial lipemia of men with impaired glucose tolerance.

Objective: Impaired glucose tolerance (IGT) has been associated with alterations in numerous coronary heart disease risk factors, including postprandial hyperlipidemia. An excess visceral adipose tissue accumulation is also predictive of IGT and of an exaggerated postprandial lipemia. The objective of the present study was therefore to compare the respective contributions of visceral adipose tissue accumulation versus IGT with the variation in postprandial lipemia.

Impact of postprandial variation in triglyceridemia on low-density lipoprotein particle size.

The fasting atherogenic dyslipidemia of visceral obesity, which includes the presence of small, dense low-density lipoprotein (LDL) particles, is predictive of an increased risk of coronary heart disease (CHD). It has also been suggested that progression of atherosclerosis may be accelerated in the presence of postprandial hyperlipidemia independently from the fasting dyslipidemic state. Studies have shown that the best predictor of postprandial hyperlipidemia and of the small, dense LDL phenotype is fasting triglyceride (TG) concentration.