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Original Article

Sustained postprandial decrease in plasma levels of LDL cholesterol in patients with type‐2 diabetes mellitus

, , , , , & show all
Pages 628-640 | Received 15 Dec 2007, Accepted 15 Feb 2008, Published online: 08 Jul 2009
 

Abstract

Objective. Low density lipoprotein cholesterol (LDL‐C) is an independent and modifiable risk factor for development of cardiovascular disease (CVD). Postprandial lipid metabolism has been linked to CVD, but little is known about the postprandial LDL‐C profile in patients with type‐2 diabetes (T2DM). We aimed to study the postprandial levels of LDL‐C in T2DM patients. Material and methods. After an overnight fast, 74 T2DM patients, mean age approximately 60 years, were served a standard fat‐rich meal of 3,515 kJ containing 54 % fat, 13 % protein and 33 % carbohydrates. Only drinking water was allowed postprandially. Blood samples were drawn at times 0 (fasting), 1.5, 3.0, 4.5 and 6.0 h (postprandial). In all samples, LDL‐C was measured with modified beta quantification (separation by ultracentrifugation followed by measurement of infranate high density lipoprotein cholesterol (HLD‐C) using a homogeneous assay). Results. At all postprandial times, levels of LDL‐C showed highly significant (p<0.005) decreases compared to time 0 (mean [95 % CI] maximum change in LDL‐C levels at 3.0 h: −0.16 mmol/L [−0.12; −0.20]; p<0.001). Independently of fasting LDL‐C levels and ongoing statin therapy, LDL‐C decreased significantly more in female compared to male patients postprandially (mean [95 % CI] maximum unadjusted change versus time 0 in LDL‐C for men [n = 56] at 3.0 h: −0.14 mmol/L [−0.19; −0.10], p<0.001; for women [n = 18] at 4.5 h: −0.26 mmol/L [−0.35; −0.18], p<0.001; −0.14 mmol/L [−0.24; −0.05], p = 0.005 between genders for the mean [95 % CI] fasting adjusted difference at 4.5 h in the change versus time 0 in LDL‐C; gender by time interaction: p = 0.007 (repeated measures mixed model)). Conclusions. In T2DM patients served a fat‐rich meal, levels of LDL‐C decreased significantly more in women compared to men postprandially, irrespective of fasting levels or ongoing statin therapy. This might have implications in the atherosclerotic process and on any difference in the risk of CVD between genders.

Acknowledgements

We thank the following people and companies for their help and support during the course of this study: The Danish Diabetes Association and the Clinical Development Foundation at the Steno Diabetes Center, for financial support; LifeScan Johnson & Johnson, for technical provision; Jørn Dyerberg, for methodological advice; Birgitte Vilsbøl Hansen, Tina Ragnholm Juhl, Berit Ruud Jensen, Lotte Pietraszek and Ingelise Rossing, the laboratory technicians; Ellis Tauber‐Lassen, the dietician; Annalise Klausen and all the staff employed in the kitchen of the Steno Diabetes Center, for preparing test meals. The Danish Diabetes Association and the Clinical Development Foundation at the Steno Diabetes Center co‐sponsored the study financially. LifeScan Johnson & Johnson supplied blood glucose hand devices and test strips. The sponsors took no part in the study design, the collection, analysis and interpretation of the data, the production of the report, or in the decision to submit the paper for publication. No conflicts of interest have been declared.

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