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Online Letters: Observations

Impaired Postprandial Metabolism of Apolipoprotein B48–Containing Remnant Particles in Normolipidemic Subjects With Brittle Type 1 Diabetes

  1. Jenny W. Su, RD1,
  2. Jennifer E. Lambert2,
  3. Michael T. Clandinin, PHD2 and
  4. Spencer D. Proctor, PHD1
  1. 1Metabolic and Cardiovascular Diseases Laboratory, Alberta Institute for Human Nutrition, University of Alberta, Edmonton, Alberta, Canada
  2. 2Alberta Institute for Human Nutrition, University of Alberta, Edmonton, Alberta, Canada
  1. Corresponding author: Spencer D. Proctor, spencer.proctor{at}ualberta.ca
Diabetes Care 2009 Feb; 32(2): e21-e21. https://doi.org/10.2337/dc08-1573
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Impaired metabolism of intestinally derived chylomicron remnants has been implicated in the development of atherosclerosis among normolipidemic patients with coronary heart disease (1,2) and, indeed, in other conditions associated with increased vascular disease such as obesity, metabolic syndrome, type 2 diabetes, and familial hypercholesterolemia (3–5). However, the role of these particles in the increased atherosclerotic risk associated with type 1 diabetes is unclear. No studies to date have examined apolipoprotein (apo)B48, a specific marker of chylomicron particle number, in the human type 1 diabetic population.

Nine normolipidemic subjects (five male and four female) with brittle type 1 diabetes and seven healthy normolipidemic control subjects (two male and five female) were studied. Subjects were matched based on sex, age (53.3 ± 3.3 vs. 46.5 ± 6.3 years; P = 0.31), and BMI (24.9 ± 1.2 vs. 23.7 ± 0.80 kg/m2; P = 0.44). The duration of diabetes in the nine diabetic subjects was 41.6 ± 3.3 years (range 20–45), and A1C concentration was 8.9 ± 0.5%.

Subjects were fasted overnight before the test day. On the test day, blood samples were drawn at 0, 2, 4, 6, and 8 h following the breakfast (0.5 h) and lunch (4.5 h) meals in order to stimulate a free-living environment. In statistical comparisons determined by unpaired Student's t tests, there were no differences in fasting glucose, insulin, or lipid parameters among subjects with type 1 diabetes compared with those in the control population. In contrast, fasting apoB48 was the only fasting lipid-associated parameter to be higher among subjects with type 1 diabetes relative to that in the control population (22.8 ± 2.5 and 12.3 ± 1.0 μg/ml; P < 0.01). The fed response, calculated as postprandial area under the curve (AUC) (0–8 h), revealed no differences in postprandial insulin, cholesterol, or triglyceride AUC between the two groups. However, the postprandial response of plasma apoB48 showed that subjects with type 1 diabetes had a progressive and significant delay in clearance of remnant particles over the 8-h time period. Total plasma apoB48 AUC indicated that circulating apoB48 mass was 31% higher in subjects with type 1 diabetes versus the control population (222.9 ± 11.3 vs. 169.8 ± 15.9 μg · ml−1 · 8 h−1; P < 0.01). Ingestion of sequential meals, consistent with a free-living situation, resulted in a biphasic response of plasma apoB48, peaking at 2 h following both the initial (breakfast) and the second (lunch) meal. Participants with type 1 diabetes demonstrated circulating apoB48 levels that were 45% higher at 6 h (P < 0.01), which progressively increased to 69% by 8 h (P < 0.01), following the second (lunch) meal.

In conclusion, apoB48 metabolism may be altered in individuals with brittle type 1 diabetes even in the absence of classic dyslipidemia. Further studies using larger sample sizes should examine whether disturbed plasma apoB48 remnants can potentially predict coronary artery disease in this population.

Acknowledgments

No potential conflicts of interest relevant to this article were reported.

Footnotes

  • Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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References

  1. ↵
    Meyer E, Westerveld HT, de Ruyter-Meijstek FC, van Greevenbroek MM, Rienks R, van Rijn HJ, Erkelens DW, de Bruin TW: Abnormal postprandial apolipoprotein B48 and triglyceride responses in normolipidemic women with greater than 70% stenotic coronary artery disease: a case-control study. Atherosclerosis 124:221–235, 1996
    OpenUrlCrossRefPubMedWeb of Science
  2. ↵
    Weintraub MS, Grosskopf I, Rassin T, Miller H, Charach G, Rotmensch HH, Liron M, Rubinstein A, Iaina A: Clearance of chylomicron remnants in normolipidaemic patients with coronary artery disease: case control study over three years. BMJ 312:935–939, 1996
    OpenUrlAbstract/FREE Full Text
  3. ↵
    Mekki N, Christofilis A, Charbonnier M, Atlan-Gepner C, Defoort C, Juhel C, Borel P, Portugal H, Pauli AM, Vialettes AM, Lairon D: Influence of obesity and body fat distribution on postprandial lipemia and triglyceride-rich lipoproteins in adult women. J Clin Endocrinol Metab 84:184–191, 1999
    OpenUrlCrossRefPubMedWeb of Science
  4. Curtin A, Deegan P, Owens D, Collins P, Johnson A, Tomkin GH: Elevated triglyceride-rich lipoproteins in diabetes: a study of apolipoprotein B-48. Acta Diabetol 33:205–210, 1996
    OpenUrlCrossRefPubMedWeb of Science
  5. ↵
    Dane-Stewart CA, Watts GF, Mamo JC, Dimmitt SB, Barrett PH, Redgrave TG: Elevated apolipoprotein B-48 and remnant-like particle-cholesterol in heterozygous familial hypercholesterolaemia. Eur J Clin Invest 31:113–117, 2001
    OpenUrlCrossRefPubMed
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Impaired Postprandial Metabolism of Apolipoprotein B48–Containing Remnant Particles in Normolipidemic Subjects With Brittle Type 1 Diabetes
Jenny W. Su, Jennifer E. Lambert, Michael T. Clandinin, Spencer D. Proctor
Diabetes Care Feb 2009, 32 (2) e21; DOI: 10.2337/dc08-1573

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Impaired Postprandial Metabolism of Apolipoprotein B48–Containing Remnant Particles in Normolipidemic Subjects With Brittle Type 1 Diabetes
Jenny W. Su, Jennifer E. Lambert, Michael T. Clandinin, Spencer D. Proctor
Diabetes Care Feb 2009, 32 (2) e21; DOI: 10.2337/dc08-1573
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