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Letters to the Editor |
1 Department of Internal Medicine, Cardiology, Philipps-University of Marburg, Marburg, Germany and 2 St. Nikolaus-Stiftshospital, Andernach, Germany
aAddress correspondence to this author at: Department of Internal Medicine-Cardiology, Philipps-University of Marburg, Baldinger Strasse, D-35033 Marburg, Germany. E-mail schaefe5{at}staff.uni-marburg.de.
To the Editor:
Apolipoprotein A-IV (apo A-IV) is a 46-kDa plasma protein (1) with different isoforms (2). It is secreted with chylomicrons into the circulation (3). Within the plasma compartment, apo A-IV dissociates from chylomicrons (4) and associates with HDL, triglyceride-rich lipoproteins, and the lipoprotein-free fraction (5).
Apo A-IV is influenced by dietary intervention, and a low-fat, low-cholesterol diet (NCEP Step II diet) and is able to decrease apo A-IV secretion rates significantly (6). Apo A-IV is catabolized rapidly with a fractional catabolic rate of 
2.4 pools/day (7). Apo A-IV is higher in patients with renal impairment (8). In ad-libitum-fed rats, serum apo A-IV concentrations showed a circadian rhythm associated with the feeding pattern (9). The role of apo A-IV as a risk indicator in coronary artery disease is currently unclear. Some studies have shown that apo A-IV concentrations are lower in patients with coronary artery disease (10), indicating that apo A-IV is an antiatherogenic protein. However, some questions remain unanswered because apo A-IV is also closely linked to several highly atherogenic situations in humans. For example, high triglyceride concentrations, renal impairment, or fat-enriched diets cause an increase in apo A-IV concentrations.
Because apo A-IV is linked to triglyceride concentrations, we were interested to study apo A-IV concentrations in the fasting and nonfasting state. We studied 28 normolipidemic healthy persons (13 men and 15 women; mean age, 30 years) with normal body weight for 24 h in the fasting and nonfasting states. Apo A-IV and lipoprotein concentrations were determined every 3 h for a total of 24 h by standard techniques as described recently (11). Each study sequence started at 0700 in the morning. For the fasting group, members were asked to skip their usual breakfast and remained fasting for at least 24 h. In contrast, for the nonfasting group, members were permitted to follow their typical food intake during the study. During prolonged fasting, the apo A-IV concentration decreased to 50% of the starting concentration, from a mean (SD) of 150 (37) to 84 (26) mg/L (Fig. 1
). Triglycerides decreased slightly, reaching a plateau within 6–12 h [decrease from 910 (370) to 750 (220) mg/L]. In the nonfasting state, apo A-IV concentrations were rather stable for 24 h, whereas triglycerides showed an increase over the daytime [between 1080 (530) and 1340 (690) mg/L], which correlated with apo A-IV (r = 0.238; P <0.01). We found no circadian rhythm of apo A-IV concentrations in our study participants; however, the decrease in apo A-IV plasma concentrations during extended fasting periods took surprisingly long. The usual 10- to 12-h fasting periods before blood drawing for lipid evaluations do not appear to be sufficient to reach baseline apo A-IV concentrations. Therefore, apo A-IV requires well-defined protocols when this protein is studied.
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References
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).