European journal of nutrition · 2026
Amino acids: Missing link in preeclampsia pathogenesis?
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод в очереди
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Gezer Iclal Sena, Altinsoy Hasan, Bastemur Ayse Gulcin, Dogan Ozlem, Tanacan Atakan, Ocal Fatma Doga, Sahin Dilek, Yazihan Nuray
Аннотация
PURPOSE: This study was designed to determine maternal dietary and serum amino acid (AA) levels as risk factors for preeclampsia (PE), aiming to identify the potential of specific AAs as biomarkers that could lead to novel dietary intervention strategies.
METHODS: This prospective observational study included a total of 84 pregnant women (27 with PE and 57 controls). Maternal serum AA profiles were quantified using liquid chromatography-mass spectrometry (LC-MS), and dietary AA intake was assessed via three-day dietary recalls, usual intake was estimated using the Multiple Source Method (MSM) to correct for within-person variability. The potential of AA as a risk factor was evaluated using the Receiver Operating Characteristic (ROC) curve analysis, and key mechanisms involved in AA metabolism were identified through pathway analysis.
RESULTS: Dietary assessment uncovered a altered dietary amino acid pattern (AUC > 0.8), characterized by low intake of arginine, alanine, and glycine, glutamic acid, histidine, proline, serine, threonine, and tryptophan, alongside high total branched-chain amino acid (BCAA) and leucine consumption. Although dietary total protein intake was lower in PE, a higher intake of animal protein was observed. Concurrently, serum glutamine, asparagine, phenylalanine, 3-methylhistidine, cysteine, threonine, valine, BCAA, EAA, and aromatic AAs (AUC > 0.8) in serum were found to be potential risk factors for PE. Our results establish that dietary AA patterns and serum AA changes are independent, key risk factors, together providing a more comprehensive etiological model of PE.
CONCLUSION: This study showed that a dietary imbalance in specific AAs represents a modifiable risk factor for PE. This finding, alongside an altered serum AA profile, opens new avenues for targeted nutritional interventions in high-risk pregnancies.
METHODS: This prospective observational study included a total of 84 pregnant women (27 with PE and 57 controls). Maternal serum AA profiles were quantified using liquid chromatography-mass spectrometry (LC-MS), and dietary AA intake was assessed via three-day dietary recalls, usual intake was estimated using the Multiple Source Method (MSM) to correct for within-person variability. The potential of AA as a risk factor was evaluated using the Receiver Operating Characteristic (ROC) curve analysis, and key mechanisms involved in AA metabolism were identified through pathway analysis.
RESULTS: Dietary assessment uncovered a altered dietary amino acid pattern (AUC > 0.8), characterized by low intake of arginine, alanine, and glycine, glutamic acid, histidine, proline, serine, threonine, and tryptophan, alongside high total branched-chain amino acid (BCAA) and leucine consumption. Although dietary total protein intake was lower in PE, a higher intake of animal protein was observed. Concurrently, serum glutamine, asparagine, phenylalanine, 3-methylhistidine, cysteine, threonine, valine, BCAA, EAA, and aromatic AAs (AUC > 0.8) in serum were found to be potential risk factors for PE. Our results establish that dietary AA patterns and serum AA changes are independent, key risk factors, together providing a more comprehensive etiological model of PE.
CONCLUSION: This study showed that a dietary imbalance in specific AAs represents a modifiable risk factor for PE. This finding, alongside an altered serum AA profile, opens new avenues for targeted nutritional interventions in high-risk pregnancies.