Autor: |
Aleidi SM; Department of Biopharmaceutics and Clinical Pharmacy, School of Pharmacy, The University of Jordan, Amman 11942, Jordan., Al-Ansari MM; Department of Botany and Microbiology, College of Science, King Saud University, Riyadh 11451, Saudi Arabia., Alnehmi EA; Department of Botany and Microbiology, College of Science, King Saud University, Riyadh 11451, Saudi Arabia.; Metabolomics Section, Department of Clinical Genomics, Center for Genomics Medicine, King Faisal Specialist Hospital & Research Center (KFSHRC), Zahrawi Street, Al Maather, Riyadh 11211, Saudi Arabia., Malkawi AK; Department of Chemistry and Biochemistry, The University of Quebec at Montreal, Montreal, QC H3C 3P8, Canada., Alodaib A; Metabolomics Section, Department of Clinical Genomics, Center for Genomics Medicine, King Faisal Specialist Hospital & Research Center (KFSHRC), Zahrawi Street, Al Maather, Riyadh 11211, Saudi Arabia., Alshaker M; Department of Family Medicine and Polyclinic, King Faisal Specialist Hospital & Research Center (KFSHRC), Zahrawi Street, Al Maather, Riyadh 11211, Saudi Arabia., Benabdelkamel H; Proteomics Resource Unit, Obesity Research Center, College of Medicine, King Saud University, P.O. Box 2925 (98), Riyadh 11461, Saudi Arabia., Abdel Rahman AM; Metabolomics Section, Department of Clinical Genomics, Center for Genomics Medicine, King Faisal Specialist Hospital & Research Center (KFSHRC), Zahrawi Street, Al Maather, Riyadh 11211, Saudi Arabia.; Department of Biochemistry and Molecular Medicine, College of Medicine, Al Faisal University, Riyadh 11533, Saudi Arabia. |
Abstrakt: |
The relationship between lipid metabolism and bone mineral density (BMD) is still not fully elucidated. Despite the presence of investigations using osteoporotic animal models, clinical studies in humans are limited. In this work, untargeted lipidomics profiling using liquid chromatography-mass spectrometry (LC-MS) analysis of human serum samples was performed to identify the lipidomics profile associated with low bone mineral density (LBMD), with a subsequent examination of potential biomarkers related to OP risk prediction or progression. A total of 69 participants were recruited for this cohort study, including the osteoporotic group (OP, n = 25), osteopenia group (ON, n = 22), and control (Ctrl, n = 22). The LBMD group included OP and ON patients. The lipidomics effect of confounding factors such as age, gender, lipid profile, body mass index (BMD), chronic diseases, and medications was excluded from the dataset. The results showed a clear group separation and clustering between LBMD and Ctrl (Q 2 = 0.944, R 2 = 0.991), indicating a significant difference in the lipids profile. In addition, 322 putatively identified lipid molecules were dysregulated, with 163 up- and 159 down-regulated in LBMD, compared with the Ctrl. The most significantly dysregulated subclasses were phosphatidylcholines (PC) ( n = 81, 25.16% of all dysregulated lipids 322), followed by triacylglycerol (TG) ( n = 65, 20.19%), and then phosphatidylethanolamine (PE) ( n = 40, 12.42%). In addition, groups of glycerophospholipids, including LPC (7.45%), LPE (5.59%), and PI (2.48%) were also dysregulated as of LBMD. These findings provide insights into the lipidomics alteration involved in bone remodeling and LBMD. and may drive the development of therapeutic targets and nutritional strategies for OP management. |