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Background: This Mendelian randomization (MR) study aimed to explore the causal relationship between polyunsaturated fatty acids (PUFAs) and bone mineral density (BMD).
Methods: We conducted a two-sample MR analysis to figure out if there is any causal effect of PUFAs on BMD through the summary data from the genome-wide association study (GWAS). Relationships were evaluated through inverse variance weighted (IVW), MR-Egger, weighted median, and maximum likelihood methods. The MR Pleiotropy RESidual Sum and Outlier (MR-PRESSO) test was performed to detect the horizontal pleiotropy.
Results: Our findings revealed that omega-6 fatty acids were negatively related to the TB-BMD (beta-estimate: -0.0515; 95% confidence interval [CI]: -0.0911 to -0.0119; standard error [SE]: 0.0201; p-value: 0.0106). The reverse direction MR analysis showed that TB-BMD was linked to the omega-6 FAs (beta-estimate: -0.0699; 95% CI: -0.1304 to -0.0095; SE: 0.0308; p-value: 0.0265). No statistically significant correlations between PUFAs and BMD were observed after adjusting the interactions between metabolites.
Conclusion: This two-sample MR analyses produced strong and new genomic evidence that there was a causal relationship between omega-6 FAs and BMD. Further investigations are still required to elucidate the potential mechanism.
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http://dx.doi.org/10.3389/fendo.2022.858851 | DOI Listing |
Circ Genom Precis Med
September 2025
Clinical Pharmacology and Precision Medicine, William Harvey Research Institute, London, United Kingdom (W.J.Y., M.M.S., J.R., S.v.D., H.R.W., A.T., P.B.M.).
Background: There is a higher prevalence of heart rate corrected QT (QTc) prolongation in patients with diabetes and metabolic syndrome. QT interval genome-wide association studies have identified candidate genes for cardiac energy metabolism, and experimental studies suggest that polyunsaturated fatty acids have direct effects on ion channel function. Despite this, there has been limited study of metabolite concentration relationships with QT intervals.
View Article and Find Full Text PDFObesity (Silver Spring)
September 2025
Division of Diabetes and Endocrinology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Objective: Vertical sleeve gastrectomy (VSG) promotes significant metabolic improvements, though the underlying molecular mechanisms are not fully understood. Emerging evidence suggests that small extracellular vesicles (sEVs) contribute to metabolic improvements post VSG, such as improved fatty liver disease or adipose tissue function; however, it is unclear how different organ-specific sEVs interact with various metabolic parameters. The objective of this study is to establish the role of organ-specific sEVs in the metabolic improvements post VSG.
View Article and Find Full Text PDFLeukemia
September 2025
I.R.C.C.S Santa Lucia Foundation, Via del Fosso di Fiorano, Rome, Italy.
At present there is no metabolic characterization of acute promyelocytic leukemia (APL). Pathognomonic of APL, PML::RARα fusion protein rewires metabolic pathways to feed anabolic tumor cell's growth. All-trans retinoic acid (ATRA) and arsenic trioxide (ATO)-based therapies render APL the most curable subtype of AML, yet approximately 1% of cases are resistant and 5% relapse.
View Article and Find Full Text PDFRev Gastroenterol Mex (Engl Ed)
September 2025
Facultad de Nutrición, Universidad Federal de Bahía (UFBA), Salvador, Bahía, Brazil.
Introduction And Aims: Metabolic dysfunction-associated steatotic disease (MASLD) is the most common cause of chronic liver disease in children and adolescents. The development of MASLD is associated with dietary habits, and dietary intake characteristics are a relevant risk factor. The aim of the present study was to analyze dietary intake characteristics in children and adolescents and study how diet varies in subjects with and without MASLD.
View Article and Find Full Text PDFTrends Mol Med
September 2025
Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address:
Ferroptosis, a regulated cell death pathway driven by iron-catalyzed lipid peroxidation, has recently been implicated as a major cause of hepatic injury in metabolic dysfunction-associated fatty liver disease (MAFLD). This review highlights how the identification of hyperoxidized peroxiredoxin 3 (PRDX3) as a ferroptosis-specific marker has led to the discovery that ferroptosis contributes to liver injury in MAFLD, and summarizes other emerging evidence connecting ferroptosis to MAFLD pathogenesis. These new findings suggest that dietary fat composition and genetic variants such as PNPLA3(I148M) may affect the progression of MAFLD by regulating cellular sensitivity to ferroptosis.
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