Low serum 25-hydroxyvitamin D [25(OH)D] is linked to an altered lipid profile. Monocytes play an important role in inflammation and lipid metabolism. Recently, monocyte percentage to HDL-cholesterol ratio (MHR) has emerged as a novel marker of inflammation. We investigated the association between serum 25(OH)D concentrations and MHR and serum lipids in young healthy adults. Data from the Qatar Biobank were utilized to investigate the relation between serum 25(OH)D and inflammation and serum lipid concentrations in healthy Qatari adults using multivariate regression analysis. Prevalence of serum 25(OH)D concentrations <12 ng/mL (deficiency), 12–20 ng/mL (insufficiency), and ≥20 ng/mL (sufficiency) were 55.8%, 29.9%, and 14.3%, respectively. Serum 25(OH)D was significantly inversely associated with monocyte percentage, MHR, total cholesterol, LDL-cholesterol, and triacylglycerol in multivariable adjusted analysis. MHR could be a potential biomarker to predict cardiometabolic diseases among young healthy Qataris.

Vitamin D deficiency is a global disorder associated with several chronic illnesses including dyslipidemia and metabolic syndrome. The impact of this association with both dyslipidemia and vitamin D deficiency on metabolomics profile is not yet fully understood. This study analyses the metabolomics and lipidomic signatures in relation to vitamin D status and dyslipidemia. Metabolomics data were collected from Qatar Biobank database and categorized into four groups based on vitamin D and dyslipidemia status. Metabolomics multivariate analysis was performed using the orthogonal partial least square discriminate analysis (OPLS-DA) whilst linear models were used to assess the per-metabolite association with each of the four dyslipidemia/vitamin D combination groups. Our results indicate a high prevalence of vitamin D deficiency among the younger age group, while dyslipidemia was more prominent in the older group. A significant alteration of metabolomics profile was observed among the dyslipidemic and vitamin D deficient individuals in comparison with control groups. These modifications reflected changes in some key pathways including ceramides, diacylglycerols, hemosylceramides, lysophospholipids, phosphatidylcholines, phosphatidylethanol amines, and sphingomyelins. Vitamin D deficiency and dyslipidemia have a deep impact on sphingomyelins profile. The modifications were noted at the level of ceramides and are likely to propagate through downstream pathways.

Stress granules (SGs) are assemblies of selective messenger RNAs (mRNAs), translation factors, and RNA-binding proteins in small untranslated messenger ribonucleoprotein (mRNP) complexes in the cytoplasm. Evidence indicates that different types of cells have shown different mechanisms to respond to stress and the formation of SGs. In the present work, we investigated how human-induced pluripotent stem cells (hiPSCs/IMR90-1) overcome hyperosmotic stress compared to a cell line that does not harbor pluripotent characteristics (SH-SY5Y cell line). Gradient concentrations of NaCl showed a different pattern of SG formation between hiPSCs/IMR90-1 and the nonpluripotent cell line SH-SY5Y. Other pluripotent stem cell lines (hiPSCs/CRTD5 and hESCs/H9 (human embryonic stem cell line)) as well as nonpluripotent cell lines (BHK-21 and MCF-7) were used to confirm this phenomenon. Moreover, the formation of hyperosmotic SGs in hiPSCs/IMR90-1 was independent of eIF2α phosphorylation and was associated with low apoptosis levels. In addition, a comprehensive proteomics analysis was performed to identify proteins involved in regulating this specific pattern of hyperosmotic SG formation in hiPSCs/IMR90-1. We found possible implications of microtubule organization on the response to hyperosmotic stress in hiPSCs/IMR90-1. We have also unveiled a reduced expression of tubulin that may protect cells against hyperosmolarity stress while inhibiting SG formation without affecting stem cell self-renewal and pluripotency. Our observations may provide a possible cellular mechanism to better understand SG dynamics in pluripotent stem cells.

Background: Red meat, a significant source of heme iron, may influence iron status and metabolic health, particularly in Qatar, where consumption is high. Understanding these associations is essential for addressing iron deficiency and cardiovascular risk in this population. Methods: We conducted a cross-sectional study using data from 13,778 Qatari adults enrolled in the Qatar Biobank (men: n = 5770; women: n = 8008). Red meat intake was assessed via the Food Frequency Questionnaire and categorized as low (≤1/month), moderate (2–4/month), and high (≥5/month) intake. Hematological and metabolic biomarkers were analyzed. Two-sample t-tests compared biomarker levels by gender. Multiple linear regression examined associations between red meat intake and iron profile indicators, adjusting for age, gender, supplement use, diabetes, hypercholesterolemia, and hypertension. Results: High red meat consumption was associated with increased ferritin (Coef = 134.685, p < 0.001) and hemoglobin (Coef = 0.918, p = 0.017). Males showed higher hemoglobin (14.8–14.9 vs. 12.4–12.5 g/dL, p < 0.0001) and total cholesterol (5.17 ± 1.10 vs. 5.02 ± 1.01 mmol/L, p = 0.0125). TIBC showed no significant gender differences across categories (p > 0.15) but varied significantly within each gender across red meat consumption categories (males: p < 0.0000; females: p < 0.0000). Conclusions: Higher red meat intake is associated with improved iron status, particularly ferritin levels, and gender-specific effects on hemoglobin and cholesterol levels. Moderate red meat intake may support iron health while maintaining a favorable lipid profile.