Genes and Nutrition最新文献

Purpose: Prior observational studies and experimental research have suggested a link between dietary patterns and the risk of developing chronic renal failure (CRF). Nevertheless, the causality of that relationship is still uncertain. The aim of the present study was to investigate the causal relationship between the dietary intake of 18 different foods/beverages and the risk of developing CRF through the application of Mendelian randomization (MR) analysis.

Methods: We conducted a two-sample MR study. The exposure and outcome data were obtained from the UK Biobank and European Bioinformatics Institute (EBI) databases, respectively. All the data were obtained from the IEU Open GWAS Project. Five methods were used in this MR analysis. We also conducted a series of sensitivity analyses to ensure the validity of the results.

Results: Dried fruit intake (OR (95% CI) = 0.447(0.271-0.737), p = 0.002) and cheese intake (OR (95% CI) = 0.678(0.515-0.893), p = 0.006) were associated with a reduced risk of developing CRF, whereas frequent alcohol intake (OR (95% CI) = 1.238(1.052-1.456), p = 0.010) was associated with an increased risk of developing CRF. The sensitivity analysis revealed that our results were robust.

Conclusions: Our research provides genetic evidence that dried fruit and cheese intake are associated with a decreased risk of developing CRF, whereas frequent alcohol intake is associated with an increased risk of developing CRF. However, additional investigations are needed to verify our findings.

Background: Chronic renal failure (CRF), the end-stage of chronic kidney disease, affects approximately 10% of the global population. While associations between beverage consumption and renal function have been reported, their causal relationships remain unclear. This study aimed to investigate the causal relationships between different beverage consumption and CRF, as well as the mediating effects of serum metabolites.

Methods: Using a two-sample Mendelian randomization (MR) approach, we analyzed genetic data from the UK Biobank and GWAS databases. We examined bidirectional causal relationships between water, coffee, tea, and alcohol consumption with CRF, and screened metabolites significantly associated with CRF from 1,400 metabolites for mediation analysis. Additionally, we evaluated the mediating effects of these metabolites in the relationship between beverage consumption and CRF.

Results: MR analysis showed evidence for a causal association between tea consumption and reduced CRF risk (OR = 0.314, 95% CI: 0.155-0.634, p = 0.001), while alcohol consumption was causally associated with increased CRF risk (OR = 1.275, 95% CI: 1.046-1.553, p = 0.016). Water and coffee consumption showed no significant associations with CRF. Further analysis identified 11 metabolites significantly associated with CRF. Salicylate demonstrated a positive mediating effect (12.5%) in the association between tea consumption and CRF risk, while 3-methyl catechol sulfate (-25.70%), glutarate (C5-DC) (-14.60%), and X-23,655 (-18.7%) showed negative mediating effects. In the alcohol consumption-CRF pathway, the ornithine-to-phosphate ratio exhibited a positive mediating effect, while X-23,655 showed a negative mediating effect.

Conclusion: This study provides evidence for a potential protective association of tea consumption and a potential harmful association of alcohol consumption with CRF risk, partially mediated through specific serum metabolites. These findings contribute new insights into potential CRF prevention strategies and may inform dietary guidelines.

Bacteria play a crucial role in human health and disease pathogenesis. In recent years, the therapeutic potential of probiotics has gained increasing attention, with studies suggesting their application in treating various diseases, including cancer. We evaluated clinical data supporting the use of oral and topical probiotics for skin malignancies by conducting a literature search in PubMed and Google Scholar. Although limited, clinical trials investigating probiotics in cancer prevention and treatment have shown promising results, particularly in controlling tumor progression and enhancing therapeutic outcomes. Emerging research suggests that probiotics may contribute to skin cancer prevention by modulating the gut and skin microbiomes, enhancing immune responses, exerting antioxidant and anti-inflammatory effects, and inducing apoptosis. Given their antiproliferative and pro-apoptotic effects on carcinoma cells, probiotic-based therapies may serve as potential cancer-preventive agents and adjunctive treatments during conventional therapies. Key findings from our review highlight the ability of probiotics to influence cancer progression through immune regulation, apoptosis induction, and modulation of inflammatory pathways. However, further well-designed clinical trials are needed to validate these findings and establish probiotics as a viable therapeutic approach in oncology.

Background: Osteosarcoma (OS) is a bone tumor characterized by a high recurrence rate and poor prognosis. Arjunolic acid (AA), the most abundant triterpene component in Cyclocarya paliurus, is reported to have anti-tumor effects. Its specific role in OS is still unknown, which we aim to investigate in our study.

Methods: An OS mouse model was established to investigate the effects of AA. Subsequently, M2 macrophages and M0 macrophages pretreated with AA were co-cultured with OS cells. The impact of AA on OS cell behavior (proliferation, apoptosis, migration, and invasion) was evaluated via EdU staining, flow cytometry, and Transwell assays. Concurrently, the expression of M1- and M2-associated genes (CD86, CD163, IL-6, Arg1) was quantified to assess AA's regulatory role in macrophages within the tumor microenvironment (TME). Knockdown or overexpression of Wnt3a in AA-treated M0 macrophages to determine whether AA modulates Wnt3a-mediated M2 polarization, which was further validated in vivo.

Results: In vivo, AA inhibited tumor progression in OS mice. Concurrently, AA-treated macrophages inhibited OS cell malignant behavior, and AA inhibited OS cell-mediated macrophage M2-type polarization. Mechanistically, AA inhibits the malignant behavior of OS cells and inhibits tumor progression in OS mice by suppressing Wnt3a-mediated macrophage M2 polarization. Additionally, AA-induced macrophage conversion to a pro-inflammatory phenotype in the TME of OS mice.

Conclusion: Our experiment demonstrated that AA from Cyclocarya paliurus inhibits Wnt3a-mediated M2 macrophage polarization to suppress the progression of osteosarcoma, providing a pharmacological foundation for developing therapies against OS.

Ischemic stroke remains a leading cause of mortality and disability globally, emphasizing the urgent need for innovative preventative and therapeutic strategies. Taurine, a critical amino sulfonic acid, has garnered attention for its neuroprotective effects, yet its precise role in ischemic stroke remains elusive. This study utilized a bidirectional Mendelian Randomization (MR) approach to explore the causal relationship between plasma taurine levels and ischemic stroke risk, employing genome-wide association study (GWAS) datasets. In parallel, a novel high-sensitivity liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was developed to quantify plasma taurine levels in ischemic stroke patients and healthy controls. Our findings reveal a significant inverse association between taurine levels and stroke risk, with IVW analysis showing beta = -0.001 and P = 0.0085. Furthermore, LC-MS/MS analysis demonstrated that plasma taurine levels in patients with ischemic stroke were notably lower at 36.07 ± 5.37 μmol/L compared to controls at 108.66 ± 25.11 μmol/L, confirming taurine's potential as a protective factor. These results suggest taurine as a promising biomarker and therapeutic target for stroke prevention and recovery. This study not only highlights the importance of taurine in cerebrovascular health but also provides a foundation for personalized intervention strategies.

Background: The mammalian liver executes its vital functions through intricate hepatic biochemistry. However, the complexity of the liver metabolome and its dynamic alterations during metabolic dysfunction-associated steatotic liver disease (MASLD) remain poorly understood.

Methods: We established progressive MASLD mouse models through high-fat diet (HFD) and high-fat/high-cholesterol (HFHC) dietary-feeding across multiple time points. Utilizing liquid chromatography-mass spectrometry (LC-MS)-based metabolomics and lipidomics, we systematically mapped the metabolome atlas of the mouse liver across five anatomical segments during the progression of MASLD.

Results: By integration of data from two assays, we structurally annotated 426 lipids and 118 polar metabolites. The temporal progression of HFD feeding (0, 8, and 16 weeks) resulted in gradual metabolic deterioration across various liver segments. In HFHC-fed mice, metabolic alterations surged sharply from 0 to 8 weeks, followed by moderate progression until 16 weeks in different liver segments. Elevated levels of glycerolipids and cholesteryl esters, along with fluctuating acylcarnitine and fatty acid levels across various liver segments, suggested impaired energy metabolism and disrupted fatty acid oxidation. As MASLD progresses, a shift in sphingolipid metabolism, linked to inflammation, was observed, accompanied by significant alterations in phospholipid turnover patterns. Additionally, amino acid profiles in the livers of HFD-fed and HFHC-fed mice were altered, potentially influencing the regulation of energy metabolism, inflammation, and oxidative stress. These metabolic changes in lipids and amino acids displayed segment-specific patterns, indicating varying sensitivities to inflammation and mitochondrial β-oxidation across different liver lobes. Notably, the left lateral lobe showed heightened sensitivity to metabolic disturbances during MASLD progression.

Conclusion: Our findings provided in-depth understanding in hepatic metabolites of MASLD, offering a comprehensive resource for further investigation.

Background: With the global population aging, age-related eye diseases (AREDs) such as senile cataract (SC), age-related macular degeneration (AMD), glaucoma, and diabetic retinopathy (DR) are becoming increasingly significant public health concerns. The rising prevalence of AREDs underscores the urgent need for effective prevention and treatment strategies. This study aimed to explore the causal relationships between circulating micronutrients (CMs) and AREDs.

Methods: A bidirectional two-sample Mendelian randomization (MR) analysis was conducted using genetic variants as instrumental variables to assess the effects of fifteen CMs (vitamin A, vitamin B6, vitamin B12, vitamin C, vitamin D, vitamin E, folate, carotene, copper, calcium, iron, magnesium, potassium, selenium, zinc) on AREDs. Data were sourced from large-scale genome-wide association studies (GWAS). The primary analytical method employed was inverse-variance weighted (IVW), supplemented by sensitivity analyses to confirm the robustness of the results.

Results: The MR analysis revealed significant protective effects of selenium against SC (OR = 0.961, 95% CI = 0.932-0.991, P = 0.012) and DR (OR = 0.927, 95% CI = 0.870-0.987, P = 0.019). Furthermore, higher genetically predicted magnesium levels were associated with a reduced risk of AMD (OR = 0.679, 95% CI = 0.515-0.895, P = 0.006). However, no significant causal relationships were observed between the other CMs and glaucoma or other AREDs.

Conclusions: These findings provided valuable insights into the complex interplay between CMs and AREDs, offering potential pathways for developing targeted nutritional interventions and public health strategies to mitigate the risk of these debilitating conditions.

Background: Nutrigenomics, the study of nutrient-gene interactions, holds immense potential for alleviating India's overburdened healthcare system and improving overall health-related quality of life. Yet, its utility remains in the nascent stages. To understand the factors affecting the implementation of nutrigenomics, we investigate the perceptions of practising dietetic professionals.

Objective: The purpose of this study was to investigate the perceptions of Indian dietetic professionals related to the implementation of Nutrigenomics and to understand the factors affecting it.

Methods: A total of 249 Indian dietetic professionals participated in an online survey between April 2024 - May 2024. This data was then statistically analyzed using the Chi-square test and Fisher's Exact test. Furthermore, in-depth interviews were conducted for 10 out of the 249 participants, the data collected from the interviews were analysed using reflexive thematic analysis.

Results: Majority of the dietetic professionals had high awareness (97.2%) and interest (87.5%) in incorporating genetic testing into their practice. While the survey identified several barriers to its integration, such as high costs, (p-value = 0.000), lack of clinical trials (p-value = 0.013), and ethical concerns (p-value = 0.023). The in-depth interviews highlighted the need for increased education, standardization of testing panels, and collaboration among healthcare professionals to enhance the feasibility of nutrigenomics integration.

Conclusion: Indian dietetic professionals express a positive outlook on integrating nutrigenomics into mainstream healthcare practice. However, successful establishment of personalized nutrition in India also requires addressing key challenges with respect to education, cost, training, development of regulatory frameworks and raising public awareness.

Nigella sativa (N. sativa) L. (Ranunculaceae), commonly referred to as black cumin, has a long history of usage as an herbal remedy. It has been utilized conventionally and in clinical settings to treat various illnesses. Six groups of male Wister rats were randomly selected as Gp I, represented as control; Gp II administered N. sativa aqueous extract (NSAE); 200 mg/kg/d, Gp III received N. sativa silver nanocomposite (NS-Ag-NC); 0.25 mg/kg/d; Gp IV administered thioacetamide (TAA);100 mg/kg; thrice weekly and Gps V and VI administered NSAE and NS-Ag-NC with TAA for six weeks, respectively. Findings showed that GC-MS analysis of NSAE has a high concentration of phytochemicals with strong antioxidant activity. Results revealed that TAA administration elevated TBARS, H₂O₂, PCC, NO levels, kidney function parameters, LDH activity, and up-regulated TNF-α, IL-1β, NF-kβ, and COX-2 gene expressions. In contrast, enzymatic and non-enzymatic antioxidants and ALP activity were extensively diminished. Also, severe abnormalities in lipid profile, hematological parameters, and histopathological features were noted. On the other hand, the administration of NSAE or NS-Ag-NC followed by TAA intoxication reduces renal impairment, restores the antioxidant system, and downregulates the expression of TNF-α, IL-1β, NF-kβ, and COX-2 genes in rats' renal tissues. Collectively, NS-Ag-NC has more prevalent nephroprotective impacts than NSAE and can adjust the oxidant/antioxidant pathways besides their anti-inflammatory efficacy against TAA toxicity.