DHA dietary intervention caused different hippocampal lipid and protein profile in ApoE-/- and C57BL/6J mice.

BACKGROUND: Changes in protein and lipid levels may occur in the Alzheimer's disease brain, and DHA can have beneficial effects on it. To investigate the impact of DHA dietary intervention on brain protein and lipid profile in ApoE-/- mice and C57 mice. METHOD: Three-month-old ApoE-/- mice and C57 mice were randomly divided into two groups respectively, and fed with control diet and DHA-fortified diet for five months. Cortical TC, HDL-C and LDL-C levels and cholesterol metabolism-related protein expression were measured by ELISA or immunohistochemistry methods. Hippocampus were collected for proteomic and lipidomics analysis by LC-MS/MS and differential proteins and lipid metabolites were screened and further analyzed by GO functional annotation and KEGG pathway enrichment analysis. RESULTS: DHA intervention decreased cortical TC level in both C57 and ApoE-/- mice (P < 0.05), but caused different change of cortical HDL-C, LDL-C level and LDL-C/HDL-C ratio in C57 and ApoE-/- mice (P < 0.05). Discrepant cortical and hippocampal LDLR, ABCG1, Lox1 and SORT1 protein expression was found between C57 and ApoE-/- mice (P < 0.05), and DHA treatment caused different changes of these proteins in C57 and ApoE-/- mice (P < 0.05). Differential hippocampal proteins and lipids profile were found in C57 and ApoE-/- mice before and after DHA treatment, which were mainly involved in vesicular transport and phospholipid metabolic pathways. CONCLUSION: ApoE genetic defect caused abnormal cholesterol metabolism, and affected protein and lipid profile, as well as discrepant response of hippocampal protein and lipids profile in the brain of mice given DHA fortified diet intervention.

Suboptimal diet quality is associated with the incidence of type 2 diabetes mellitus in middle-aged and older populations in China: evidence from a population-based cross-sectional study.

The association between dietary quality and type 2 diabetes mellitus (T2DM) based on the Chinese Dietary Balance Index (DBI-16) is seldom reported. We hypothesized that poor dietary quality might increase the risk of T2DM in the middle-aged and older populations. A total of 1816 individuals (≥50 years) were included in the study. Demographic characteristics and dietary intake data were collected. Logistic regression and restricted cubic spline (RCS) analyses were conducted to explore the association between DBI-16 indexes and the risk of T2DM. The insufficient intake of vegetables and dairy might decrease the risk of T2DM (ORVegetable = 0.77, 95% CI = 0.60-0.97; ORDairy = 0.58, 95% CI = 0.35-0.96), but the individuals with insufficient intake of fruit were more likely to have a higher risk of T2DM (ORfruit = 2.26, 95% CI = 1.69-3.06). Compared with the subjects with the lowest quartile of Low Bound Score (LBS) or Diet Quality Distance (DQD), the individuals with Q2 and Q3 level of LBS (ORQ2 = 1.40, 95% CI = 1.03-1.90, P = .033; ORQ3 = 1.52, 95% CI = 1.11-2.08, P < .01) or DQD (ORQ2 = 1.45, 95% CI = 1.06-1.99, P = .021; ORQ3 = 1.64, 95% CI = 1.20-2.24, P < .01) showed increased risk of T2DM with a nonlinear association observed by RCS analysis. We concluded that imbalanced dietary intake, especially insufficient daily fruit intake, might predict an increased risk of T2DM in the middle-aged and elderly Chinese.

Exploring patient delay in people with chronic kidney disease: A cross-sectional study.

To examine the factors that contribute to patient delays among individuals with chronic kidney disease (CKD) and offer insights to help develop specific risk management strategies. Conducted as a cross-sectional study between September 2021 and April 2022, this study used a convenient sampling technique to select 245 individuals diagnosed with CKD from a Grade 3 Class A hospital located in Shanxi Province. These individuals were chosen as the subjects of the study. The research participants underwent an investigation using several assessment tools, including socio-demographic information questionnaire, medical behavior, the social support rating scale, the simplified coping style questionnaire, and the General Self-efficacy Scale. The study revealed that 35.4% of individuals with CKD experienced patient delay (the interval between the initial onset and the time of seeking medical attention being longer than or equal to 3 months). Through a multifactorial logistic regression analysis, it was determined that various factors independently influenced patient delay in patients with CKD. These factors included the level of knowledge about CKD, educational level, frequency of attending physical examinations, severity of initial symptoms, social support, self-efficacy, positive coping, and negative coping. Numerous factors contribute to the Patient Delay. To effectively enhance awareness and coping abilities regarding CKD in high-risk groups, it is essential to implement focused and continuous interventions throughout the medical seeking process.

Gender-specific association of SLC19A1 and MTHFR genetic polymorphism with oxidative stress biomarkers and plasma folate levels in older adults.

BACKGROUND: Plasma folate levels are closely related to antioxidant capacity and are regulated by folate pathway gene polymorphism. However, few studies have explored the gender-specific association of folate pathway gene polymorphism with oxidative stress biomarkers. The present study was designed to explore the gender-specific independent and combined impacts of solute carrier family 19 member 1 (SLC19A1) and methylenetetrahydrofolate reductase (MTHFR) genetic polymorphisms on oxidative stress biomarkers in older adults. METHODS: A total of 401 subjects were recruited, including 145 males and 256 females. Demographic characteristics of the participants were collected by using a self-administered questionnaire. Fasting venous blood samples were taken for folate pathway gene genotyping, circulating lipids parameters and erythrocyte oxidative stress biomarkers measurement. The difference of genotype distribution and the Hardy-Weinberg equilibrium was calculated by the Chi-square test. The general linear model was applied to compare the plasma folate levels and erythrocyte oxidative stress biomarkers. Multiple linear regression was used to explore the correlation between genetic risk scores and oxidative stress biomarkers. Logistic regression was used to explore the association of genetic risk scores of folate pathway gene with folate deficiency. RESULTS: The male subjects have lower plasma folate and HDL-C levels than the female ones, and the male carrying MTHFR rs1801133 (CC) or MTHFR rs2274976 (GA) genotypes have higher erythrocyte SOD activity. The plasma folate levels, erythrocyte SOD and GSH-PX activities were negatively correlated with genetic risk scores in the male subjects. A positive correlation between the genetic risk scores and folate deficiency was observed in the male subjects. CONCLUSIONS: There was association between folate pathway gene polymorphism of Solute Carrier Family 19 Member 1 (SLC19A1) and Methylenetetrahydrofolate Reductase (MTHFR) with erythrocyte SOD and GSH-PX activities, and folate levels in male but not in female aging subjects. Genetic variant of genes involved in folate metabolism has strong impact on plasma folate levels in the male aging subjects. Our data demonstrated that there was a potential interaction of gender and its genetic background in affecting the body's antioxidant capacity and the risk of folate deficiency in aging subjects.

Effects of distinct n-6 to n-3 polyunsaturated fatty acid ratios on insulin resistant and AD-like phenotypes in high-fat diets-fed APP/PS1 mice.

Type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) are prevalent diseases with similar pathophysiological characteristics and genetic predispositions. Polyunsaturated fatty acids (PUFAs) are essential in maintaining normal brain function. However, little is known about the effect of dietary n-6/n-3 PUFA ratio on AD-like pathology, particularly in high-fat diet (HFD)-fed AD model mice. In the present study, the APP/PS1 mice were fed with 60 % HFD for 3.5 months to induce insulin resistance. After that, 45 % HFD with various n-6/n-3 PUFA ratios (n-6/n-3 = 1:1, 5:1 or 16:1) was applied for an additional 3.5 months of treatment. The behavior of mice was observed using the water maze after dietary intervention. The animals were euthanized after behavioral testing, and serum and tissue samples were collected for biochemical, histological, and pathological tests and evaluation. HFD caused insulin resistance, increased serum IL-6 and TNF-α levels, cortical soluble Aß1-40, Aß1-42 content, and cortical n-6/n-3 PUFA ratio in APP/PS1 mice. Increased APP and BACE1 protein expression and p-IR/IR ratio but decreased pro-inflammatory cytokines mRNA expression was detected in the cortex of 60 % HFD-fed APP/PS1 mice. N-3 PUFAs-rich diet (n-6/n-3 = 1:1) alleviated insulin resistance and hyperlipidemia caused by 60 % HFD. Cortical soluble Aß1-40 and Aß1-42 contents, as well as the expression of cortical APP, GLUT1, GLUT3, insulin metabolism-related molecules, and NF-κB pathway downstream pro-inflammatory cytokines, were found to be n-6/n-3 PUFAs ratio-dependent, indicating that dietary n-6/n-3 PUFA ratio plays a critical role in modifying the responses of serum inflammatory cytokines, AD pathology, cortical n-6/n-3 PUFAs ratio, insulin signaling, and neuroinflammation to HFD treatment.

A novel material Cs2RbxAg1-xIn0.875Bi0.125Cl6 with a special blue shift and application for white light LED devices.

Perovskite microcrystals have attracted wide attention and have been applied in extensive optical applications. The CsPbX3 perovskite poses a great threat to the environment due to the presence of lead (Pb), and there is an urgent need to improve the photoluminescence quantum yield. Therefore, a lead-free perovskite microcrystal material Cs2RbxAg1-xIn0.875Bi0.125Cl6 with a high photoluminescence quantum yield (PLQY) was synthesized by a convenient hydrothermal method, with comprehensive characterization of both the structure and optical performance at varying Rb ratios. Optimal properties were observed at x = 0.15 with bright white emission and a PLQY of 32.15%. Superior stability of the novel material in ethanol was observed under the radiation of an excitation light of 365 nm. Interestingly, a blue shift of the emission peak occurred after exposure to humid air, possibly due to the reconstruction of the crystal structure. Moreover, a LED device packaged with this novel material was developed with a desirable color temperature of 3190 K, promising for further lighting applications.

Association of cluster determinant 36, scavenger receptor class B type 1, and major facilitator superfamily domain containing the 2a genetic polymorphism with serum lipid profile in aging population with type 2 diabetes mellitus.

Background: Lipid metabolism disorder commonly happens in subjects with Type 2 diabetes mellitus (T2DM) which may be linked to genetic variants of lipid metabolism-related genes. However, few studies have explored the relationship between lipid metabolism-related gene polymorphism and serum lipid profile in aging subjects with T2DM. The present study was designed to explore the impact of genetic polymorphism of cluster determinant 36 (CD36) (rs1049673, rs1054516, rs2151916), scavenger receptor class B type 1 (SCARB1) (rs5888), and major facilitator superfamily domain containing the 2a (MFSD2A) (rs12083239, rs4233508, rs12072037) on the relationship between circulating lipids in aging subjects with T2DM. Methods: 205 T2DM patients and 205 age and gender matched control subjects were recruited. Information on demographic characteristics was collected by using a self-administered questionnaire. Fasting venous blood samples were taken for lipid-related gene genotyping and serum lipid profile measurement. The Chi-square test was used to compare percentage differences and to calculate P-value for Hardy-Weinberg equilibrium. Logistic regression and multiple linear regression were used to explore the risk or correlation between variables, and general linear model (GLM) was used to compare the means of serum lipids between the groups. Results: In T2DM group, CD36 rs1054516 and MFSD2A rs12072037 were correlated with serum TC level. In control group, CD36 rs1049673 was correlated with serum HDL-C level. Meanwhile, T2DM subjects with MFSD2A rs12083239 (CG), MFSD2A rs4233508 (TT), and MFSD2A rs12072037 (AA) had higher TG level than control subjects. T2DM subjects with CD36 rs1049673 (CG, GG), CD36 rs1054516 (CT), CD36 rs2151916 (TT, CT), SCARB1 rs5888 (GG), MFSD2A rs12083239 (GG, CG), MFSD2A rs4233508 (TT), and MFSD2A rs12072037 (CA, AA) had lower HDL-C level than control subjects. T2DM subjects with MFSD2A rs12072037 (AA) had lower LDL-C level than control subjects. In dominant model, major genotype (GG) of SCARB1 gene was associated with the risk of T2DM (OR = 0.636, P = 0.032). Conclusion: The genetic polymorphism of CD36 (rs1049673, rs1054516, rs2151916), SCARB1 (rs5888), and MFSD2A (rs12083239, rs4233508, rs12072037) were associated with serum lipids in T2DM subjects. The SCARB1 rs5888 major genotype (GG) was a protective factor for T2DM. Large scale cohort study is required to determine the relationship between lipid metabolism-related gene polymorphism, serum lipid profile and T2DM in aging subjects.

Study on the Association of Dietary Fatty Acid Intake and Serum Lipid Profiles With Cognition in Aged Subjects With Type 2 Diabetes Mellitus.

Background: The correlation between dietary fatty acid (FA) intake and serum lipid profile levels with cognition in the aged population has been reported by previous studies. However, the association of dietary FA intake and serum lipid profile levels with cognition in subjects with type 2 diabetes mellitus (T2DM) is seldom reported. Objective: A cross-sectional study was conducted to explore the correlation between dietary FA intake and serum lipid profiles with cognition in the aged Chinese population with T2DM. Methods: A total of 1,526 aged Chinese subjects were recruited from communities. Fasting blood samples were collected for parameter measurement. The food frequency questionnaire (FFQ) method was applied for a dietary survey. Cognition was assessed using the Montreal Cognitive Assessment (MoCA) test. Dietary FA intake and serum lipid levels were compared between subjects with T2DM and control subjects. A logistic regression analysis was carried out for analyzing the association of FA intake and serum lipid levels with the risk of mild cognitive impairment (MCI) in subjects with T2DM and control subjects. Results: There was a significant difference in the serum lipid level between the T2DM group and the control group. Results of the logistic regression analysis demonstrated the potential associations of serum total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c), and dietary n-3 polyunsaturated fatty acids (PUFAs) intake with the risk of MCI in subjects with T2DM, but the associations were not observed in control subjects. Conclusion: The T2DM phenotype might affect the relationship between dietary FA intake, circulating lipids, and cognitive performance. Large prospective cohort studies are needed to uncover the underlying mechanism of how dietary FA intake and serum lipid levels affect cognition in aged subjects with T2DM.

Effects of DHA dietary intervention on hepatic lipid metabolism in apolipoprotein E-deficient and C57BL/6J wild-type mice.

Lipid metabolic disorder occurs when ApoE gene is deficient. However, the role of Docosahexaenoic acid (DHA) in relieving hepatic lipid metabolic disorder in apolipoprotein E-deficient (ApoE -/-) mice remains unknown. We fed 3-month-old C57BL/6J wild-type (C57 wt) and ApoE -/- mice respectively with normal or DHA fortified diet for 5 months. We found ApoE gene deficiency caused hepatic lipid deposition and increased lipid levels in plasma and liver. Hepatic gene expression of SRB1, CD36 and FABP5 in ApoE -/- mice, protein expression of HMGCR, LRP1 in C57 wt mice and protein expression of LRP1 in ApoE -/- mice increased after DHA intervention. In DHA-fed ApoE -/- mice, LXRα/ß and PPARα protein expression down-regulated in cytoplasm, but LXRα/ß protein expression up-regulated in nucleus. DHA treatment decreased RXRα and RXRß expression in C57 wt and ApoE -/- female mice. Deletion of ApoE gene caused lipid metabolism disorder in liver of mice. DHA treatment efficiently meliorated lipid metabolism caused by ApoE deficient through the regulation of gene and protein expressions of molecules involved in liver fatty acids transport and lipid metabolism.