Protein, amino acid, and peptide supplementation for the treatment of sarcopaenia.

Sarcopaenia is an age-related disease affected by many factors, nutrition being one. Reduced protein intake and decreased diet quality are correlated with sarcopaenia. Protein, amino acid, or peptide supplementation is a commonly used clinical practice to increase protein intake. However, whether supplementation plays a key role in preventing and treating sarcopaenia and whether it needs to be combined with other interventions is worthy of study. This review focuses on protein, amino acid, and peptide supplementation for the prevention and treatment of sarcopaenia.

Activating SIRT1 deacetylates NF-κB p65 to alleviate liver inflammation and fibrosis via inhibiting NLRP3 pathway in macrophages.

Background and aims: Macrophages play a critical role in the development of liver diseases. As an NAD+-dependent histone deacetylase, SIRT1 inhibits liver inflammation and fibrosis, but the mechanisms are not fully understood. Our aim was to investigate the molecular mechanism of SIRT1 in macrophages in liver inflammation and fibrosis. Methods: We employed the CCl4-induced hepatic fibrosis rat models and cultured murine macrophages RAW 264.7 in vitro to explore the anti-fibrosis effect of SIRT1. The content of cytokines was measured with ELISA. The expression of proteins associated with the NF-κB /NLPR3 signaling pathway was detected by Western blot, co-immunoprecipitation, and immunofluorescence. SIRT1, NF-κB, and NLRP3 genes were knocked down in RAW 264.7 cells by small interfering RNA (siRNA) transfection. Results: The expression of NF-κB p65, NLRP3, α-SMA, and iNOS increased in liver tissue, with high plasma LPS level and low expression of SIRT1 in CCl4-induced rat models. Overexpressing SIRT1 could inhibit these protein levels, decrease plasma LPS level, and attenuate liver injury and fibrosis. In vitro, LPS induced cytomorphology changes and up-regulated NF-κB/NLRP3 pathway, with the low expression of SIRT1 in RAW 264.7; meanwhile, the secretion of inflammatory factors increased. Nevertheless, knockdown of NF-κB or NLRP3 and activation of SIRT1 inhibited inflammation of macrophages; inhibition or knockdown of SIRT1 enhanced macrophage inflammation. Furthermore, activation of SIRT1 could inhibit LPS-treated macrophages from activating hepatic stellate cells (HSCs). Conclusions: Activating SIRT1 inhibits the inflammation in macrophages by down-regulating NLRP3 pathway through deacetylating NF-κB p65, which in turn inhibits the activation of HSCs to alleviate hepatic inflammation and fibrosis.

Simultaneous Enhancement of Magnetothermal and Photothermal Responses by Zn, Co Co-Doped Ferrite Nanoparticles.

Reducing nanoparticle (NP) dosage for hyperthermia therapy has remained a great challenge. In this work, efficiencies of alternating current (AC) magnetic field and near-infrared (NIR) heating are simultaneously enhanced by Zn and Co co-doping of magnetite NPs. The optimum magnetic anisotropy for maximized loss power under each magnetic field is achieved by tuning the doping concentration. The specific loss power of Zn0.3 Co0.08 Fe2.62 O4 @SiO2 NPs reaches 2428 W g-1 under an AC field of 27 kA m-1 at 430 kHz; 12 296 W g-1 under NIR laser irradiation at 808 nm and 2.5 W cm-2 ; and an unprecedented value of 14 724 W g-1 under dual mode. These values far exceed what has been achieved previously in iron oxide NPs. Ex vivo experiments on sacrificial mice show that while the NP dosage is substantially reduced to that used for magnetic resonance imaging, the surface body temperature of the mice reaches 50 °C after exposure to both AC field and laser irradiation under field parameters and laser intensity below safety limits. This nanoplatform is thus promising for multi-modal local hyperthermia therapy.

Dietary patterns, oxidative Stress, inflammation and biological variation in hemoglobin A1c: Association and Mediation analysis in a rural community in north China.

OBJECTIVE: The aim is to assess the relationship between the hemoglobin glycation index(HGI) and dietary patterns, and investigates whether inflammation and oxidative stress mediate the relationship. METHODS: Cross-sectional data were collected from 453 dwellers in a Chinese rural community. Diet was assessed using 24 h food recalls. Based on the energy intake ratio from three macronutrients, dietary patterns were identified by cluster analysis. The HGI was defined as the observed HbA1c minus predicted HbA1c. Indicators of inflammation and oxidative stress were assessed. RESULT: 3 dietary patterns were clustered, namely "fat(n = 100)", "balance(n = 186)" and "carbohydrate(n = 167)". The fat dietary patterns had lower HGI than the other two dietary patterns. TNFα was higher in the carbohydrate dietary pattern. Linear regression analysis suggested that the carbohydrate dietary pattern was correlated with higher HGI levels(ß = 0.204,95 %CI(0.071,0.338)), compared with the fat dietary pattern. The relationship disappeared after accounting for biomarkers of inflammation and oxidative stress. Mediation analyses indicated that TNFα might explain for 19.15 % effects of the carbohydrate dietary pattern on HGI, compared with the fat dietary pattern. CONCLUSION: The carbohydrate dietary pattern had positive associations with HGI and TNFα. TNFα partly mediated the relationship between dietary patterns and HGI.

Contemporary Research Progress on the Detection of Polycyclic Aromatic Hydrocarbons.

Polycyclic aromatic hydrocarbons (PAHs) are a class of the most common and widespread contaminants. The accumulation of PAHs has made a certain impact on the environment and is seriously threatening human health. Numerous general analytical methods suitable for PAHs were developed. With the development of economy, the environmental problems of PAHs in modern society are more extensive and prominent, and attract more attention from environmental scientists and analysts. Deeper understanding of the properties of PAHs depends on the advent of detection methods, which can also be more conducive to promoting the protection of the environment. Till now, more sensitive, more high-speed and more high-throughput analytical tools are being invented and have played important roles in the research of PAHs. In this short review article, we focused mainly on the contemporary analytical methods about PAHs. We started with a brief review on the hazards, migration, distribution and traditional analysis methods of PAHs in recent years, including liquid chromatography, gas chromatography, surface enhanced Raman spectroscopy and so on. We also presented the applications of the modern ambient mass spectrometry, especially microwave plasma torch mass spectrometry, in the detection of PAHs, as well as the far out novel results in our lab by using microwave plasma torch (MPT) mass spectrometry; for example, some new insights about Birch reduction, regular hydrogen addition and the robustness of molecular structure. These studies have demonstrated the versatility of MPT MS as a platform in the research of PAHs.

Bone Tumor Suppression in Rabbits by Hyperthermia below the Clinical Safety Limit Using Aligned Magnetic Bone Cement.

Demonstrating highly efficient alternating current (AC) magnetic field heating of nanoparticles in physiological environments under clinically safe field parameters has remained a great challenge, hindering clinical applications of magnetic hyperthermia. In this work, exceptionally high loss power of magnetic bone cement under the clinical safety limit of AC field parameters, incorporating direct current field-aligned soft magnetic Zn0.3 Fe2.7 O4 nanoparticles with low concentration, is reported. Under an AC field of 4 kA m-1 at 430 kHz, the aligned bone cement with 0.2 wt% nanoparticles achieves a temperature increase of 30 °C in 180 s. This amounts to a specific loss power value of 327 W gmetal-1 and an intrinsic loss power of 47 nHm2 kg-1 , which is enhanced by 50-fold compared to randomly oriented samples. The high-performance magnetic bone cement allows for the demonstration of effective hyperthermia suppression of tumor growth in the bone marrow cavity of New Zealand White Rabbits subjected to rapid cooling due to blood circulation, and significant enhancement of survival rate.

High Hemoglobin Glycation Index Is Associated With Telomere Attrition Independent of HbA1c, Mediated by TNFα.

CONTEXT: The hemoglobin glycation index (HGI) is correlated with metabolic diseases and inflammation. Whether the HGI is associated with the aging process and how inflammation and oxidative stress affect the relationship remain unclear. OBJECTIVE: We aimed to analyze links between the HGI and aging biomarkers, and to explore a potential role of inflammation and oxidative stress in the correlations. METHODS: A cross-sectional study of 434 subjects with different glucose intolerances in a rural community was enrolled. The HGI was calculated as the difference between the measured and predicted hemoglobin A1c (HbA1c). The population was categorized into tertiles of the HGI. Telomere length (LTL) and mitochondrial DNA copy number (mtDNAcn) determined by polymerase chain reaction assay. Tumor necrosis factor (TNF) α and interleukin (IL) 6, 8-oxo-2'-deoxyguanosine (8-oxo-dG), superoxide dismutase (SOD) activities, and glutathione reductase (GR) were measured. RESULTS: Participants in the high HGI group were older and reported a shorter LTL, higher levels of TNFα, SOD activities, and HbA1c. Correlation analyses demonstrated that HGI was correlated with LTL (r = -0.25, P < .001) and TNFα (r = 0.19, P < .001) regardless of HbA1c levels. No relationship was found between HGI and mtDNAcn. HGI (ß = -0.238, 95% CI -0.430, -0.046, P = .015) and TNFα (ß = -0.02, 95% CI -0.030, -0.014, P < .001) were proved to be correlated with LTL independently, using multiple linear regression analysis. Ordinal logistic regression models showed that compared with subjects the high HGI group, the possibilities of a higher-level LTL was 5.29-fold in the low HGI group (OR 5.29, 95% CI (2.45, 11.41), P < .001), 2.41-fold in the moderate HGI group (OR 2.41, 95% CI 1.35, 4.30, P = .003) after controlling for confounding variables. Mediation analyses indicated that TNFα accounted for 30.39% of the effects of the HGI on LTL. CONCLUSION: HGI was negatively related to telomere attrition, independent of HbA1c. TNFα acted as a mediator of the relationship between HGI and LTL.

Association of Serum Antioxidant Minerals and Type 2 Diabetes Mellitus in Chinese Urban Residents.

Antioxidant minerals including zinc, copper and selenium play critical roles in the maintenance of the redox balance in the body. However, their influences on type 2 diabetes mellitus (T2DM) are still inconclusive in Chinese populations. To elucidate the relationship between antioxidant minerals and T2DM, serum zinc, copper and selenium concentrations were measured in 1443 Chinese urban residents using a 1:2 matched case-control study. Conditional logistic regression models (CLR) were used to obtain the odds ratios (ORs) and 95% confidence intervals (CIs), and restricted cubic splines (RCS) were used to examine their dose−response associations. Serum zinc (OR = 0.52 [0.35, 0.77]) and copper concentrations (OR = 0.25 [0.17, 0.37]) were negatively associated with T2DM in a fully adjusted model. An L-shaped zinc-T2DM association (Poverall association = 0.003, and Pnonlinearity = 0.005) and a negative linear copper-T2DM association (Poverall association < 0.0001, and Pnonlinearity = 0.395) were observed. No association was found between serum selenium and T2DM in fully adjusted CLR or RCS models. In addition, joint associations with T2DM were identified between serum zinc and copper and between serum selenium and copper. In conclusion, our study emphasizes the importance of an adequate intake of antioxidant minerals for T2DM prevention in the Chinese population.

Genome-wide identification, phylogeny and expression analysis of AP2/ERF transcription factors family in sweet potato.

BACKGROUND: In recent years, much attention has been given to AP2/ERF transcription factors because they play indispensable roles in many biological processes, such as plant development and biotic and abiotic stress responses. Although AP2/ERFs have been thoroughly characterised in many plant species, the knowledge about this family in the sweet potato, which is a vital edible and medicinal crop, is still limited. In this study, a comprehensive genome-wide investigation was conducted to characterise the AP2/ERF gene family in the sweet potato. RESULTS: Here, 198 IbAP2/ERF transcription factors were obtained. Phylogenetic analysis classified the members of the IbAP2/ERF family into three groups, namely, ERF (172 members), AP2 (21 members) and RAV (5 members), which was consistent with the analysis of gene structure and conserved protein domains. The evolutionary characteristics of these IbAP2/ERF genes were systematically investigated by analysing chromosome location, conserved protein motifs and gene duplication events, indicating that the expansion of the IbAP2/ERF gene family may have been caused by tandem duplication. Furthermore, the analysis of cis-acting elements in IbAP2/ERF gene promoters implied that these genes may play crucial roles in plant growth, development and stress responses. Additionally, the available RNA-seq data and quantitative real-time PCR (qRT-PCR) were used to investigate the expression patterns of IbAP2/ERF genes during sweet potato root development as well as under multiple forms of abiotic stress, and we identified several developmental stage-specific and stress-responsive IbAP2/ERF genes. Furthermore, g59127 was differentially expressed under various stress conditions and was identified as a nuclear protein, which was in line with predicted subcellular localization results. CONCLUSIONS: This study originally revealed the characteristics of the IbAP2/ERF superfamily and provides valuable resources for further evolutionary and functional investigations of IbAP2/ERF genes in the sweet potato.

Erratum to "Sex-Specific Negative Association between Iron Intake and Cellular Aging Markers: Mediation Models Involving TNFα".

[This corrects the article DOI: 10.1155/2019/4935237.].

Hemoglobin A1c modifies the association between triglyceride and time in hypoglycemia determined by flash glucose monitoring in adults with type 1 diabetes: implications for individualized therapy and decision-making.

BACKGROUND: We aimed to investigate the associations of flash glucose monitoring (FGM)-derived metrics with lipid profiles and identify potential modifiers of these associations among adults with type 1 diabetes (T1D). METHODS: A cross-sectional study was conducted among 108 Chinese adults with T1D who used FGM for 14 consecutive days. The relationship between FGM-derived metrics and lipid variables and potential modifiers were identified using interaction and subgroup analysis. RESULTS: Serum triglyceride level inversely correlated with time below range (glucose <3.9 mmol/L) and time in range (glucose 3.9-10.0 mmol/L) and positively correlated with time above range (glucose >10.0 mmol/L) (Spearman's r=-0.34, -0.25, 0.34, respectively, all P<0.01). Additionally, triglyceride levels had positive correlation with absolute measures of glycemic variability (GV) but not with the coefficient of variation for glucose (Spearman's r=0.12, P>0.05), a relative measure. Multivariate linear regression analysis adjusting for potential confounders including gender, age, disease duration, body mass index (BMI), daily insulin dose, fasting C-peptide, and dyslipidemia medication use showed that higher triglyceride level independently predicted decrease in time below range and time in range and increase in time above range (all P<0.01). Furthermore, interaction analysis found that the interaction between HbA1c and triglyceride was significant in the time below range (P for interaction =0.034). The association between triglyceride and time below range differed substantially after stratification by HbA1c, which was significant in those with HbA1c <7.0% whereas inconsequential among those with HbA1c ≥7.0%. In those with HbA1c <7.0% (n=44), the area under receiver operating characteristic curve of triglyceride predicting achievement of targets of time below range (<4%) was 0.856 (95% confidence interval 0.688-1.000, P=0.042) with an optimal cutoff value of 0.50 mmol/L (sensitivity 100%, specificity 66.7%, positive predictive value 94.4%). CONCLUSIONS: In adults with T1D, HbA1c may be a potential modifier of the association between triglyceride and time below range, suggesting it might be necessary for those with HbA1c <7.0% accompanied by lower triglyceride levels to set a less intensive glycemic target to minimize risk of hypoglycemia.

Association between glucose fluctuation during 2-hour oral glucose tolerance test, inflammation and oxidative stress markers, and ß-cell function in a Chinese population with normal glucose tolerance.

BACKGROUNDS: Glucose fluctuation (GF) may have detrimental effects in individuals with diabetes; however, clinical data on the association between short-term GF, inflammation/oxidative stress markers, and islet ß-cell function based on a population with normal glucose tolerance (NGT) are insufficient. Therefore, we aimed to explore these associations in a Chinese population of 209 individuals with NGT in a cross-sectional analysis. METHODS: Individuals were categorized based on GF tertiles, calculated as the maximum-minimum glucose levels among four time points (0, 30, 60, 120 min) during 2-hour oral glucose tolerance test (OGTT). Plasma inflammation markers tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), and oxidative stress markers superoxide dismutase (SOD), and 8-oxo-2'-deoxyguanosine (8-oxo-dG) were measured. Islet ß-cell function was estimated according to the disposition index (DI) at the early (30 min) and total (120 min) phase of the OGTT, adjusted for insulin sensitivity. RESULTS: Individuals in the middle and highest tertile of GF had reduced ß-cell function, and increased plasma SOD and TNF-α levels compared with those in the lowest tertile of GF (P<0.05). Multiple linear regression analysis indicated that GF was positively associated with TNF-α, 8-oxo-dG and SOD levels, but negatively associated with ß-cell function, whereas IL-6, TNF-α, 8-oxo-dG and SOD levels were negatively associated with ß-cell function (P<0.05). CONCLUSIONS: GF may increase inflammation and oxidative stress markers in individuals with NGT, which could contribute to reduced ß-cell function. Thus, maintaining glucose stability after a meal may have beneficial effects on delaying ß-cell dysfunction, suggesting that diet and exercise strategies to decrease diet related GF are warranted.

Sirtuin 1 ameliorates defenestration in hepatic sinusoidal endothelial cells during liver fibrosis via inhibiting stress-induced premature senescence.

OBJECTIVE: Premature senescence is related to progerin and involves in endothelial dysfunction and liver diseases. Activating sirtuin 1 (SIRT1) ameliorates liver fibrosis. However, the mechanisms of premature senescence in defenestration of hepatic sinusoidal endothelial cells (HSECs) and how SIRT1 affects HSECs fenestrae remain elusive. METHODS: We employed the CCl4 -induced liver fibrogenesis rat models and cultured primary HSECs in vitro, administered with the SIRT1-adenovirus vector, the activator of SIRT1 and knockdown NOX2. We measured the activity of senescence-associated ß-galactosidase (SA-ß-gal) in HSECs. Meanwhile, the protein expression of SIRT1, NOX2, progerin, Lamin A/C, Ac p53 K381 and total p53 was detected by Western blot, co-immunoprecipitation and immunofluorescence. RESULTS: In vivo, premature senescence was triggered by oxidative stress during CCl4 -induced HSECs defenestration and liver fibrogenesis, whereas overexpressing SIRT1 with adenovirus vector lessened premature senescence to relieve CCl4 -induced HSECs defenestration and liver fibrosis. In vitro, HSECs fenestrae disappeared, with emerging progerin-associated premature senescence; these effects were aggravated by H2 O2 . Nevertheless, knockdown of NOX2, activation of SIRT1 with resveratrol and SIRT1-adenovirus vector inhibited progerin-associated premature senescence to maintain fenestrae through deacetylating p53. Furthermore, more Ac p53 K381 and progerin co-localized with the abnormal accumulation of actin filament (F-actin) in the nuclear envelope of H2 O2 -treated HSECs; in contrast, these effects were rescued by overexpressing SIRT1. CONCLUSION: SIRT1-mediated deacetylation maintains HSECs fenestrae and attenuates liver fibrogenesis through inhibiting oxidative stress-induced premature senescence.

Liraglutide Inhibits Osteoclastogenesis and Improves Bone Loss by Downregulating Trem2 in Female Type 1 Diabetic Mice: Findings From Transcriptomics.

Background: The mechanisms of bone fragility in type 1 diabetes (T1D) are not fully understood. Whether glucagon-like peptide-1 receptor (GLP-1R) agonists could improve bone quality in T1D context also remains elusive. Aims: We aimed to explore the possible mechanisms of bone loss in T1D and clarify whether liraglutide has effects on bone quality of T1D mice using transcriptomics. Methods: Female streptozotocin-induced diabetic C57BL/6J mice were randomly divided into four groups and received the following treatments daily for 8 weeks: saline as controls, insulin, liraglutide, and liraglutide combined with insulin. These groups were also compared with non-STZ-treated normal glucose tolerance (NGT) group. Trunk blood and bone tissues were collected for analysis. Three tibia from each of the NGT, saline-treated, and liraglutide-treated groups were randomly selected for transcriptomics. Results: Compared with NGT mice, saline-treated T1D mice manifested markedly hyperglycemia and weight loss, and micro-CT revealed significantly lower bone mineral density (BMD) and deficient microarchitectures in tibias. Eight weeks of treatment with liraglutide alone or combined with insulin rescued the decreased BMD and partly corrected the compromised trabecular microarchitectures. Transcriptomics analysis showed there were 789 differentially expressed genes mainly mapped to osteoclastogenesis and inflammation pathways. The RT-qPCR verified that the gene expression of Trem2, Nfatc1, Trap, and Ctsk were significantly increased in the tibia of T1D compared with those in the NGT group. Liraglutide treatment alone or combined with insulin could effectively suppress osteoclastogenesis by downregulating the gene expression of Trem2, Nfatc1, Ctsk, and Trap. Conclusions: Taken together, increased osteoclastogenesis with upregulated expression of Trem2 played an important role in bone loss of T1D mice. Liraglutide provided protective effects on bone loss in T1D mice by suppressing osteoclastogenesis.

C-Peptide: A Mediator of the Association Between Serum Uric Acid to Creatinine Ratio and Non-Alcoholic Fatty Liver Disease in a Chinese Population With Normal Serum Uric Acid Levels.

Background: The data on the relationship between normal-ranged serum uric acid (SUA), ß-cell function, and non-alcoholic fatty liver disease (NAFLD) are complicated and insufficient. Moreover, uric acid is excreted by kidney, and SUA levels may be affected by renal function. Thus, we introduced a renal function-normalized index [serum uric acid to creatinine ratio (SUA/Cr)] into the study and explored the association between SUA/Cr, C-peptide and NAFLD in a Chinese population with normal SUA levels by a cross-sectional analysis. Materials and Methods: A total of 282 individuals with normal SUA levels and different glucose tolerance status from a diabetes project were included in the study (mean age = 53.7± 10.5 years; women = 64.50%). NAFLD was diagnosed by abdominal ultrasonography (NAFLD, n=86; without NAFLD, n=196). Trapezoid formula was used to calculate area under the curve of C-peptide (AUCCP) from 4 points (including 0, 30,60, and 120min) during 2-h oral glucose tolerance test. Spearman correlation analysis was used to explore the correlation between SUA/Cr, AUCCP and NAFLD risk factors. Multiple logistic regression analysis was used to explore the association between SUA/Cr or AUCCP and NAFLD. Mediation analysis was used to explore whether AUCCP mediated the association between SUA/Cr and NAFLD. Results: Individuals with NAFLD had significantly higher SUA/Cr and AUCCP than those without NAFLD(P<0.05). Spearman correlation analysis showed that both SUA/Cr and AUCCP were significantly associated with many NAFLD risk factors, and SUA/Cr was positively correlated with AUCCP (P<0.05). Multiple logistic regression analysis indicated that SUA/Cr and AUCCP were positively associated with NAFLD incidence (P<0.05). Medication analysis indicated that SUA/Cr had a significant direct effect on NAFLD (ß =0.5854, 95% CI: 0.3232-0.8966), and AUCCP partly mediated the indirect effect of SUA/Cr on NAFLD incidence (ß =0.1311, 95% CI: 0.0168-0.4663). Conclusions: SUA/Cr was positively associated with NAFLD incidence, and AUCCP partly mediated the association in a Chinese population with normal SUA levels. Thus, we should pay more attention to high-normal SUA and C-peptide levels due to their predictive power in NAFLD incidence.

Association Between Leukocyte Mitochondrial DNA Copy Number and Non-alcoholic Fatty Liver Disease in a Chinese Population Is Mediated by 8-Oxo-2'-Deoxyguanosine.

Background: Alterations in mitochondrial DNA are potentially associated with oxidative stress and may be involved in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). However, the association between mitochondrial DNA copy number (mtDNAcn) and NAFLD was not consistent. In addition, the association between inflammation and NAFLD has not been established yet. The present study, based on a Chinese population of individuals with different glucose statuses, aimed to explore the association between leukocyte mtDNAcn, markers of oxidative stress, and inflammation and NAFLD. Methods: A total of 318 participants from a diabetes project were included. NAFLD was diagnosed by ultrasonography. Leukocyte mtDNAcn was determined by PCR assay. The levels of the inflammation markers tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) and the oxidative stress markers glutathione reductase (GR), superoxide dismutase (SOD), and 8-oxo-2'-deoxyguanosine (8-oxo-dG) were also measured. Results: Participants with NAFLD (n = 105) exhibited significantly higher leukocyte mtDNAcn, IL-6, and 8-oxo-dG (all P < 0.05). Pearson correlation analysis indicated mtDNAcn was negatively associated with age, uric acid, SOD, and TNF-α, but was positively associated with 8-oxo-dG (all P < 0.05). Univariate logistic regression analysis revealed that mtDNAcn was positively associated with NAFLD [odds ratio (OR) = 1.617, 95% confidence interval (CI) = 1.036-2.525; P = 0.034]. However, after adjustment for 8-oxo-dG, this association was no longer statistically significant (OR = 1.534, 95% CI = 0.979-2.403, P = 0.062). Moreover, the stress marker 8-oxo-dG was independently associated with NAFLD after adjustment for mtDNAcn, IL-6, glucose tolerance status, and other conventional NAFLD risk factors (OR = 1.707, 95% CI =1.142-2.550, P = 0.009). Mediation analysis indicated that 8-oxo-dG fully mediated the effect of mtDNAcn on the incidence of NAFLD (direct effect ß = 0.5221, 95% CI = -0.0648 to 1.2504; indirect effect ß = 0.0946, 95% CI = 0.0049-0.2463). Conclusions: In a Chinese population, the association between leukocyte mtDNAcn and NAFLD was fully mediated by high levels of 8-oxo-dG. Thus, oxidative stress may be an important driver of NAFLD, and clinical interventions aimed at decreasing oxidative stress to improve NAFLD warrant further research.

Negative association between antioxidant vitamin intake and non-alcoholic fatty liver disease in Chinese non-diabetic adults: mediation models involving superoxide dismutase.

We aimed to explore the association between antioxidant vitamin intake, oxidative stress related markers and non-alcoholic fatty liver disease (NAFLD) by a cross-sectional analysis. A total of 241 non-diabetic participants from a Chinese rural cohort were included. NAFLD was diagnosed by abdominal ultrasound (NAFLD, n = 71; Non-NAFLD, n = 171). Dietary intake was assessed by a 24-h food recall. Plasma oxidative stress related markers superoxide dismutase (SOD), glutathione reductase (GR) and 8-oxo-2'-deoxyguanosine(8-oxo-dG) were measured. The association between dietary antioxidant vitamin intake, oxidative stress related markers and NAFLD were analysed by Spearman correlation analysis and multiple logistic regression analysis. Mediation models were established to examine whether SOD mediated the association between dietary vitamin A or α-tocopherol intake and NAFLD. Spearman correlation analysis indicated that dietary vitamin A and α-tocopherol intake were positively correlated with SOD (p < .05). Multiple logistic regression analysis found plasma SOD, dietary vitamin A and α-tocopherol intake were inversely associated with NAFLD (all p < .05). Mediation analysis indicated that SOD significantly mediated the indirect effect of dietary α-tocopherol (mediated effect = 13.21% total effect) or vitamin A (mediated effect = 3.12% total effect) intake on NAFLD. Our study indicated that dietary vitamin A and α-tocopherol intake may contribute to protect from NAFLD in Chinese non-diabetics, and the associations were partly mediated by SOD. However, SOD only accounted for a minor percentage of the association between vitamin A intake and NAFLD. Thus, other mechanisms underlying antioxidant vitamin' protective effect on NAFLD need further exploration.

Corrigendum to "Dietary Magnesium Intake and Leukocyte Telomere Attrition in Adults: The Regulatory Role of Serum Tumor Necrosis Factor α".

[This corrects the article DOI: 10.1155/2020/7610436.].

Negative Association between Caloric Intake and Estimated Glomerular Filtration Rate in a Chinese Population: Mediation Models Involving Mitochondrial Function.

BACKGROUND: With the shortening of leukocyte telomere length (LTL) and decrease in the copy number of mitochondrial DNA, mitochondrial dysfunction and oxidative stress are considered important drivers of the aging process. Although previous experimental studies report that caloric intake is associated with age-related renal dysfunction through the changes in mitochondrial function, there are insufficient epidemiological data to establish this association. OBJECTIVE: We aimed to explore the association between caloric intake and renal function and to investigate whether mitochondrial DNA copy number (mtDNAcn) mediated this association by cross-sectional analysis. METHODS: A total of 403 individuals from a Chinese rural cohort (women = 66.50%; mean age = 53.94 ± 10.27 years) with an estimated glomerular filtration rate (eGFR) ≥60 mL/min/1.73 m2 and with differences in the glucose tolerance status (diabetes, n = 106; prediabetes, n = 125; normal glucose tolerance, n = 172) were included. Dietary data were obtained by a 24-h food recall, and caloric intake was normalized by ideal body weight. The mtDNAcn and LTL were detected using real-time PCR assay. The associations between caloric intake, aging markers, and renal function were analyzed by partial correlation analysis and multiple linear regression analysis. Mediation analysis was applied to examine the role of mtDNAcn in the association between caloric intake and eGFR. RESULTS: Caloric intake was higher while age-adjusted mtDNAcn was lower in individuals with eGFR <90 mL/min/1.73 m2 (n = 140) than in those with eGFR ≥90 mL/min/1.73 m2 (n = 263). After adjusting for multiple factors, linear regression analysis revealed that caloric intake was negatively associated with eGFR and mtDNAcn, while mtDNAcn was positively associated with eGFR. Moreover, mediation analysis indicated that the indirect effect of caloric intake on eGFR through mtDNAcn was significant (ß = -0.0505, 95% confidence interval -0.0931 to -0.0190). CONCLUSIONS: Caloric intake was negatively associated with eGFR in a Chinese population, and the association was partly mediated by decreased mtDNAcn.