Dietary phytochemical index and its relationship with diabetic sensorimotor polyneuropathy: a case-control study.

Phytochemicals are compounds found in fruits, vegetables, whole grains, nuts and legumes that are non-nutritive but have bioactive properties. A high intake of these compounds is essential for optimal health and disease prevention. No study has investigated the association between Dietary Phytochemical Index (DPI) and polyneuropathy in patients with diabetes. This study aimed to examine the association between DPI and Diabetic Sensory-motor Polyneuropathy (DSPN) in a case-control study. In this case-control study, a total of 185 diabetic patients with DSPN (case group) and 185 sex- and age-matched diabetic patients without neuropathy (control group) were enrolled in this study. Participants were 30-60 years old. A validated food frequency questionnaire was used to measure the dietary intake of all participants. Daily energy derived from phytochemical-rich foods was used to calculate the DPI score. Toronto clinical neuropathy score was applied to define DSPN. Anthropometric data and fasting blood glucose levels were measured using standard methods. The Binary logistic regression was used to estimate Crude and multivariable-adjusted OR (95% CI) for DSPN across tertiles of DPI for the whole population. In the crude model, there was a significant trend across the tertile of DPI (OR highest vs. lowest tertile of DPI = 0.33; 95%CI 0.18, 0.52; P-trend < 0.001). After controlling for age, sex, and energy, a significant reverse association was observed between DPI and DSPN (OR highest vs. lowest tertile of DPI = 0.27; 95%CI 0.15, 0·48; P-trend < 0.001). Moreover, after adjusting for a wide range of confounding variables such as energy intake, physical activity, education, smoking status, and HbA1c, participants in the third tertile of DPI had 75% reduced odds for DSPN (95%CI 0.14, 0.45; P-trend < 0.001). Finally in the full adjusted model, after further adjustment for BMI, observed significant association was remained (OR highest vs. lowest tertile of DPI: 0.24; 95% CI 0.13, 0.14; P-trend < 0.001). Higher intakes of phytochemical-rich foods are associated with lower odds of DSPN.

Silibinin as a major component of milk thistle seed provides promising influences against diabetes and its complications: a systematic review.

Silibinin, or silybin, is a polyphenolic flavonoid and the main active component of silymarin, isolated from the seeds of the milk thistle plant (Silybum marianum). It has been shown to have antioxidant, antineoplastic, hepatoprotective, neuroprotective, anti-inflammatory, antimicrobial, and antidiabetic effects. In this systematic review, a literature search was conducted from inception until January 2024 on major electronic databases (PubMed, Scopus, Web of Science, and Google Scholar) to identify studies assessing the effects of silibinin on diabetes and its associated complications in different molecular, cellular, animal, and clinical studies. Silibinin has been shown to improve diabetic conditions through a variety of mechanisms, including reducing insulin resistance (IR), lowering reactive oxygen species (ROS) levels, and affecting glycolysis, gluconeogenesis, and glycogenolysis. Silibinin treatment reduced blood glucose (BG) levels, oxidative stress markers, and inflammatory cytokines while increasing glycosylated hemoglobin (HbA1C) and antioxidative marker levels in various cellular and animal models of diabetes. It also ameliorated levels of triglyceride (TG), cholesterol, low-density lipoprotein (LDL), and high-density lipoprotein (HDL). Furthermore, silibinin has been identified as an effective treatment for diabetic complications, including hepatic damage, endothelial dysfunction, neuropathy, nephropathy, retinopathy, and osteoporosis. The promising anti-inflammatory, antioxidant, antidiabetic, and insulin-sensitizing activities of silibinin were also supported in clinical studies. The administration of silibinin could possess multiple protective impacts in improving DM and its complications. Nevertheless, further well-designed investigations are necessary to better understand its mechanisms.

Association of SOD2 rs2758339, rs5746136 and rs2842980 polymorphisms with increased risk of breast cancer: a haplotype-based case-control study.

BACKGROUND: A growing body of evidence indicates that oxidative stress, high levels of reactive oxygen species (ROS), is implicated in the pathogenesis of breast cancer (BC). Superoxide dismutase (SOD2), a mitochondria-resident antioxidant enzyme, protects cells from ROS by catalytically converting the superoxide radicals into less reactive species. OBJECTIVE: We aimed to investigate whether SOD2 rs2758339, rs5746136 and rs2842980 polymorphisms are associated with increased risk of BC. METHODS: A total of 100 patients with BC and 100 healthy controls were enrolled in the study. We used polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay for genotyping the SOD2 single-nucleotide polymorphisms (SNPs). Under co-dominant, dominant and recessive inheritance models, the genotypic and allelic associations of SOD2 SNPs with susceptibility to BC were evaluated using logistic regression analysis. The haplotype analysis was performed on the SOD2 SNPs to determine their combined effect on the BC risk. RESULTS: We found that SOD2 rs5746136 was significantly associated with decreased risk of developing BC in co-dominant and dominant inheritance models (P < 0.05). The SOD2 rs5746136 T allele confers an apparent protective effect against breast carcinogenesis (OR: 1.956; 95% CI 1.312-2.916; P < 0.0001). The SOD2 rs5746136/rs2842980 combined genotypes (CT/AA, CT/AT and TT/AA) were significantly more frequent in healthy subjects compared to BC patients (P < 0.05). The CTA and ACA haplotypes (rs2758339, rs5746136, rs2842980) were found to be a protective and a risk factor for BC, respectively. CONCLUSION: These data strongly suggest that SOD2 rs5746136 was significantly associated with reduced risk of BC, indicating its protective role in BC development.

Association of childhood and adolescence obesity with incidence and mortality of adulthood cancers. A systematic review and meta-analysis.

Background: Prevalence and subsequent conditions of childhood and adolescent obesity are increasing. It has been seen that obesity in youth is associated with adulthood cancer. This systematic review and meta-analysis aimed to determine the pooled association of childhood obesity with cancers in adulthood. Methods: In this systematic review, international electronic databases such as Scopus, PubMed, Web of Science, and EMBASE were searched using relevant keywords until February 2022. All Cohort studies assessing the association of childhood and adolescent obesity (under 18 years old) with the incidence and mortality of all types of cancers were included. Two independent reviewers screened and carried out the quality assessment of included studies. Between-studies heterogeneity was assessed using the I squared and Cochran's Q tests. Random/fixed-effect meta-analyses were used to pool the appropriate effect sizes (Hazard ratios (HR)). Results: Overall, 46 studies were found to be relevant and were included in this study. Based on the random-effects model meta-analysis, childhood obesity increased the hazard of cancer incidence and mortality in adulthood by 33% (HR: 1.33, 95%CI (1.25, 1.41)) and by 28% (HR: 1.28, 95%CI (1.13, 1.42)), respectively. In the subgroups meta-analysis, the HR of childhood obesity and adulthood cancer incidence mortality in women was higher than in men (HR=1.39, 95%CI (1.25, 1.53) vs HR= 1.20, 95%CI (1.07, 1.32)) and (HR= 1.40, 95%CI (1.10, 1.69) vs HR=1.20, 95%CI (1.04, 1.36)) respectively. Conclusion: This study found that obesity in childhood and adolescence is associated with a significant increase in the incidence and mortality of cancers in adulthood. Prevention of childhood obesity, in addition to its short-term beneficial effects, can reduce the burden of cancer in adulthood. The data sets of this study are present in the Tables of the current manuscript. Moreover this study was registered online in PROSPERO (registration code: CRD42022331958). Systemic review registration: https://www.crd.york.ac.uk/Prospero/, identifier CRD42022331958.

Association between Dietary Inflammatory Index Scores and Diabetes Sensorimotor Polyneuropathy in Patients with Type 2 Diabetes Mellitus: A Case-Control Study.

Background: Diabetes sensorimotor polyneuropathy (DSPN) is a common complication of diabetes. Diet has been previously related to DSPN. However, no studies have investigated the relationship between the inflammatory potential of the whole diet and DSPN. So, we aimed to examine the association between dietary inflammatory index (DII) and DSPN in Iranian adults. Methods: A total of 185 subjects with DSPN and 185 sex- and age-matched controls were selected in this case-control study. A 168-item validated food frequency questionnaire (FFQ) was used to assay dietary intakes. DII was calculated based on the developed formula. The Toronto clinical neuropathy score was applied to define DSPN. Binary logistic regression was used to estimate the odds ratios (ORs) and 95% confidence intervals (95% CIs) of DII in relation to DSPN. Results: Mean values of age and BMI for all the participants were reported as 50.79 and 28.60, respectively. Also, the median (IQR) of DII for all the participants was estimated as -0.091 (-0.93, 1.07). Our findings suggest that participants in the highest quartile of the DII had higher odds of DSPN (OR = 1.76; 95% CI: 1.03, 3.36) (p-trend = 0.01) compared to subjects in the lowest quartile of DII scores after adjustment for age and sex. Additionally, a strong association was observed after adjusting for energy intake, physical activity, education, smoking status, economic status, marital status, job, BMI, and WC in model 2 (OR = 2.23, 95% CI = 1.13-4.39) (p-trend = 0.0048). Conclusion: Higher DII score was associated with an increased risk of DSPN. Therefore, it is possible that a diet rich in anti-inflammatory nutrients and foods could improve and prevent DSPN.

Combined therapies with exercise, ozone and mesenchymal stem cells improve the expression of HIF1 and SOX9 in the cartilage tissue of rats with knee osteoarthritis.

PURPOSE: Knee osteoarthritis (OA) is a common type of degenerative joint disease which decreases the quality of life. Sex-determining region Y box 9 (SOX9) and hypoxia-inducible factor-1 (HIF1) are considered as the key regulators of OA. We investigated the effect of combined therapies with mesenchymal stem cells (MSCs), ozone (O3) and exercise training on SOX9 and HIF1 expression in the cartilage of rats with knee OA. METHODS: Knee OA was induced by surgical method. OA rats were divided into model, MSCs, ozone, exercise, MSCs + ozone, MSCs + exercise, ozone + exercise and MSCs + ozone + exercise groups. Rats in the MSCs group received intraarticular injection of 1 × 106 cells/kg. Rats in the ozone group received O3 at the concentration of 20 µg/mL, once weekly for 3 weeks. Rats in the exercise group were trained on rodent treadmill three times per week. 48 hours after the programs, cartilage tissues were isolated and the expression of SOX9 and HIF1 was determined using Real-Time PCR. RESULTS: Significant differences were found in the expression of SOX9 and HIF1 between groups (P < 0.0001). Although combined therapies with exercise, MSCs and O3 significantly increased the expression of SOX9 and HIF1 in the cartilage tissue of rats with knee OA, combination of exercise with O3 was significantly more effective compared to the other combined therapies (P < 0.001). CONCLUSIONS: Combined therapy with exercise, MSCs and O3 significantly increased the expression of SOX9 and HIF1 genes in the cartilage of rats with knee OA; however, exercise + O3 was significantly more effective.

Genetic Analysis of MECP2 Gene in Iranian Patients with Rett Syndrome.

OBJECTIVES: Rett syndrome is an X linked dominant neurodevelopmental disorder which almost exclusively affects females. The syndrome is usually caused by mutations in MECP2 gene, which is a nuclear protein that selectively binds CpG dinucleotides in the genome. MATERIALS & METHODS: To provide further insights into the distribution of mutations in MECP2 gene, we investigated 24 females with clinical characters of Rett syndrome referred to Alzahra University Hospital in Isfahan, Iran during 2015-2017. We sequenced the entire MECP2 coding region and splice sites for detection of point mutations in this gene. Freely available programs including JALVIEW, SIFT, and PolyPhen were used to find out the damaging effects of unknown mutations. RESULTS: Direct sequencing revealed MECP2 mutations in 13 of the 24 patients. We identified in 13 patients, 10 different mutations in MECP2 gene. Three of these mutations have not been reported elsewhere and are most likely pathogenic. CONCLUSION: Defects in MECP2 gene play an important role in pathogenesis of Rett syndrome. Mutations in MECP2 gene can be found in the majority of Iranian RTT patients. We failed to identify mutations in MECP2 gene in 46% of our patients. For these patients, further molecular analysis might be necessary.