Chronic obstructive pulmonary disease (COPD) is one of the common chronic respiratory diseases, which causes a heavy burden to patients and society. Increasing studies suggest that ABCA1 plays an important role in COPD. ABCA1 belongs to a large class of ATP-binding (ABC) transporters. It is not only involved in the reverse transport of cholesterol, but also in the regulation of apoptosis, pyroptosis, cellular inflammation and cellular immunity. Meanwhile, ABCA1 is involved in several signaling pathways, such as SREBP pathway, LXR pathway, MAPK pathway, p62/mTOR pathway, CTRP1 pathway and so on. In addition, the ABCA1 participates in the disorder of lipid metabolism in COPD by regulating the formation of RCT and HDL, regulates the inflammation of COPD by removing excess cholesterol in macrophages, and promotes the differentiation of COPD phenotype into emphysema type. Accordingly, the ABCA1 may be a therapeutic target for COPD.

Vitamin D deficiency is implicated in the development of prediabetes. However, it is unclear whether vitamin D deficiency showed any relationship with different phenotypes of prediabetes. This study was designed to address this issue.

We included participants from the National Health and Nutrition Examination Survey 2011-2016. Prediabetes is classified into the following phenotypes: an isolated defect (that is, impaired fasting glucose [IFG], impaired glucose tolerance [IGT], or impaired hemoglobin A1c[IA1c]), two defects (that is, IFG+IGT, IFG+IA1c, or IGT+IA1c), or three defects (that is, IFG+IGT+IA1c). Multivariate logistic regression analysis was used to obtain the odds ratio (OR) and 95% confidence intervals (CIs).

A total of 4126 participants (2332 with prediabetes and 1794 with normal glycemia) were included in this study. Multivariate logistic regression analysis showed that prediabetes was associated with an increased odds of vitamin D deficiency than normal glycemia (OR 1.216, 95% CI 1.023-1.444). Further analysis showed that prediabetes phenotypes of IGT+IFG (OR 1.549, 95% CI 1.050-2.283) and IFG+IGT + IA1c (OR 1.507, 95% CI 1.062-2.138) had an increased odds of vitamin D deficiency. The odds of vitamin D deficiency was higher in individuals with glucose-defined prediabetes, but not in those with HbA1c-defined prediabetes when compared with individuals with normal glycemia.

Prediabetes was associated with an increased odds of vitamin D deficiency, and glucose-defined prediabetes might be a better predictor of vitamin D deficiency.

Background/Objectives: Nutritional needs for people with chronic spinal cord injury (SCI) are inadequately addressed due to the lack of comprehensive evidence and scattered research. We established a consensus-based framework for addressing the nutritional needs of community-dwelling adults with chronic SCI who can ingest food orally. Methods: A web-based Delphi design was employed to ascertain an expert consensus. The Delphi panel consisted of physicians, registered dietitians (RDs), and researchers knowledgeable in SCI and nutrition. Informed by a literature review, 18 nutrition statements were rated by 15 panelists. The survey included statements about SCI-specific dietary energy assessments and macro- and micronutrients. Results: The response rate for the panel (N = 15) was 100%. Consensus levels, scores, stability levels, and response numbers were documented for each statement. The statements received consensus scores ranging from 4.14 to 8.13 on a 9-point Likert scale. Alternative expert comments and suggestions were also provided for each statement. Conclusion: Engaging a diverse panel of experts, the real-time Delphi process yielded expert-reviewed nutrition statements based on an extensive literature review and expert opinions. The rated statements contribute to the ongoing dialogue in SCI-specific nutrition, providing a practical resource for healthcare professionals working with adults with chronic SCI.

Background/Objectives: Vitamin D deficiency in children has been linked to various metabolic disturbances, including dyslipidemia, which contributes to cardiovascular risk. This study aims to investigate the relationship between vitamin D levels and lipid profiles in children. Methods: A cohort of 332 children with either normal vitamin D or diagnosed vitamin D deficiency was recruited. Serum vitamin D levels were measured, and lipid profiles, including total cholesterol, low-density lipoproteins (LDLs), high-density lipoproteins (HDLs), and triacylglycerols (TAGs), were assessed. The data were analyzed using statistical methods. Results: This study found that children with higher serum vitamin D concentrations had significantly lower TAG (p = 0.033) and very-low-density lipoprotein (VLDL) (p = 0.038) levels and higher HDL levels (p = 0.042), indicating a more favorable lipid profile compared to those with lower vitamin D levels. Conclusions: This study demonstrates that vitamin D deficiency can be associated with dyslipidemia in children. These findings suggest that vitamin D supplementation may be an effective strategy for managing dyslipidemia and reducing cardiovascular risk in pediatric populations. Further research is needed to determine the long-term effects and optimal dosing of vitamin D in this context.

Polycystic ovary syndrome (PCOS) is a prevalent endocrine condition affecting both metabolic and reproductive health in women. The impact of vitamin D on metabolic regulation has attracted growing interest. The purpose of this study is to investigate the impact of vitamin D supplementation on key metabolic parameters-namely blood glucose, insulin, and lipid levels-in individuals with PCOS.

A systematic review was conducted to identify relevant studies in PubMed, Embase, Cochrane Library, Web of Science, and ClinicalTrials.gov. The search focused on randomized controlled trials (RCTs) evaluating the impact of vitamin D supplementation in patients with PCOS. Meta-analysis was performed using RevMan 5.3 software, and study quality was evaluated with the Cochrane Risk of Bias Tool. In addition, outcome-related evidence was graded using the GRADE system, and TSA was performed to determine if the number of participants met the required threshold.

A total of 691 individuals with PCOS from 13 RCTs were evaluated. The meta-analysis indicated that the supplementation of vitamin D led to a notable reduction in the subsequent metabolic parameters: fasting blood glucose[MD=-2.91 mg/dL, 95% CI (-4.78, -1.04) mg/dL, P = 0.002], insulin levels[MD=-1.98 µIU/mL, 95% CI (-3.32, -0.64) µIU/mL, P = 0.004], triglycerides[MD=-11.01 mg/dL, 95% CI (-16.42, -5.61) mg/dL, P < 0.0001], total cholesterol [MD=-11.69 mg/dL, 95% CI (-15.56, -7.82) mg/dL, P < 0.00001], very low-density lipoprotein cholesterol (VLDL-cholesterol) [MD=-2.64 mg/dL, 95% CI (-4.50, -0.79) mg/dL, P = 0.005], and low-density lipoprotein cholesterol (LDL-cholesterol) [MD=-5.85 mg/dL, 95% CI (-10.28, -1.42) mg/dL, P = 0.010]. Nevertheless, the supplementation of vitamin D did not exert a significant impact on high - density lipoprotein cholesterol (HDL - cholesterol) [MD=-0.21 mg/dL, 95% CI (-0.81, 1.22) mg/dL, P = 0.69]. Begg's and Egger's tests suggested a minimal probability of publication bias, and the TSA confirmed that the optimal sample size for major outcomes had been reached, supporting the robustness of the meta-analysis results.

Vitamin D supplementation shows significant benefits in improving metabolic parameters in PCOS patients, particularly in reducing fasting blood glucose, insulin, and lipid levels, suggesting a potential role of vitamin D in PCOS management. The long-term outcomes and most effective dose of vitamin D warrant further investigation in future research.

Not applicable.

Vitamin D (VD) has been implicated in regulating insulin secretion and pancreatic β-cell function. Yet, the underlying molecular mechanism of VD in glucose homeostasis is not fully understood. This study investigates the effect of VD in regulating insulin secretion and pancreatic β-cell function. INS-1 β-cells were treated with VD to assess cell viability, reactive oxygen species production (ROS), insulin secretion, glucose uptake, proliferation, gene expression alterations, mitochondria metabolism, calcium influx, as well as the effects of antidiabetic drugs on VDR expression. Additionally, RNA sequencing from human pancreatic islets were utilized to examine VDR expression in relation to clinical parameters such as HbA1c, BMI, age, and gender. VD treatment enhanced glucose-stimulated insulin secretion and elevated intracellular calcium levels without affecting insulin content, glucose uptake, ROS production, proliferation, or mitochondrial metabolism. Expression levels of key β-cell function genes, including Ins, Pdx1, and Glut2, remained unchanged with VD treatment. However, genes associated with calcium channels were upregulated. Cell exposure to rosiglitazone and dexamethasone elevated VDR expression in INS-1 cells, while metformin and insulin had no effect. RNA-seq analysis in human islets showed that VDR expression levels in human islets were significantly higher than in other metabolic tissues and were notably reduced in hyperglycemic donors compared to normoglycemic individuals. Furthermore, VDR expression positively correlated with several genes regulating voltage-gated calcium channels. In conclusion, the study indicates that VD plays a significant role in enhancing insulin secretion through modulation of intracellular calcium dynamics, highlighting its potential therapeutic implications for managing type 2 diabetes.

Background: COPD is a heterogenous disease of the respiratory tract caused by diverse genetic factors along with environmental and lifestyle-related effects such as industrial dust inhalation and, most frequently, cigarette smoking. These factors lead to airflow obstruction and chronic respiratory symptoms. Additionally, the increased risk of infections exacerbates airway inflammation in COPD patients. As a consequence of the complex pathomechanisms and difficulty in treatment, COPD is among the leading causes of mortality both in the western countries and in the developing world. Results: The management of COPD is still a challenge for the clinicians; however, alternative interventions such as smoking cessation and lifestyle changes from a sedentary life to moderate physical activity with special attention to the diet may ameliorate patients' health. Here, we reviewed the effects of different dietary components and supplements on the conditions of COPD. Conclusions: COPD patients are continuously exposed to heavy metals, which are commonly present in cigarette smoke and polluted air. Meanwhile, they often experience significant nutrient deficiencies, which affect the detoxification of these toxic metals. This in turn can further disrupt nutritional balance by interfering with the absorption, metabolism, and utilization of essential micronutrients. Therefore, awareness and deliberate efforts should be made to check levels of micronutrients, with special attention to ensuring adequate levels of antioxidants, vitamin D, vitamin K2, magnesium, and iron, as these may be particularly important in reducing the risk of COPD development and limiting disease severity.

Previous investigations have assessed the connection between vitamin D deficiency and an increased risk of gestational diabetes mellitus (GDM); however, the findings remain inconsistent. The purpose of this study was to investigate the causal relationship between 25-hydroxyvitamin D (25OHD) levels and GDM.

Summary statistics data from genome-wide association studies (GWASs) were used to perform a bidirectional two-sample Mendelian randomization (MR) study. A total of 417,580 Europeans from the UK Biobank provided summary statistics data for 25OHD. The tenth data release of the FinnGen study provided the data for GDM, comprising 14,718 cases and 215,592 controls. For the univariate MR (uvMR) investigations, we employed the inverse variance weighted (IVW) method as our major analytical approach. Multiple sensitivity analyses were performed to evaluate the robustness of the results. Moreover, multivariate MR (mvMR) studies were conducted to account for potential confounding variables, including obesity, insulin resistance, and lipid traits.

In the forward MR study, uvMR analysis did not provide evidence supporting a causal effect of 25OHD levels on the risk of GDM [IVW odds ratio (OR): 1.07, 95% confidence interval (CI): 0.95 to 1.19, p = 0.273]. After adjusting for obesity, fasting insulin levels, and lipid traits, the findings from the mvMR analysis aligned with those of the uvMR analysis. In the reverse MR study, uvMR analysis indicated that GDM had no causal effect on serum 25OHD levels (IVW β = -0.003, p = 0.804), and the robustness of this finding was confirmed in the mvMR study.

Our MR research revealed no causal effect of serum 25OHD levels on GDM, suggesting that 25OHD deficiency does not correlate with an increased risk of GDM. Furthermore, our reverse analysis revealed no causal effect of GDM on 25OHD levels.

Cardiovascular diseases (CVDs) cause about 30% of deaths worldwide, increasing social and economic burden in our societies. Although the treatment of the canonical cardiovascular risk factors has reduced the impact of CVDs on morbidity and mortality in the past few years, they continue to represent a major health problem. The definition of the biological properties of the bone-heart axis has led to new insights in the pathogenesis of CVDs; hence, the aim of this review is to try to elucidate the role of this axis on the susceptibility to CVDs. There is evidence that the bone interacts with extra-skeletal organs, including the cardiovascular system, through its endocrine functions. Clinical and experimental data strongly indicate that the interplay between the bone and the cardiovascular system represents a future tool for the prevention, diagnosis and treatment of CVDs. The identification of these non-canonical cardiovascular risk factors could prompt pharmacological research towards new target therapy aimed at precision medicine.

The (MTHFR) C677T gene polymorphism is associated with neurological disorders and schizophrenia. Patients diagnosed with schizophrenia and schizoaffective disorder and controls (n 134) had data collected for risk factors, molecular and neuro-sensory variables, symptoms, and functional outcomes. Promising gene variant-related predictive biomarkers were identified for diagnosis by Receiver Operating Characteristics and for illness duration by linear regression. These were then analyzed using Spearman's correlation in relation to the duration of illness. Significant correlations were ranked by strength and plotted on graphs for each MTHFR C677T variant. Homozygous MTHFR 677 TT carriers displayed a mid-illness switch to depression, with suicidality and a late-phase shift from lower to higher methylation, with activated psychosis symptoms. MTHFR 677 CC variant carriers displayed significant premorbid correlates for family history, developmental disorder, learning disorder, and head injury. These findings align with those of low methylation, oxidative stress, multiple neuro-sensory processing deficits, and disability outcomes. Heterozygous MTHFR 677 CT carriers displayed multiple shifts in mood and methylation with multiple adverse outcomes. The graphically presented ranked biomarker correlates for illness duration allow a perspective of psychosis development across gene variants, with the potential for phase of illness monitoring and new therapeutic insights to prevent or delay psychosis and its adverse outcomes.

Vitamin D is a key molecule in calcium and phosphate homeostasis; however, increasing evidence has recently shown that it also plays a crucial role in the immune system, both innate and adaptive. A deregulation of vitamin D levels, due also to mutations and polymorphisms in the genes of the vitamin D pathway, determines severe alterations in the homeostasis of the organism, resulting in a higher risk of onset of some diseases, including osteoporosis. This review gives an overview of the influence of vitamin D levels on the pathogenesis of osteoporosis, between bone homeostasis and immune system.

Vitamin D receptors (VDRs) are present in almost all cells of the immune system, including B cells, T cells, NK (Natural Killer) cells, dendritic cells, and monocytes, as well as the epithelial cells of many organs such as the intestine, pancreas, prostate, lungs, and cardiomyocytes. In addition, some immune cells, including dendritic cells, macrophages, and B and T cells, can synthesize calcitriol by expressing 1α-hydroxylase. Upon binding to VDRs, vitamin D (Vit D) regulates the expression of genes involved in immune responses, including those encoding for cytokines. It modulates the production of pro-inflammatory cytokines while promoting the synthesis of anti-inflammatory cytokines. Vit D also affects the differentiation and maturation of cells of the immune system. By inhibiting the nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways, Vit D reduces the expression of pro-inflammatory genes. These effects highlight the potential of Vit D as a therapeutic agent in the management of inflammatory diseases, including autoimmune disorders, cardiovascular diseases, diabetes, metabolic syndrome, cancer, neurological diseases, depression, and inflammatory bowel disease.

Adequate serum vitamin D levels correlate with a more favorable lipid profile compared to deficient levels. Despite the well-established prevalence of vitamin D deficiency in children with obesity, studies investigating its influence on lipid profiles in this population are scarce. We explored the impact of vitamin D status on lipid profiles and markers of atherogenic dyslipidemia in a cohort of children and adolescents with obesity.

A total of 271 Caucasian children and adolescents with overweight/obesity and a control group of 54 pediatric patients with normal weight. All participants underwent outpatient visits for the assessment of clinical parameters and venous blood collection for biochemical analysis such as triglycerides (TG)/HDL-C ratio, LDL-C/HDL-C ratio, atherogenic index of plasma AIP), vitamin D level. Individuals with obesity displayed severe vitamin D deficiency (25-OH-D ≤10 ng/ml) at a higher frequency compared to those with normal weight (p = 0.03). In patients with overweight/obesity and low 25-OH-D levels show higher values of glycemia (p = 0.001), insulin resistance (HOMA-IR and TRYG p < 0.001), TG (p < 0.001), TG/HDL-C (p = 0.001), AIP (p < 0.001), SBP (p = 0.01), and DBP (p = 0.04). In normal-weight individuals with low 25-OH- D levels an increased values of glycemia (p = 0.01), insulin resistance (HOMA-IR p = 0.01 and TRYG p = 0.002), TG (p = 0.01), TG/HDL-C (p = 0.02), AIP (p = 0.01). A direct correlation between 25-OH-D levels and metabolic parameters is observed.

A correlation between vitamin D levels and the lipid/atherosclerotic profile was recorded. Vitamin D deficiency may represent a preventable and easily treatable cardiometabolic risk factor, emphasizing the importance of early intervention and preventive measures.

Vitamin D deficiency has emerged as a significant concern in public health due to its potential association with various metabolic disorders. This study aimed to investigate the relationship between serum vitamin D levels and the susceptibility to hyperlipidemia among adults. Using a multi-stage sampling approach, we recruited a cohort of 2072 eligible individuals aged over 18 years. Serum 25-hydroxyvitamin D [25(OH)D] levels were measured alongside glucolipid metabolic markers, and comprehensive demographic and physical data were collected. The cohort exhibited a hyperlipidemia prevalence of 42.18%, with 19.88% demonstrating vitamin D deficiency. Notably, 23.68% of individuals with vitamin D deficiency also presented hyperlipidemia. Statistical analysis revealed a significantly higher prevalence of hyperlipidemia among those with vitamin D deficiency compared to those with sufficient levels (23.68% vs. 17.11%, P < 0.05). After adjusting for various factors including age, geographical region, exercise status, BMI, fasting glucose level, and blood pressure, lower serum 25(OH)D concentrations were found to significantly increase the risk of hyperlipidemia (Odds Ratio [OR] = 1.41; 95% CI: 1.057, 1.885; P < 0.05). Further stratification of the hyperlipidemic cohort revealed that vitamin D deficiency was associated with 1.459- and 1.578-times higher risks for total cholesterol and triglyceride abnormalities, respectively, compared to those with sufficient vitamin D levels. Moreover, each 10 ng/mL decrease in serum vitamin D level corresponded to an increased risk of total cholesterol (OR = 0.82; 95% CI: 0.728, 0.974; P < 0.05) and triglyceride abnormalities (OR = 0.79; 95% CI: 0.678, 0.927; P < 0.05). However, there were no significant differences observed between vitamin D-sufficient and-deficient groups regarding Low-Density Lipoprotein (LDL) and High-Density Lipoprotein (HDL) abnormalities. These findings underscore the potential role of serum vitamin D deficiency as an independent risk factor contributing to the elevated prevalence of hyperlipidemia in the adult population.

Current immunoassay techniques for analyzing clinically relevant parathyroid hormone (PTH) circulating fragments cannot distinguish microheterogeneity among structurally similar molecular species. This hinders the identification of molecular species and the capture of target analyte information. Since structural modifications are important in disease pathways, mass spectrometry can detect, identify, and quantify heterogeneous ligands captured by antibodies. We aimed to create a sensitive and selective multiple reaction monitoring-mass spectrometric immunoassay analysis (MRM-MSIA)-based method for detecting and quantifying PTH fragments or proteoforms for clinical research. Our study established MRM transitions using triple-quadrupole tandem mass spectrometry for the signature peptides of five PTH fragments. This method was validated according to FDA guidelines, employing the mass spectrometric immunoassay (MSIA) protocol to bolster detection selectivity and sensitivity. This validated approach was applied by analyzing samples from type 2 diabetes mellitus (T2DM) patients with and without vitamin D deficiency. We found serum PTH fragments associated with vitamin D deficiency in patients with and without T2DM. We developed and validated the MRM-MSIA technique specifically designed for the detection and quantification (amino acid (aa38-44), (aa45-51), and (aa65-75)) of these fragments associated with vitamin D deficiency and T2DM. This study is the first to accurately quantify plasma PTH fragments using MRM-MSIA, demonstrating its potential for clinical diagnostics.

Even though the role of D2 (ergocalciferol) on cardiovascular disease risk components has been studied, conflicting results have been reported. Moreover, no single study has studied all these parameters and the role of vitamin D2 individually has not been assessed; hence, this systematic review and meta-analysis of randomized controlled trials was conducted to assess the effect of vitamin D2 supplementation on lipid profile, anthropometric indices, blood pressure, and inflammatory and glycemic biomarkers in humans.

Web of Science, Scopus, PubMed/Medline, and Embase were searched from database inception to July 2024, and the random effects model, according to the DerSimonian and Laird method, was used to generate combined estimates of the intervention's effect on the outcomes.

After full-text analysis, 11 eligible articles were included in our meta-analyses. No statistically significant association was observed between vitamin D2 administration and BMI, WC, TC, HDL-C, LDL-C, TG, DBP or SBP; however, a statistically significant decrease in CRP (WMD: - 1.92 mg/dL, 95 % CI: - 3.30 to - 0.54, P = 0.006) and HbA1c levels (WMD: - 0.37 %, 95 % CI: - 0.66 to - 0.09, P = 0.009), and a non-statistically significant decrease in FBG (WMD: - 4.61 mg/dL, 95 % CI: - 14.71 to 5.47, P = 0.370, I2 = 90 %, P ˂ 0.001) and HOMA-IR (WMD: - 0.10, 95 % CI: - 0.17-0.03, P = 0.002) were detected.

In summary, our systematic review and meta-analysis discovered that vitamin D2 administration was associated with a statistically significant decrease in CRP and HbA1c levels, without a significant correlation with other outcomes.

Sodium glucose cotransporter 2 inhibitors (SGLT2is) are a newly developed class of anti-diabetics which exert potent hypoglycemic effects in the diabetic milieu. However, the evidence suggests that they also have extra-glycemic effects. The renin-angiotensin-aldosterone system (RAAS) is a hormonal system widely distributed in the body that is important for water and electrolyte homeostasis as well as renal and cardiovascular function. Therefore, modulating RAAS activity is a main goal in patients, notably diabetic patients, which are at higher risk of complications involving these organ systems. Some studies have suggested that SGLT2is have modulatory effects on RAAS activity in addition to their hypoglycemic effects and, thus, these drugs can be considered as promising therapeutic agents for renal and cardiovascular disorders. However, the exact molecular interactions between SGLT2 inhibition and RAAS activity are not clearly understood. Therefore, in the current study we surveyed the literature for possible molecular mechanisms by which SGLT2is modulate RAAS activity.

Polycystic ovary syndrome (PCOS) is a common and complex endocrine disorder in women of reproductive age. Vitamin D supplementation is a promising complementary therapy for PCOS, yet there is no consensus on an optimal dose, leading to a lack of evidence-based supplementation guidelines.

The objective of this study was to conduct a vitamin D dose-response meta-analysis among women with PCOS.

MEDLINE, CINAHL, and EMBASE databases from inception to November 2022 were searched for relevant articles.

Study screening and bias assessment were conducted by 2 independent reviewers. Eight relevant studies were identified; data for serum 25(OH)D (nmol/L) at baseline and at 12 weeks in each intervention group (mean ± SD) and vitamin D dose were extracted.

Estimates across studies were used to create a pooled curve, using restricted cubic splines with knots at the 10th, 50th, and 90th percentiles of the distribution of doses, to estimate the mean difference in effect for serum 25(OH)D at each dose compared with 0 IU/day. Sensitivity analyses were conducted fixing knots at 4000 IU/day and 7000 IU/day, which were a priori identified as potentially important thresholds, and to assess model fit and estimate heterogeneity. The pooled analysis demonstrated strong evidence of a dose-response relationship (P < .001), suggesting an increasing effect with increasing dose. An initial increase in serum 25(OH)D was evident until doses of approximately 3000 IU/day; this was followed by a plateau in effect between approximately 3000 IU/day and 5000 IU/day. The effect of supplementation with >5000 IU/day was unclear, given the minimal data at higher doses. The curve produced robust results for moderate doses (3000 IU/day to 4000 IU/day), which were not sensitive to model specification.

Women with PCOS are responsive to vitamin D supplementation, but the benefit of providing doses of >3000 IU/day appears minimal. Further data is required to determine dose-response at doses of >5000 IU/day, and whether higher intakes provide a clinically meaningful advantage in this population.

PROSPERO registration no. CRD42021259396.

Vitamin D has a significant correlation with type 2 diabetes. Insufficient levels of vitamin D can cause insulin resistance, which impairs the ability of cells to respond to insulin and worsens the progression of diseases. Furthermore, vitamin D has the potential to enhance the release of insulin, enhance the regulation of blood sugar levels, and reduce the glycemic index. Research has indicated that insufficient levels of vitamin D may elevate the likelihood of experiencing complications related to type 2 diabetes, including cardiovascular disease and neuropathy. This study employed bibliometric analysis to investigate recent advancements in research about the relationship between vitamin D and type 2 diabetes.

We searched for articles on the topic of vitamin D and type 2 diabetes published between January 1, 2004, and December 31, 2023. The search was performed on February 20, 2024, using the Web of Science Core Collection (WoSCC). Utilizing VOSviewer and CiteSpace, we conducted bibliometric analysis and visualization.

A comprehensive study was conducted on a total of 1362 papers pertaining to the relationship between vitamin D and type 2 diabetes. The United States had the biggest number of publications and the highest effect among these articles. Within the top 10 most published journals, the journal "DIABETES CARE" has the highest H-index, indicating its significant influence in this field of study. Currently, there is an extensive body of research on the supplementation of vitamin D for the improvement of type 2 diabetes and prevention of complications in type 2 diabetes, as well as its related mechanisms. Research related to bone turnover and peripheral neuropathy represents a promising area for future studies.

Overall, bibliometrics may assist researchers in comprehending the trajectory, significant themes, and scholarly influence of the field concerning vitamin D and type 2 diabetes. This, in turn, offers substantial backing for future studies that delve further into the subject matter.

X-linked hypophosphatemia (XLH) is characterized by increased concentrations of circulating fibroblast growth factor 23 (FGF-23) resulting in phosphate wasting, hypophosphatemia, atypical growth plate and bone matrix mineralization. Epidemiologic studies suggest a relationship between FGF-23, obesity, and metabolic dysfunction. The prevalence of overweight and obesity is high in children with XLH. We aimed to evaluate the prevalence of obesity and metabolic complications in adults with XLH.

We conducted a prospective cohort study in adult XLH patients from a single tertiary referral center. The proportion of patients with a BMI >25 kg/m2 was the main outcome measure. Body fat mass percentage (FM%) and adipose tissue surfaces were secondary outcome measures. Glucose homeostasis (plasma glucose and insulin concentrations after fasting and 2 hours after an oral glucose tolerance test) was explored in a subgroup of patients and compared with age-, sex-, and BMI-matched healthy controls.

Among 113 evaluated patients, 85 (75%) were female and 110 (97%) carried a PHEX mutation. Sixty-three (56%) patients were overweight or obese, with a median BMI of 25.3 [IQR, 22.7; 29.2] kg/m2. BMI was correlated with FM%, abdominal and thigh subcutaneous and intra-abdominal adipose tissue surfaces. The prevalence of impaired fasting glucose, impaired glucose tolerance, and diabetes was not different between XLH patients and matched controls.

The prevalence of overweight and obesity is high among XLH patients and is associated with excess fat mass. However, the prevalence of glucose homeostasis abnormalities is not increased in patients compared to healthy controls, suggesting that metabolically healthy overweight or obesity predominates.

Vitamin D insufficiency is a prevalent issue in patients suffering from CKD. The purpose of this study was to determine whether serum 25(OH)D levels are associated with all-cause and cardiovascular mortality in patients with CKD.

To examine the associations between 25(OH)D levels and cardiovascular mortality, this retrospective cohort study used the National Health and Nutrition Examination Survey (NHANES) and the National Death Index (NDI) 2007‒2018 database. A total of 2,668 eligible subjects were included in this study, with follow-up conducted until December 31, 2019. The associations were assessed using Cox proportional hazards regression, restricted cubic splines, Kaplan-Meier survival curves, and competing risks survival analysis. Furthermore, subgroup and sensitivity analyses were performed.

During a median follow-up of 72 months in a weighted population of 11,715,452 eligible participants, there were 665 deaths from any cause, including 196 cardiovascular-related deaths. After adjusting for covariates, lower levels of 25(OH)D were significantly associated with increased risks for both all-cause mortality (HR= 0.85, 95 % CI 0.77∼0.94) and cardiovascular mortality (SHR= 0.80, 95 % CI 0.67∼0.94). Consistent results were also observed when analyzing 25(OH)D as a categorical variable (quartile). Compared to group Q1, both group Q3 (HR = 0.71, 95 % CI 0.54‒0.93) and group Q4 (HR = 0.72, 95 % CI 0.55‒0.94) exhibited a significantly reduced mortality risk. Weighted restricted cubic splines revealed an inverse J-shaped linear association between levels of 25(OH) D and all-cause mortality ((PNonliner > 0.05). Subgroup analysis and sensitivity analysis yielded similar findings.

All-cause mortality and cardiovascular disease-related mortality were significantly increased by lower 25(OH)D levels, both as continuous and categorical variables. 25(OH)D has an inverse J-shaped linear association with all-cause and cardiovascular mortality.

Diabetes mellitus (DM) has affected over 387 million patients globally, expected to reach 592 million by the end of 2035. It is a metabolic disorder characterized by chronic hyperglycemia caused by either insulin deficiency, insulin resistance, or both.

The present study was designed to estimate the levels of different bone markers; serum Vitamin D, alkaline phosphatase, phosphorus, and calcium in patients with type 2 DM (T2DM). The study was conducted on patients aged 20-50 years diagnosed with T2DM, who were attending the outpatient/inpatient department of internal medicine.

The levels of calcium were decreased in the patients with diabetes and also the study proved a negative correlation between calcium and random plasma glucose (RPG). There was a significant negative correlation between RPG and serum 25(OH)D3.

We conclude that Vitamin D insufficiency is frequent in Moradabad, Uttar Pradesh. Sunshine exposure daily for 15 min on the face and hands is necessary to elevate the sunlight Vitamin D levels.

Vitamin D is a crucial micronutrient, critical to human health, and influences many physiological processes. Oral and skin-derived vitamin D is hydroxylated to form calcifediol (25(OH)D) in the liver, then to 1,25(OH)2D (calcitriol) in the kidney. Alongside the parathyroid hormone, calcitriol regulates neuro-musculoskeletal activities by tightly controlling blood-ionized calcium concentrations through intestinal calcium absorption, renal tubular reabsorption, and skeletal mineralization. Beyond its classical roles, evidence underscores the impact of vitamin D on the prevention and reduction of the severity of diverse conditions such as cardiovascular and metabolic diseases, autoimmune disorders, infection, and cancer. Peripheral target cells, like immune cells, obtain vitamin D and 25(OH)D through concentration-dependent diffusion from the circulation. Calcitriol is synthesized intracellularly in these cells from these precursors, which is crucial for their protective physiological actions. Its deficiency exacerbates inflammation, oxidative stress, and increased susceptibility to metabolic disorders and infections; deficiency also causes premature deaths. Thus, maintaining optimal serum levels above 40 ng/mL is vital for health and disease prevention. However, achieving it requires several times more than the government's recommended vitamin D doses. Despite extensive published research, recommended daily intake and therapeutic serum 25(OH)D concentrations have lagged and are outdated, preventing people from benefiting. Evidence suggests that maintaining the 25(OH)D concentrations above 40 ng/mL with a range of 40-80 ng/mL in the population is optimal for disease prevention and reducing morbidities and mortality without adverse effects. The recommendation for individuals is to maintain serum 25(OH)D concentrations above 50 ng/mL (125 nmol/L) for optimal clinical outcomes. Insights from metabolomics, transcriptomics, and epigenetics offer promise for better clinical outcomes from vitamin D sufficiency. Given its broader positive impact on human health with minimal cost and little adverse effects, proactively integrating vitamin D assessment and supplementation into clinical practice promises significant benefits, including reduced healthcare costs. This review synthesized recent novel findings related to the physiology of vitamin D that have significant implications for disease prevention.

Type 1 diabetes mellitus is a chronic autoimmune disease caused by insufficient production of insulin. Many studies have linked type 1 diabetes mellitus to vitamin D3 deficiency. We investigated the prevalence of vitamin D deficiency in Sudanese children and adolescents with type 1 diabetes mellitus and assessed the impact of vitamin D deficiency treatment on their glycemic control.

In 2019-2022, we conducted a quasi-experimental study on 115 children with type 1 diabetes mellitus (1-19 years old) at the Sudan Childhood Diabetes Center. Vitamin D supplements were given orally to deficient patients for 3 months. The concentrations of hemoglobin A1c, fasting blood glucose, insulin dosage, and vitamin D (25-hydroxyvitamin D (25(OH)D)) were measured before and after vitamin D3 administration. One-way ANOVA and paired sample t-tests were used to evaluate the effect of supplementation.

Only 27% of type 1 diabetes mellitus children were deficient in vitamin D, whereas 31.1% were inadequate and 40.9% were sufficient. The administration of vitamin D supplements slightly improved hemoglobin A1c levels in 67.7% of the patients, but the difference was not significant (mean 10.8 ± 2.1% before, 10.1 ± 2.5% after, p0.05 = 0.199). However, there was a significant decrease in the fasting blood glucose level (mean: 174.978.5-136.759.1 ng/ml; p0.05 = 0.049). Vitamin D levels were significantly increased after treatment (mean = 49.6 ng/mL; t-test = -11.6, 95% CI 40.8-(-28.6); p0.05 = 0.000). After vitamin D3 supplementation, 25.8% of individuals changed their insulin dosage; however, there was no significant variation in insulin needs.

The prevalence of vitamin D deficiency in children and adolescents with type 1 diabetes mellitus in Sudan is relatively high; incorporating vitamin D supplements in their treatment plan may improve their glycemic control.

Increasing evidence suggests a beneficial role of vitamin D (VitD) supplementation in addressing the widespread VitD deficiency, but currently used VitD3 formulations present low bioavailability and toxicity constrains. Hence, poly(L-lactide-co-glycolide) (PLGA) nanoparticles (NPs), solid-lipid nanoparticles (SLNs) and nanostructured lipid carriers (NLCs) were investigated to circumvent these issues. PLGA NPs prepared by emulsification or nanoprecipitation presented 74 or 200 nm, and association efficiency (AE) of 68 % and 17 %, respectively, and a rapid burst release of VitD3. Both SLN and NLCs presented higher polydispersity and larger NPs size, around 500 nm, which could be reduced to around 200 nm by use of hot high-pressure homogenization in the case of NLCs. VitD3 was efficiently loaded in both SLNs and NLCs with an AE of 82 and 99 %, respectively. While SLNs showed burst release, NLCs allowed a sustained release of VitD3 for nearly one month. Furthermore, NLCs showed high stability with maintenance of VitD3 loading for up to one month at 4 °C and no cytotoxic effects on INS-1E cells up to 72 h. A trending increase (around 30 %) on glucose-dependent insulin secretion was observed by INS-1E cells pre-treated with VitD3. This effect was consistently observed in the free form and after loading on NLCs. Overall, this work contributed to further elucidation on a suitable delivery system for VitD3 and on the effects of this metabolite on β cell function.

Vitamin D deficiency is a risk factor for liver disease, insulin resistance, and beta cell dysfunction. Individuals with alcohol use disorder (AUD) have many comorbidities, with a heavy burden of liver disease and metabolic complications, including type 2 diabetes mellitus (T2DM).

We aimed to analyze the prevalence and associations of vitamin D deficiency in patients admitted for in-hospital treatment of AUD.

A cross-sectional study was conducted in patients consecutively admitted for the treatment of AUD between January 2017 and October 2023. Sociodemographic data, substance use characteristics, and blood parameters were available at admission. Vitamin D status was assessed through the serum concentrations of 25-hydroxyvitamin D [25(OH)D] levels using a direct competitive chemiluminescent immunoassay method. Deficiency of vitamin D was defined as a concentration less than 20 ng/mL; impaired fasting glucose (IFG) was defined by fasting blood glucose >100 mg/dL (5.6 mmol/L), and advanced liver fibrosis by an FIB-4 index >3.25.

Two hundred and forty-three patients were included (75% male) with a mean age of 49 ± 10 years, mean BMI of 26.4 ± 7.3, mean alcohol consumption of 163 ± 81 g/day, and a mean duration of AUD of 18.1 ± 11.2 years. Mean 25(OH)D, fasting blood glucose, AST, ALT, and platelets were 14.4 ± 10.2 ng/mL, 103.4 ± 40.9 mg/dL, 55.1 ± 75.8 U/L, 44.8 ± 76.6 U/L, and 206.3 ± 84.8 × 109/L, respectively. The prevalence of vitamin D deficiency was 80.6%, and 41.1% of patients had levels less than 10 ng/mL. IFG was present in 32.3% of patients, and 20.5% had FIB-4 values >3.25. In the multivariable analysis, IFG (OR, 2.51; 95% CI: 1.02-6.17, p = 0.04) and advanced liver fibrosis (OR, 4.27; 95% CI: 1.21-15.0, p = 0.02) were the only factors associated with vitamin D deficiency.

Vitamin D deficiency was very prevalent in this series of patients with AUD and was associated with impaired fasting glucose and advanced liver fibrosis.

While several studies have investigated the association between vitamin D deficiency and biochemical parameters, the results are still inconsistent and mostly overlook seasonal variations. This study explored the relationships between 25-hydroxy-vitamin D (25(OH)D) concentrations, biochemical markers, and seasonal variation among young males and females.

A cross-sectional study was conducted among 203 individuals aged 18-24 years of both sexes residing in Brasilia, Brazil (latitude: 15°S). Sociodemographic variables, season of blood collection, and serum levels of 25(OH)D, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, glycated hemoglobin (HbA1c), glucose, insulin, hs-CRP, parathyroid hormone, ionized calcium, and alkaline phosphatase were included. Descriptive statistics and differences among groups, correlations, and linear regression tests were performed.

The mean age of the participants was 21.17±1.7 years, and the mean serum 25(OH)D level was 25.76±7.0 ng/mL. Of the participants, 50.7% had vitamin D insufficiency (20 to 29.9 ng/mL), and 23.2% were vitamin D deficient (≤20 ng/mL). Vitamin D deficiency was higher in the spring (53.2%) and among females (29.5%). In young men with vitamin D insufficiency/deficiency (≤29.9 ng/mL) (n = 49), 25(OH)D levels were inversely correlated with HOMA-β (r = -0.234, p = 0.032) and triglyceride (r = -0.415, p = 0.003) levels. However, there were no significant correlations between 25(OH)D concentrations and biochemical markers among women with insufficient and deficient vitamin D levels.

This study found a high prevalence of vitamin D insufficiency/deficiency among young individuals living in Brasília, Brazil, particularly women and during the spring season. Our findings suggest that lower 25(OH)D levels (≤29.9 ng/mL) may be associated with insulin resistance and an increased risk of cardiovascular disease in young men studied. However, further studies with larger representative samples are needed to explore the mechanisms underlying the association between vitamin D and biochemical parameters.

Diabetes is a metabolic illness that increases protein glycosylation in hyperglycemic conditions, which can have an impact on almost every organ system in the body. The role of vitamin D in the etiology of diabetes under RAGE (receptor for advanced glycation end products) stress has recently received some attention on a global scale. Vitamin D's other skeletal benefits have generated a great deal of research. Vitamin D's function in the development of type 1 and type 2 diabetes is supported by the discovery of 1,25 (OH)2D3 and 1-Alpha-Hydroylase expression in immune cells, pancreatic beta cells, and several other organs besides the bone system. A lower HBA1c level, metabolic syndrome, and diabetes mellitus all seems to be associated with vitamin D insufficiency. Most of the cross-sectional and prospective observational studies that were used to gather human evidence revealed an inverse relationship between vitamin D level and the prevalence or incidence of elevated HBA1c in type 2 diabetes. Several trials have reported on the impact of vitamin D supplementation for glycemia or incidence of type 2 diabetes, with varying degrees of success. The current paper examines the available data for a relationship between vitamin D supplementation and HBA1c level in diabetes and discusses the biological plausibility of such a relationship.

In our study, we aimed to investigate the negative effects of the prefrontal cortex (PFC)-associated impairment of cholinergic activity on memory and learning caused by high fructose corn syrup (HFCS) and the protective role of vitamin D in adolescent rats. Twenty-four animals were divided into three groups as control, HFCS group (11 % HFCS-55 solution, ad libitum) and HFCS+ Vit D (42 μg/kg/day). Elevated Plus Maze (EPM), Forced Swim Test (FST), and Morris Water Maze (MWM, performed from day 23) tests were applied to all animals. Fluid intake consumption of the rats was measured daily, weight gain and blood glucose were measured weekly. After 31 days of treatment, the rats were sacrificed and PFC tissue was removed for biochemical, histopathological and immunohistochemical analyses. In HFCS group, fluid consumption, blood glucose, malondialdehyde (MDA) levels, degenerative neuron count and choline acetyltransferase (ChAT) expression were significantly increased; superoxide dismutase (SOD), catalase (CAT) enzyme activity and brain-derived neurotrophic factor (BDNF) expression were significantly decreased. In addition, the time spent in the enclosed arm in EPM was increased, the immobility time in FST was, and the time spent in the target quadrant in MWM was significantly decreased. Vitamin D treatment reversed all these parameters. In conclusion, HFCS caused an increase in the number of degenerative neurons in the PFC, disrupted cholinergic activity and negatively affected learning-memory functions. Vitamin D, decreased the number of degenerative neurons, increased cholinergic activity and positively affected learning and memory performance. BRIEF SYNOPSIS: In this study, prefrontal cortex damage was investigated in adolescent rats fed high fructose corn syrup. The effect of vitamin D on prefrontal cortex damage was evaluated.

Diabetes mellitus is a metabolic disorder characterized by high blood sugar levels. In recent years, T2DM has become a worldwide health issue due to an increase in incidence and prevalence. Diabetic kidney disease (DKD) is one of the devastating consequences of diabetes, especially owing to T2DM and the key clinical manifestation of DKD is weakened renal function and progressive proteinuria. DKD affects approximately 1/3rd of patients with diabetes mellitus, and T2DM is the predominant cause of end-stage kidney disease (ESKD). Several lines of studies have observed the association between vitamin D deficiency and the progression and etiology of type II diabetes mellitus. Emerging experimental evidence has shown that T2DM is associated with various kinds of kidney diseases. Recent evidence has also shown that an alteration in VDR (vitamin D receptor) signaling in podocytes leads to DKD. The present review aims to examine vitamin D metabolism and its correlation with T2DM. Furthermore, we discuss the potential role of vitamin D and VDR in diabetic kidney disease.

Ultraviolet (UV) radiation has both harmful and beneficial effects on human skin and health. It causes skin damage, aging, and cancer; however, it is also a primary source of vitamin D. Additionally, UV radiation can impact energy metabolism and has protective effects on several cardiovascular and metabolic disorders in mice and humans. However, the mechanisms of UV protection against these diseases have not been clearly identified.

This review summarizes the systemic effects of UV radiation on hypertension and several metabolic diseases such as obesity, diabetes, and nonalcoholic fatty liver disease (NAFLD) in mice, and we also consider the mechanisms of action of the related regulators nitric oxide (NO) and vitamin D.

UV exposure can lower blood pressure and prevent the development of cardiovascular diseases and metabolic disorders, such as metabolic syndrome, obesity, and type 2 diabetes, primarily through mechanisms that depend on UV-induced NO. UV radiation may also effectively delay the onset of type 1 diabetes through mechanisms that rely on UV-induced vitamin D. UV-induced NO and vitamin D play roles in preventing and slowing the progression of NAFLD.

UV exposure is a promising nonpharmacological intervention for cardiovascular and metabolic disorders. NO and vitamin D may play a crucial role in mediating these effects. However, further investigations are required to elucidate the exact mechanisms and determine the optimal dosage and exposure duration of UV radiation.

The association of vitamin D deficiency, which is prevalent in type 2 diabetes mellitus (T2DM), with liver disease and related mortality has not been quantified. Our study aimed to (1) investigate whether there is a synergistic association of vitamin D deficiency and T2DM with liver-related outcomes and (2) explore whether high 25-hydroxyvitamin D [25(OH)D] concentrations are associated with a lower risk of liver-related outcomes in T2DM.

Leveraging the data from UK Biobank, we conducted 2 studies: study I assessed the joint associations of vitamin D deficiency [25(OH)D <50 nmol/L] and T2DM with liver-related outcomes among 439,276 participants, and study II explored the associations of vitamin D status with liver-related outcomes among 21,519 individuals with T2DM. Baseline T2DM was identified through medication, laboratory test, and electronic health-related records. Serum 25(OH)D was measured by direct competitive chemiluminescent immunoassay. Liver-related outcomes included 6 liver disease end points and mortality by overall liver disease, chronic liver disease, and severe liver disease.

During an average follow-up duration of 11.6 years, we observed a significant positive additive interaction effect (all synergy index>1.0) of T2DM and vitamin D deficiency on the risk of liver-related outcomes. Compared with participants without either T2DM or vitamin D deficiency, the multivariable-adjusted HRs of overall liver diseases were 1.29 for participants without T2DM but with vitamin D deficiency, 1.73 for participants with T2DM but without vitamin D deficiency, and 2.19 for participants with both T2DM and vitamin D deficiency. In individuals with T2DM, we observed that participants without vitamin D deficiency were inversely associated with incident liver disease and related mortality (multivariable-adjusted HRs 0.41-0.81) when compared with individuals with vitamin D deficiency.

There are positive synergistic associations of vitamin D deficiency and T2DM with liver-related outcomes. Inverse associations between serum 25(OH)D concentrations and liver-related outcomes were observed in individuals with T2DM.

Serum vitamin D (VitD) levels have been inversely related with metabolic syndrome (MetS), although the direct impact of VitD is still debated. This study examined 879 subjects of working age from an obesity and occupational clinic in Milan, Italy. Among these participants, 316 had MetS, while 563 did not. A multiple logistic regression analysis was conducted to determine the odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) for MetS in relation to serum VitD levels. After controlling for age, sex, leisure time physical activity, and body mass index (BMI), individuals with VitD levels between 20 and 29.9 ng/dL, or at least 30 ng/dL, had approximately half the risk of developing MetS (OR: 0.52, 95% CI: 0.32-0.86 and OR: 0.50, 95% CI: 0.25-0.99, respectively) compared to those with VitD levels below 10 ng/dL. This study presents further evidence of the beneficial effect of adequate VitD levels on the risk of MetS in a population of overweight/obese workers, even after adjusting for BMI. This study supports the importance of testing for and-if required-supplementing VitD in individuals with metabolic risk factors.

Prior research has established noteworthy correlations between inadequate glycemic management and a multitude of problems in individuals diagnosed with diabetes mellitus (DM).

This is a cross-sectional retrospective study that was conducted at the Jeddah Center for the Care of Diabetes and Blood Pressure Patients, Jeddah, Kingdom of Saudi Arabia. The medical records of patients diagnosed with DM between 2015 and 2022 were identified and reviewed for the purpose of this study. Pearson correlation coefficient was used to examine the correlation between glycated haemoglobin (HbA1c) and vitamin D levels. Multiple linear regression analysis was applied to identify the association between HbA1c and vitamin D levels.

A total of 152 patients were included in this study. The mean HbA1c level for the patients in this study was 8.2% (SD: 1.7). The median vitamin D level for the patients was 20.9 ng/ml (interquartile range (IQR): 13-30.4). More than half of the patients (n= 92; 60.5%) were found to have vitamin D insufficiency. Pearson correlation coefficient identified that there is an inverse correlation between the level of HbA1c and vitamin D level (r= -0.21 (95%CI -0.36 to -0.06; p-value= 0.007). Multiple linear regression analysis (adjusting for age and type of DM) identified that poor glycaemic control has a negative association with vitamin D level (regression coefficient (B) = -0.027; 95%CI -0.053 to - 0.001; p-value= 0.039).

Poor glycaemic control is associated with vitamin D deficiency in DM patients. It is recommended that patients with DM adhere to their medications and maintain a healthy lifestyle in order to manage their condition. This will improve their overall health, specifically their vitamin D status.

Vitamin D is among the vitamins necessary for both adults' and children's health. It plays a significant role in calcium absorption, the immune system, cell proliferation and differentiation, bone protection, skeletal health, rickets, muscle health, heart health, disease pathogenesis and severity, glucose metabolism, glucose intolerance, varying insulin secretion, and diabetes. Because the 25-hydroxyvitamin D (25OHD) test, which is used to measure vitamin D is expensive and may not be covered in healthcare benefits in many countries, this study aims to predict vitamin D deficiency in diabetic patients. The prediction method is based on data mining techniques combined with feature selection by using historical electronic health records. The results were compared with a filter-based feature selection algorithm, namely relief-F. Non-valuable features were eliminated effectively with the relief-F feature selection method without any performance loss in classification. The performances of the methods were evaluated using classification accuracy (ACC), sensitivity, specificity, F1-score, precision, kappa results, and receiver operating characteristic (ROC) curves. The analyses have been conducted on a vitamin D dataset of diabetic patients and the results show that the highest classification accuracy of 97.044% was obtained for the support vector machines (SVM) model using radial kernel that contains 18 features.

Both 25-autoimmunity and(25(OH)D: calcifediol) and its active form, 1,25-dihydroxyvitamin D (1,25(OH)2D: calcitriol), play critical roles in protecting humans from invasive pathogens, reducing risks of autoimmunity, and maintaining health. Conversely, low 25(OH)D status increases susceptibility to infections and developing autoimmunity. This systematic review examines vitamin D's mechanisms and effects on enhancing innate and acquired immunity against microbes and preventing autoimmunity. The study evaluated the quality of evidence regarding biology, physiology, and aspects of human health on vitamin D related to infections and autoimmunity in peer-reviewed journal articles published in English. The search and analyses followed PRISMA guidelines. Data strongly suggested that maintaining serum 25(OH)D concentrations of more than 50 ng/mL is associated with significant risk reduction from viral and bacterial infections, sepsis, and autoimmunity. Most adequately powered, well-designed, randomized controlled trials with sufficient duration supported substantial benefits of vitamin D. Virtually all studies that failed to conclude benefits or were ambiguous had major study design errors. Treatment of vitamin D deficiency costs less than 0.01% of the cost of investigation of worsening comorbidities associated with hypovitaminosis D. Despite cost-benefits, the prevalence of vitamin D deficiency remains high worldwide. This was clear among those who died from COVID-19 in 2020/21-most had severe vitamin D deficiency. Yet, the lack of direction from health agencies and insurance companies on using vitamin D as an adjunct therapy is astonishing. Data confirmed that keeping an individual's serum 25(OH)D concentrations above 50 ng/mL (125 nmol/L) (and above 40 ng/mL in the population) reduces risks from community outbreaks, sepsis, and autoimmune disorders. Maintaining such concentrations in 97.5% of people is achievable through daily safe sun exposure (except in countries far from the equator during winter) or taking between 5000 and 8000 IU vitamin D supplements daily (average dose, for non-obese adults, ~70 to 90 IU/kg body weight). Those with gastrointestinal malabsorption, obesity, or on medications that increase the catabolism of vitamin D and a few other specific disorders require much higher intake. This systematic review evaluates non-classical actions of vitamin D, with particular emphasis on infection and autoimmunity related to the immune system.

To compare and assess the efficacy of two vitamin D delivery systems (oil-based and microencapsulated) on 25-hydroxy-vitamin D (25(OH)D) levels, body mass index (BMI) and insulin resistance (IR) in women with established polycystic ovary syndrome (PCOS) and vitamin D deficiency.

A monocentric, retrospective study was conducted, using the data of 70 female patients, who visited the endocrinology department of the "Dr. Shterev" Hospital, Sofia, Bulgaria between May 2020 and September 2020. The patients were divided into two groups according to the type of vitamin D3 supplementation: either a microencapsulated liposomal form (n=35), or a conventional oil-based form (n=35). The following clinical measures were analysed and compared: BMI, serum levels of 25(OH)D, fasting plasma glucose levels, fasting immunoreactive insulin (IRI), homeostatic model assessment (HOMA) index, levels of antimullerian hormone (AMH) II generation, and testosterone. In all selected patients, these measurements were performed at baseline and 3 months after initiation of vitamin D supplementation.

Significantly increased serum levels of 25(OH)D were observed in patients supplemented with the microencapsulated form of vitamin D3 in the third month from the beginning of therapy, compared with the control group (p=0.003). In the microencapsulated vitamin D group, there was a decrease in IRI serum levels (p=0.023), HOMA-IR (p=0.021), serum AMH (p=0.010) and testosterone levels (p=0.006). The fasting plasma glucose levels did not change significantly.

The results of our study show that the patients supplemented with a microencapsulated form of vitamin D3 achieved faster compensation of 25(OH)D levels, which in turn, under equal conditions, led to significant improvement in the metabolic profile, in particular insulin sensitivity.

Vitamin D deficiency (VDD) is commonly observed in people with late-stage chronic kidney disease (CKD) and end-stage renal disease; it has also been associated with the progression of kidney disease. We hypothesized that VDD played a role in early-stage chronic kidney disease as well. Thus, this cross-sectional study aimed to evaluate the association between serum 25-hydroxyvitamin D concentration and CKD stages 1 through 3 (early-stage CKD) in a relatively healthy population in China. A total of 3142 Chinese individuals were included in this cross-sectional study. VDD was observed in 108 (5.6%) males and 307 (25.33%) females. We found a significant inverse association between serum 25(OH)D concentration with CKD stages in both sexes. Furthermore, VDD was associated with CKD stages 1 through 3 in males (adjusted odds ratio, 15.84; 95% confidence interval, 7.85-31.98; P < .001), but not in females. Vitamin D status should be evaluated in people who are newly diagnosed with CKD stages 1 through 3 or decreased estimated glomerular filtration rate, especially in males.

The association between vitamin D deficiency and lipid profiles in adults with overweight or obesity remains unclear and inconsistent. The aim of our study was to determine the relationship between lipid profiles and vitamin D deficiency in the overweight and obese adults.

Four databases, including PubMed, the Web of Science, EMBASE and the Cochrane Library, were used to identify all studies on vitamin D status and lipid levels, including the serum levels of triglycerides (TGs), total cholesterol (TC), low-density lipoprotein cholesterol (LDL), and high-density lipoprotein cholesterol (HDL). The Weighted mean difference (WMD) with 95% confidence intervals (CIs) using random-effects models was used to assess the association between the lipid profile and vitamin D deficiency.

Twenty-one articles that included a total of 7952 adults with overweight or obesity (BMI ≥ 25 kg/m2) were included. The overall results revealed that compared with the controls, individuals with vitamin D deficiency showed higher levels of TG (WMD = 15.01; 95%CI, 2.51-27.52) and TC (WMD = 8.61; 95%CI, 1.31-15.92). Moreover, vitamin D deficiency was related to an increased level of LDL (WMD = 6.12; 95%CI, 0.02-12.23). HDL level was inversely associated with the vitamin D deficiency status (WMD = -2.57; 95%CI, -4.26, -0.88).

Among the adults with overweight or obesity, the vitamin D deficient group displayed impaired lipid profiles, including increased TG, TC and LDL levels and reduced HDL level.

The relationship between vitamin D deficiency and sensitivity to thyroid hormones was unclear. We aimed to explore the association of 25-hydroxyvitamin D (25(OH)D) levels with thyroid hormone sensitivity in euthyroid adults. A total of 3143 subjects were included. The serum 25(OH)D, free thyroxine (FT3), free thyrotropin (FT4), thyroid-stimulating hormone (TSH), and other clinical variables were measured. Vitamin D deficiency was defined as 25(OH)D < 20 ng/mL. Thyroid feedback quantile-based index (TFQI), parametric thyroid feedback quantile-based index (PTFQI), thyroid-stimulating hormone index (TSHI), thyrotrophic thyroxine resistance index (TT4RI), and FT3/FT4 were calculated to assess thyroid hormone sensitivity. Results showed that 58.8% of the participants had vitamin D deficiency. They had significantly higher levels of triglyceride, insulin, FT3, FT4, TSH, TFQI, PTFQI, TSHI, and TT4RI and lower levels of high-density lipoprotein cholesterol than those with sufficient vitamin D (all p < 0.05). Logistic regression analysis showed that the risk of impaired sensitivity to thyroid hormones evaluated by TFIQ, PTFQI, TSHI, and TT4RI increased by 68% (OR: 1.68; 95%CI: 1.45-1.95; and p < 0.001), 70% (OR: 1.70; 95%CI: 1.46-1.97; and p < 0.001), 66% (OR: 1.66; 95%CI: 1.43-1.92; and p < 0.001), and 50% (OR: 1.50; 95%CI: 1.30-1.74; and p < 0.001), respectively, in participants with vitamin D deficiency compared with those with sufficient vitamin D after adjusting for multiple confounders. In conclusion, in euthyroid populations, vitamin D deficiency was associated with impaired sensitivity to thyroid hormones.

Diabetic foot ulcer (DFU) is a form of chronic wound which becomes a serious complication in diabetes mellitus (DM). Recently, the role of vitamin D on T cell-mediated immunity, pancreatic insulin secretion, and its mechanism on cell growth and healing processes have been reported. This study aims to compare the vitamin D level of DM patients with DFU and without DFU to assess the duration and severity of DFU and its correlation with vitamin D levels. The sociodemographic characteristics and DFU duration were documented. The severity was examined in accordance with PEDIS classification. 25-hydroxyvitamin D (25[OH]D) was analysed using in-vitro chemiluminescent immunoassay (CLIA). Statistical analysis was performed and the P-value <.05 was considered as statistically significant. The vitamin D levels in DM patients with and without DFU were 8.90 ng/mL (6.52-10.90) and 16.25 ng/mL (13-19.59), respectively, with P < .001. There was no correlation between the duration of DFU and DFU severity by PEDIS score with vitamin D levels. Vitamin D levels in DM patients with DFU are lower than those in patients without DFU. However, there was insufficient evidence to conclude that there is no correlation between the DFU duration and DFU severity by PEDIS score with vitamin D levels.