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Endogenous ligands for alicarboxylic acid receptors are important metabolic intermediates that play a significant role in regulating body energy and maintaining homeostasis. However, the molecular mechanism of alicarboxylate ligand-mediated counterpart receptors is currently unclear. We resolve the active state structure of HCA2-niacin, and the structural analysis explains the mechanism of niacin selectivity in the alicarboxylic acid receptors family. Homology modeling, molecular dynamics simulation and mutagenesis experiments reveal different ligand recognition modes and activation mechanisms of the alicarboxylic acid receptors, analyze the flexibility of the binding pocket and elucidate the important role of disulfide bonds on receptor activation and ligand binding. These more detailed molecular mechanisms further elucidate the relevant mechanisms of human metabolism and provide key clues for subsequent drug development of alicarboxylic acid receptors.

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The role of redox mediators in improving electron transport from electrochemically active bacteria to the anode is crucial for enhanced bioelectricity output from microbial fuel cells (MFCs), which makes the selection of an ideal mediator very important. This study aims at exploring a new redox mediator niacin (vit B3) for enhanced bioelectricity generation in MFC while treating distillery wastewater through facile modification of anode electrode by niacin doping (MFC-NME) and simple application of niacin to the anolyte (MFC-NAA). Fourier transform infrared (FTIR) spectroscopy, scanning electron microscopy (SEM), and X-ray diffraction (XRD) of NME confirmed the effective adsorption of niacin onto the carbon felt surface. Notably, MFC-NME exhibited a significantly higher power density (PD) of 6.36 W/m3 compared to MFC-NAA (4.59 W/m3) and control MFC (3.49W/m3). The charge transfer resistance (RCT) in MFC-NME (1.73 Ω) and MFC-NAA (2.06 Ω) were lowered by more than half than that in control MFC (4.33 Ω), which underscores the efficacy of niacin as a redox mediator. SEM analysis revealed improved bacterial attachment over the bioanode in the MFC-NME as compared to that of MFC-NAA and control MFC. Removal of chemical oxygen demand (COD) was higher in MFC-NAA (85%) and MFC-NME (80%) than in control MFC (73%) suggesting that niacin in the anolyte supported greater organic matter removal due to enriched microbial activity. Niacin used in anode modification shows great potential for improved electron transfer and enhanced bioelectricity production and supports greater wastewater treatment performance. The modified bioanode NME exhibits excellent stability.

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A conventional questionnaire-based assessment of acetic acid intake is based on the intake of seasonings such as mayonnaise, which could thereby lead to an underestimation. We here determine the relationships of acetic acid intake with nutrient intake estimated using a food recording app (Asken) based on meal recipes. A total of 141 individuals (48 men and 93 women) used the app for at least 7 days per month. The mean daily intake of acetic acid was 0.16 ± 0.19 g and the mean frequency of acetic acid intake was 2.77 ± 1.66 days per week. A multivariate regression analysis adjusted for age, sex, BMI, and energy intake revealed that the amount of acetic acid consumed was significantly and positively associated with the intake of protein (11.9 (5.1, 18.6), p < 0.001), cholesterol (80.7 (4.5, 156.9), p = 0.04), and all vitamins except vitamin K. The frequency of acetic acid intake was significantly and positively associated with protein (1.04 (0.20, 1.87), p = 0.015), vitamin B1 (0.3 (0.02,0.5), p = 0.031), niacin (0.5 (0.04,1.0), p = 0.032), and vitamin B12 (0.4 (0.1,0.7), p = 0.002) intake, suggesting that individuals who frequently consume acetic acid tend to consume more protein and some vitamins. Thus, the amount and frequency of acetic acid may reflect protein and vitamin intake.

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Objective: The relationship between dietary niacin intake (DNI) and mortality rates among patients afflicted with chronic kidney disease (CKD) is a subject of debate. Utilizing data derived from the National Health and Nutrition Examination Survey (NHANES), this study adopts a retrospective cohort design with an aim to investigate the association in the American adult patients with CKD. Methods: A cohort study was conducted in the National Health and Nutrition Examination Survey (NHANES) between 2009 and 2018 that enrolled 6,191 CKD patients aged 20 years and above. We collected data on mortality through 31 December 2018. DNI was measured using a 24-h recall method. The relationship between DNI levels and mortality from all causes and cardiovascular causes was analyzed using weighted Cox proportional hazards models. The Kaplan-Meier (K-M) survival curve was plotted to illustrate these associations. Results: Following a median monitoring period of 85 months, it was observed that 2,419 individuals (33.08%) succumbed to all causes, whereas cardiovascular-related deaths were recorded for 746 participants (10.45%). When controlling for confounders, an inverse relationship was established between DNI and mortality rates. Specifically, a marginal increase of 1 mg/day in DNI corresponded to a reduced Hazard Ratios (HRs) of 0.993 (0.987, 0.999; p = 0.027) for all-cause mortality and 0.980 (0.969, 0.991; p < 0.001) for cardiovascular mortality. A further stratified analysis by quartiles of DNI, with the lowest quartile serving as the reference, revealed that the highest quartile was associated with HRs of 0.820 (0.697, 0.966) for all-cause mortality and 0.663 (0.465, 0.944) for cardiovascular mortality, both displaying a significant trend (p < 0.001). However, a subdivision of CKD patients by age showed that the protective effects of higher DNI were only confined to individuals aged 60 years and above but not to those under 60 years of age. Conclusion: A negative correlation between DNI and mortality due to all causes and cardiovascular issues among CKD patients aged 60 and above was revealed based on the datasets; however, this association was not observed in younger individuals under 60. Consequently, enhancing DNI might serve as a beneficial therapeutic strategy specifically for the older CKD demographic.

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BACKGROUND: Chronic kidney disease (CKD), which has become a global public health issue, is associated with mitochondrial dysfunction. Niacin is a necessary coenzyme for mitochondrial energy metabolism. However, the association between dietary niacin intake and CKD remains uncertain. This study aimed to investigate the association between dietary niacin intake and CKD in American adults. METHODS: This is a cross-sectional study. 25,608 individuals aged ≥20 years from the National Health and Nutrition Examination Survey from 2007 to 2018 were involved.Dietary niacin intake was estimated based on 24-hour dietary recalls conducted by trained personnel. CKD was determined by an estimated glomerular filtration rate (eGFR) (<60 ml/min/1.73 m2) or a urinary albumin-to-creatinine ratio (ACR) (≥30mg/g). The association between dietary niacin intake and CKD was investigated using multivariable logistic regression analysis. RESULTS: Of 25,608 participants, 17.14% (4388/25,608) had CKD. Compared to individuals with lower niacin intake (quartile [Q]1, ≤15.30 mg/day), those with higher niacin intake in Q2 (15.31-22.07 mg/day), Q3 (22.08-31.09 mg/day), and Q4 (≥31.10 mg/day) exhibited adjusted odds ratios for CKD of 0.89 (95% confidence interval [CI]:0.81-0.99, p = 0.024), 0.83 (95% CI:0.75-0 .92, p < 0 .001), and 0.83 (95% CI:0.75-0.93, p = 0.001) respectively. The relationship between dietary niacin intake and CKD among U.S. adults follows an L-shaped pattern, with an inflection point at approximately 28.04 mg/day. CONCLUSIONS: These results suggest an L-shaped association between dietary niacin intake and CKD. Individuals with low dietary niacin intake levels should be alert to the risk of CKD.

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The probiotic Bacillus subtilis 29784 (Bs29784) sustains chicken's intestinal health, enhancing animal resilience and performance through the production of the bioactive metabolites hypoxanthine (HPX), niacin (NIA), and pantothenate (PTH). Here, using enterocyte in vitro models, we determine the functional link between these metabolites and the three pillars of intestinal resilience: immune response, intestinal barrier, and microbiota. We evaluated in vitro the capacity of Bs29784 vegetative cells, spores, and metabolites to modulate global immune regulators (using HT-29-NF-κB and HT-29-AP-1 reporter cells), intestinal integrity (HT-29-MUC2 reporter cells and Caco-2 cells), and cytokine production (Caco-2 cells). Finally, we simulated intestinal fermentations using chicken's intestinal contents as inocula to determine the effect of Bs29784 metabolites on the microbiota and their fermentation profile. Bs29784 vegetative cells reduced the inflammatory response more effectively than spores, indicating that their benefit is linked to metabolic activity. To assess this hypothesis, we studied Bs29784 metabolites individually. The results showed that each metabolite had different beneficial effects. PTH and NIA reduced the activation of the pro-inflammatory pathways AP-1 and NF-κB. HPX upregulated mucin production by enhancing MUC2 expression. HPX, NIA, and PTH increased cell proliferation. PTH and HPX increased epithelial resilience to an inflammatory challenge by limiting permeability increase. In cecal fermentations, NIA increased acetate, HPX increased butyrate, whereas PTH increased acetate, butyrate, and propionate. In ileal fermentations, PTH increased butyrate. All molecules modulated microbiota, explaining the different fermentation patterns. Altogether, we show that Bs29784 influences intestinal health by acting on the three lines of resilience via its secreted metabolites. IMPORTANCE: Probiotics provide beneficial metabolites to its host. Here, we describe the mode of action of a commonly used probiotic in poultry, Bs29784. By using in vitro cellular techniques and simulated chickens' intestinal model, we show the functional link between Bs29784 metabolites and the three lines of animal resilience. Indeed, both Bs29784 vegetative cells and its metabolites stimulate cellular anti-inflammatory responses, strengthen intestinal barrier, and positively modulate microbiota composition and fermentative profile. Taken together, these results strengthen our understanding of the effect of Bs29784 on its host and explain, at least partly, its positive effects on animal health, resilience, and performance.

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Objective: This investigation aims to elucidate the correlations between dietary intakes of vitamin E, B6, and niacin and the incidence of cataracts, utilizing the comprehensive NHANES 2005-2008 dataset to affirm the prophylactic roles of these nutrients against cataract formation. Methods: Using data from the NHANES 2005-2008 cycles, this analysis concentrated on 7,247 subjects after exclusion based on incomplete dietary or cataract data. The identification of cataracts was determined through participants' self-reported ophthalmic surgical history. Nutritional intake was gauged using the automated multiple pass method, and the data were analyzed using logistic and quantile regression analyses to investigate the relationship between vitamin consumption and cataract prevalence. Results: Our analysis identified significant inverse associations between the intake of vitamins E, B6, and niacin and the risk of cataract development. Specifically, higher intakes of vitamin B6 (OR = 0.85, 95% CI = 0.76-0.96, p = 0.0073) and niacin (OR = 0.98, 95% CI = 0.97-1.00, p = 0.0067) in the top quartile were significantly associated with a reduced likelihood of cataract occurrence. Vitamin E intake showed a consistent reduction in cataract risk across different intake levels (OR = 0.96, 95% CI = 0.94-0.99, p = 0.0087), demonstrating a nonlinear inverse correlation. Conclusion: The outcomes indicate that elevated consumption of vitamin B6 and niacin, in conjunction with regular vitamin E intake, may have the potential to delay or prevent cataract genesis. These results suggest a novel nutritional strategy for cataract prevention and management, advocating that focused nutrient supplementation could be instrumental in preserving eye health and reducing the risk of cataracts. Further research is recommended to validate these findings and establish optimal dosages for maximum benefit.

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Myopathy is a common manifestation in mitochondrial disorders, but the pathomechanisms are still insufficiently studied in children. Here, we report a severe, progressive mitochondrial myopathy in a four-year-old child, who died at eight years. He developed progressive loss of muscle strength with nocturnal hypoventilation and dilated cardiomyopathy. Skeletal muscle showed ragged red fibers and severe combined respiratory chain deficiency. Mitochondrial DNA sequencing revealed a novel m.5670A>G mutation in mitochondrial tRNAAsn (MTTN) with 88 % heteroplasmy in muscle. The proband also had systemic NAD+ deficiency but rescuing this with the NAD+ precursor niacin did not stop disease progression. Targeted metabolomics revealed an overall shift of metabolism towards controls after niacin supplementation, with normalized tryptophan metabolites and lipid-metabolic markers, but most amino acids did not respond to niacin therapy. To conclude, we report a new MTTN mutation, secondary NAD+ deficiency in childhood-onset mitochondrial myopathy with metabolic but meager clinical response to niacin supplementation.

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Niacin was found in the lysolecithin model of multiple sclerosis (MS) to promote the phagocytic clearance of debris and enhance remyelination. Lysolecithin lesions have prominent microglia/macrophages but lack lymphocytes that populate plaques of MS or its experimental autoimmune encephalomyelitis (EAE) model. Thus, the current study assessed the efficacy of niacin in EAE. We found that niacin inconsistently affects EAE clinical score, and largely does not ameliorate neuropathology. In culture, niacin enhances phagocytosis by macrophages, but does not reduce T cell proliferation. We suggest that studies of niacin for potential remyelination in MS should include a therapeutic that targets adaptive immunity.

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Objective: This study aims to explore the association between niacin intake and stroke within a diverse, multi-ethnic population. Methods: A stringent set of inclusion and exclusion criteria led to the enrollment of 39,721 participants from the National Health and Nutrition Examination Survey (NHANES). Two interviews were conducted to recall dietary intake, and the USDA's Food and Nutrient Database for Dietary Studies (FNDDS) was utilized to calculate niacin intake based on dietary recall results. Weighted multivariate logistic regression was employed to examine the correlation between niacin and stroke, with a simultaneous exploration of potential nonlinear relationships using restricted cubic spline (RCS) regression. Results: A comprehensive analysis of baseline data revealed that patients with stroke history had lower niacin intake levels. Both RCS analysis and multivariate logistic regression indicated a negative nonlinear association between niacin intake and stroke. The dose-response relationship exhibited a non-linear pattern within the range of dietary niacin intake. Prior to the inflection point (21.8 mg) in the non-linear correlation between niacin intake and stroke risk, there exists a marked decline in the risk of stroke as niacin intake increases. Following the inflection point, the deceleration in the decreasing trend of stroke risk with increasing niacin intake becomes evident. The inflection points exhibit variations across diverse populations. Conclusion: This investigation establishes a negative nonlinear association between niacin intake and stroke in the broader American population.

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Parkinson's disease (PD) is one of the most common neurodegenerative diseases and involves various pathogenic mechanisms, including oxidative stress and neuroinflammation. Niacin, an important cofactor in mitochondrial energy metabolism, may play a key role in the pathogenesis of PD. An in-depth exploration of the relationship between niacin and mitochondrial energy metabolism may provide new targets for the treatment of PD. The present study was designed to examine the association between dietary niacin intake and the risk of PD in US adults. Data from adults aged 40 years and older collected during cycles of the United States (US) National Health and Nutrition Examination Survey (NHANES) from 2005 to 2018 were used. A multiple logistic regression model was used to analyze the relationship between dietary niacin intake and the risk of PD. Further linear tests using restricted cubic splines (RCS) were performed to explore the shape of the dose-response relationship. Subgroup stratification and interaction analyses were conducted according to years of education, marital status, smoking, and hypertension to evaluate the stability of the association between different subgroups. A total of 20,211 participants were included in this study, of which 192 were diagnosed with PD. In the fully adjusted multiple logistic regression model, dietary niacin intake was negatively associated with the risk of PD (OR: 0.77, 95%CI: 0.6-0.99; p = 0.042). In the RCS linear test, the occurrence of PD was negatively correlated with dietary niacin intake (nonlinearity: p = 0.232). In stratified analyses, dietary niacin intake was more strongly associated with PD and acted as an important protective factor in patients with fewer years of education (OR: 0.35, 95%CI: 0.13-0.93), married or cohabitating (OR: 0.71, 95%CI: 0.5-0.99), taking dietary supplements (OR: 0.6, 95%CI: 0.37 0.97), non-smokers (OR: 0.57, 95%CI: 0.39-0.85), those with hypertension (OR: 0.63, 95%CI: 0.63-0.95), coronary artery disease (OR: 0.77, 95%CI: 0.6-1), and stroke (OR: 0.75, 95%CI: 0.88-0.98), but the interaction was not statistically significant in all subgroups. Dietary niacin intake was inversely associated with PD risk in US adults, with a 23% reduction in risk for each 10 mg increase in niacin intake.

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PURPOSE: Benign prostatic hyperplasia (BPH) commonly impacts the quality of life in older men. However, there is lack of research on relationship between dietary niacin intake and the risk of BPH. The purpose of this study was to investigate the relationship between dietary niacin intake and the risk of BPH. METHODS: Data from the NHANES spanning 2003 to 2008 were utilized. BPH was determined using a self-report questionnaire, while dietary niacin intake was calculated based on the mean of two distinct diet interviews. Multivariate logistic regressions were performed to explore the association, supplemented with restricted cubic splines and subgroup analysis. RESULTS: A total of 700 males were enrolled, of which 653 men had BPH. After adjusting for all covariates, a high dietary intake of niacin was associated with an increased risk of BPH (OR: 1.04; 95%CI: 1.01-1.07). Furthermore, when the lowest dietary niacin intake is used as the reference, the highest tertile is associated with an increased risk of BPH (OR: 2.34, 95% CI: 1.24-4,42). Restricted cubic splines demonstrated a positive correlation between dietary niacin intake and BPH risk. CONCLUSIONS: The study results demonstrated a positive association between dietary niacin intake and the risk of BPH in elderly men in the US. These findings underscore the importance of systematic assessment before supplementing micronutrients in elderly men.

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Background: NAXE-encephalopathy or early-onset progressive encephalopathy with brain edema and/or leukoencephalopathy-1 (PEBEL-1) and NAXD-encephalopathy (PEBEL-2) have been described recently as mitochondrial disorders causing psychomotor regression, hypotonia, ataxia, quadriparesis, ophthalmoparesis, respiratory insufficiency, encephalopathy, and seizures with the onset being usually within the first three years of life. It usually leads to rapid disease progression and death in early childhood. Anecdotal reports suggest that niacin, through its role in nicotinamide adenine dinucleotinde (NAD) de novo synthesis, corrects biochemical derangement, and slows down disease progression. Reports so far have supported this observation. Methods: We describe a patient with a confirmed PEBEL-1 diagnosis and report his clinical response to niacin therapy. Moreover, we systematically searched the literature for PEBEL-1 and PEBEL-2 patients treated with niacin and details about response to treatment and clinical data were reviewed. Furthermore, we are describing off-label use of a COX2 inhibitor to treat niacin-related urticaria in NAXE-encephalopathy. Results: So far, seven patients with PEBEL-1 and PEBEL-2 treated with niacin were reported, and all patients showed a good response for therapy or stabilization of symptoms. We report a patient exhibiting PEBEL-1 with an unfavorable outcome despite showing initial stabilization and receiving the highest dose of niacin reported to date. Niacin therapy failed to halt disease progression or attain stabilization of the disease in this patient. Conclusion: Despite previous positive results for niacin supplementation in patients with PEBEL-1 and PEBEL-2, this is the first report of a patient with PEBEL-1 who deteriorated to fatal outcome despite being started on the highest dose of niacin therapy reported to date.

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Niacin (Vitamin B3) plays a crucial role as a vitamin in cellular energy production, metabolism, and DNA repair. A severe deficiency of this vitamin can lead to pellagra, which is characterized by dermatitis, dementia, diarrhoea and eventually death if untreated. A 68-year-old woman with a poor socioeconomic background presented with photosensitive dermatitis, fever, abdominal pain, and diarrhoea. Her urine changed to port wine colour following sun exposure. Porphyria cutanea tarda was excluded in the absence of demonstrable urine spectrophotometry. A diagnosis of pellagra was made, and timely management led to a complete cure. Proper diagnosis and effective treatment of pellagra are imperative as this condition can be life-threatening if left untreated.

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Background: The pathogenesis of pulmonary senescence involves immune system dysregulation, oxidative stress, and mitochondrial dysfunction. The effects on lung function of niacin, an essential coenzyme involved in mitochondrial energy metabolism with known antioxidant properties, are poorly understood. Methods: This cross-sectional study used data from the 2007-2012 National Health and Nutrition Examination Survey, including spirometry data and niacin intake information of 9706 adults. This study investigated various spirometry measures, such as forced expiratory volume in 1 s, forced vital capacity, pulse expiratory flow, (forced expiratory volume in 1 s)/(forced vital capacity)ratio, and predicted forced expiratory volume in 1 s and forced vital capacity percentages. Additionally, a secondary analysis was conducted using Global Initiative for Chronic Obstructive Lung Disease and chronic obstructive pulmonary disease. Foundation Spirometry Grade criteria to assess the relationship between niacin intake, airflow limitation, and obstruction. Multivariate regression models were used to adjust for relevant covariates. Results: The study included 9706 U S. adults (4788 men and 4918 women) with a median age of 46.2 years. After adjusting for relevant factors, a positive correlation was observed between niacin intake and lung function. Compared to the lowest quintile of niacin intake (Q1, ≤14.5 mg/day), individuals in the highest quintile (Q5, >34.5 mg/day) exhibited significant increases in lung function parameters, including forced expiratory volume in 1s (69.84 mL, p = 0.003), pulse expiratory flow (254.48 mL, p < 0.001), (forced expiratory volume in 1 s)/(forced vital capacity)(0.01, p = 0.041), percent predicted forced expiratory volume in 1 s(2.05, p = 0.002), and percent predicted forced vital capacity(1.29, p = 0.042).Subset analyses of individuals with spirometry-defined airflow obstruction showed associations of high niacin intake with significantly improved forced expiratory volume, pulse expiratory flow, and percent predicted pulse expiratory flow and an interaction among race, education, and smoking status with respect to the relationship between niacin intake and lung function parameters. Conclusions: Higher niacin intake was associated with increased measures of lung function. A diet rich in niacin-containing foods may play a role in improving lung health.

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We describe a 28-year-old Caucasian female with vigorexy, who had no previous ocular history. She presented with bilateral gradual painless reduction in vision over the past 3 weeks. She had been taking niacin supplements, averaging 500 mg daily, for 7 years. Fundus examination revealed bilateral CME, which was confirmed by ocular coherence tomography scan. Fundus fluorescein angiography did not reveal any fluid leakage. Niacin supplementation was discontinued, and after 2 months, the CME had completely resolved, and the best corrected visual acuities improved to 1 in both eyes.

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Niacin is a cofactor in many biological reactions related to energy metabolism, redox reactions, DNA repair and longevity. Although it has been considered that increasing energy expenditure increases NAD consumption, little study has directly demonstrated the effect of exercise on niacin nutritional status. We have recently established the niacin insufficient model mice using kynurenine 3-monooxygenase knock out (KMO-/-) mice with niacin-limited diet, which lack the de novo NAD synthesis pathway from tryptophan. To evaluate the effects of chronic endurance exercise on niacin nutritional status, 4 wk old KMO-/- mice were fed 4 or 30 mg/kg nicotinic acid containing diets, and forced to swim in a running water pool every other day for 35 d. The swim-exercised mice fed 4 mg/kg nicotinic acid diet showed lower body weight gain and niacin nutritional markers such as liver and blood NAD, and urine nicotinamide metabolites than the sedentary mice. These animals did not show any difference in the NAD synthesis, NAD salvage and nicotinamide catabolic pathways. Chronic endurance exercise failed to affect any indices in the mice fed the 30 mg/kg nicotinic acid diet. When the diet was exchanged the 4 mg/kg for 30 mg/kg nicotinic acid diet to the mice showed chronic endurance exercise-induced growth retardation, their body weight rapidly increased. These results show that chronic endurance exercise impairs niacin nutritional status in the niacin insufficient mice, and enough niacin intake can prevent this impairment. Our findings also suggest that chronic endurance exercise increases niacin requirement by increase of NAD consumption.

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BACKGROUND: There are contradictory effects regarding the effect of NAD + precursor on glucose metabolism and liver enzymes. In order to obtain a better viewpoint from them, this study aimed to comprehensively investigate the effects of NAD + precursor supplementation on glucose metabolism, C-reactive protein (CRP), and liver enzymes. METHODS: PubMed/MEDLINE, Web of Science, SCOPUS, and Embase databases were searched using standard keywords to identify all controlled trials investigating the glucose metabolism, CRP, and liver enzymes effects of NAD + precursor. Pooled weighted mean difference (WMD) and 95% confidence intervals (95% CI) were achieved by random-effects model analysis for the best estimation of outcomes. RESULTS: Forty-five articles with 9256 participants' were included in this article. The pooled findings showed that NAD + precursor supplementation had a significant increase in glucose (WMD: 2.17 mg/dL, 95% CI: 0.68, 3.66, P = 0.004) and HbA1c (WMD: 0.11, 95% CI: 0.06, 0.16, P < 0.001) as well as a significant decrease in CRP (WMD: -0.93 mg/l, 95% CI -1.47 to -0.40, P < 0.001) compared with control group, and was not statistically significant with respect to insulin and homeostasis model assessment of insulin resistance (HOMA-IR). However, we found no systemic changes in aspartate transaminase (AST), alanine transaminase (ALT), or alkaline phosphatase (ALP) levels after NAD + precursor supplementation. The results of the subgroup analysis showed that the intake of NAD + precursor during the intervention of more than 12 weeks caused a greater increase in the glucose level. Furthermore, Nicotinic acid supplementation (NA) causes a greater increase in glucose and HbA1c levels than nicotinamide (NE) supplementation. CONCLUSIONS: Overall, these findings suggest that NAD + precursor supplementation might have an increase effect on glucose metabolism as well as a decrease in CRP.

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BACKGROUND: Niacin, an established therapeutic for dyslipidemia, is hindered by its propensity to induce significant cutaneous flushing when administered orally in its unmodified state, thereby constraining its clinical utility. OBJECTIVE: This study aimed to fabricate, characterize, and assess the in-vitro and in-vivo effectiveness of niacin-loaded polymeric films (NLPFs) comprised of carboxymethyl tamarind seed polysaccharide. The primary objective was to mitigate the flushing-related side effects associated with oral niacin administration. METHODS: NLPFs were synthesized using the solvent casting method and subsequently subjected to characterization, including assessments of tensile strength, moisture uptake, thickness, and folding endurance. Surface characteristics were analyzed using a surface profiler and scanning electron microscopy (SEM). Potential interactions between niacin and the polysaccharide core were investigated through X-ray diffraction experiments (XRD) and Fourier transform infrared spectroscopy (FTIR). The viscoelastic properties of the films were explored using a Rheometer. In-vitro assessments included drug release studies, swelling behavior assays, and antioxidant assays. In-vivo efficacy was evaluated through skin permeation assays, skin irritation assays, and histopathological analyses. RESULTS: NLPFs exhibited a smooth texture with favorable tensile strength and moisture absorption capabilities. Niacin demonstrated interaction with the polysaccharide core, rendering the films amorphous. The films displayed slow and sustained drug release, exceptional antioxidant properties, optimal swelling behavior, and viscoelastic characteristics. Furthermore, the films exhibited biocompatibility and non-toxicity towards skin cells. CONCLUSION: NLPFs emerged as promising carrier systems for the therapeutic transdermal delivery of niacin, effectively mitigating its flushing-associated adverse effects.

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PURPOSE: Niacin (nicotinic acid), known for its lipid-modifying effects, has been explored for its potential anti-inflammatory properties and potential to affect adipokines secretion from adipose tissue. The aim of this systematic review and meta-analysis was to assess the effects of niacin on inflammatory markers and adipokines. METHODS: A comprehensive search was conducted across five databases: PubMed, Scopus, Cochrane Library, Embase, and ISI Web of Science. Randomized controlled trials exploring the effects of niacin on inflammatory markers (CRP, IL-6, TNF-α) and adipokines (Adiponectin, Leptin) were included. Pooled effect sizes were analysed using a random-effects model, and additional procedures including subgroup analyses, sensitivity analysis and dose-response analysis were also performed. RESULTS: From an initial 1279 articles, fifteen randomized controlled trials (RCTs) were included. Niacin administration demonstrated a notable reduction in CRP levels (SMD: -0.88, 95% CI: -1.46 to -0.30, p = 0.003). Subgroup analyses confirmed CRP reductions in trials with intervention durations ≤ 24 weeks, doses ≤ 1000 mg/day, and elevated baseline CRP levels (> 3 mg/l). The meta-analysis of IL-6 and TNF-α revealed significant TNF-α reductions, while IL-6 reduction did not reach statistical significance. Niacin administration also substantially elevated Adiponectin (SMD: 3.52, 95% CI: 0.95 to 6.1, p = 0.007) and Leptin (SMD: 1.90, 95% CI: 0.03 to 3.77, p = 0.04) levels. CONCLUSION: Niacin treatment is associated with significant reductions in CRP and TNF-α levels, suggesting potential anti-inflammatory effects. Additionally, niacin positively influences adipokines, increasing Adiponectin and Leptin levels. These findings provide insights for future research and clinical applications targeting inflammation and metabolic dysregulation.

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