Role Of B12 Research Articles

Impact of vitamin B12 on the reproductive health of women with sickle cell disease: a narrative review.

Sickle cell disease (SCD) poses an increased risk of infertility, pregnancy complications and maternal and perinatal mortality among women of reproductive age. This risk is particularly higher for women in sub-Saharan Africa, where the disease burden is highest and access to comprehensive health care is limited, as well as in other countries with a high SCD prevalence due to migration. Disease modifying treatments for SCD could directly and indirectly harm the ovaries, potentially compromising quality and quantity of existing oocytes. Therefore, it is essential to explore alternative interventions, such as nutritional modifications that are less harmful and cost-effective in order to improve reproductive outcomes, and enhance the overall well-being of both mother and child in this population. Maintaining optimal levels of B12 may possibly provide benefits to the ovaries and pregnancy by decreasing homocysteine levels, increasing nitric oxide (NO) bioavailability, and promoting antioxidant and anti-inflammatory activities. Individuals living with SCD are more susceptible to vitamin B12 (B12) deficiency. However, there is a lack of clinical data investigating the relationship between systemic levels of B12, its supplementation, and reproductive outcome measures in SCD women. Therefore, this review aims to examine the current evidence regarding the impact of SCD on female reproductive health and the role of B12 in the reproductive biology of women living with SCD.

Structural Analyses of CrtJ and Its B12-Binding Co-Regulators SAerR and LAerR from the Purple Photosynthetic Bacterium Rhodobacter capsulatus.

Among purple photosynthetic bacteria, the transcription factor CrtJ is a major regulator of photosystem gene expression. Depending on growing conditions, CrtJ can function as an aerobic repressor or an anaerobic activator of photosystem genes. Recently, CrtJ’s activity was shown to be modulated by two size variants of a B12 binding co-regulator called SAerR and LAerR in Rhodobacter capsulatus. The short form, SAerR, promotes CrtJ repression, while the longer variant, LAerR, converts CrtJ into an activator. In this study, we solved the crystal structure of R. capsulatus SAerR at a 2.25 Å resolution. Hydroxycobalamin bound to SAerR is sandwiched between a 4-helix bundle cap, and a Rossman fold. This structure is similar to a AerR-like domain present in CarH from Thermus termophilus, which is a combined photoreceptor/transcription regulator. We also utilized AlphaFold software to predict structures for the LAerR, CrtJ, SAerR-CrtJ and LAerR-CrtJ co-complexes. These structures provide insights into the role of B12 and an LAerR N-terminal extension in regulating the activity of CrtJ.

Telomere length and vitamin B12.

Telomeres are non-coding nucleoprotein structures consisting of a highly conserved tandem repeat DNA sequence that caps the ends of chromosomes in eukaryotes. Telomeres confer chromosomal stability, protect the genome from nucleolytic degradation, avoid aberrant recombination and improper repair, and prevent random fusion of chromosomes. The end-replication problem results in telomere shortening with every cell division, eventually leading to cellular senescence and aging. Telomere length (TL) is thereby an ideal candidate for "biological aging." Telomeres possess guanine-rich repeats, which are highly susceptible to oxidative stress. Epidemiological studies have indicated the association of telomere attrition with mortality and various age-related diseases. Micronutrients comprising vitamins and minerals act as potential modulators of stress and can influence TL. Research has indicated that vitamin B12 (B12) regulates oxidative stress and maintains genomic stability, thereby influencing telomere integrity and cellular aging. The deficiency of B12 leads to elevated levels of homocysteine, which reduces the methylation potential and increases oxidative stress, thereby compromising the TL. Telomere shortening and mitochondrial dysfunction are independently linked to aging. However, they are connected through telomerase reverse transcriptase activity, which regulates mitochondrial biogenesis. Further, experimental evidence indicated the positive association of B12 with relative TL and mitochondrial DNA copy number, an indirect index of mitochondrial biogenesis. The present chapter provides some insights into the role of B12 in influencing TL. Exploring their association might open new avenues to understand the pathophysiology of aging and age-related diseases.

Vitamin B6 Regulates Muscle Satellite Cell Function: A Novel Possible Role of Vitamin B6 in Muscle Regeneration

Abstract Objectives So far, there is scarce information on potential roles of vitamin B6 (B6) in muscle regeneration. Thus, we examined if B6 has any effects on satellite cells (SCs), the muscle stem cells crucial for muscle regeneration. Methods Male ICR mice were divided into two groups receiving a B6 deficient level diet (1 mg pyridoxine (PN) HCl/kg diet) or a B6 supplement level diet (35 mg PN HCl) for 6 weeks (n = 6/group). Single fibers were isolated from EDL muscles and cultured in plating medium at 37°C, for 0 or 48 hr. Then, fixed fibers were co-immunostained for Pax7 and MyoD. Without culturing (0 hr), SCs are in quiescent state and stained positive with Pax7 +. Following 48 hr of culture, SCs will be activated and enter cell cycle for proliferation (stained positive with MyoD + Pax7+), commitment to differentiation (stained positive with MyoD+), or self-renew (stained positive with Pax7+). Results Without culturing (0 hr), the number of SCs on single fibers isolated from the muscles of the B6-deficient mice was lower than that in the B6-supplement mice (4.0 vs. 7.2 Pax7 + nuclei/fiber, P < 0.01), suggesting that B6 deficiency possibly induced a decline in the quiescent population of SCs. At 48 hr of culture, as compared to the B6-supplement mice, the B6-deficient mice showed the lower number of MyoD + Pax7 + clusters (3.7 vs. 8.1 clusters/fiber, P < 0.01) and the lower number of Pax7 + nuclei (P < 0.01), but no effects on the number of MyoD + nuclei. This suggested that B6 deficiency might affect the self-renewal function of SCs, while had less effects on proliferation and differentiation. Next, we hypothesized that the adverse effects of B6 deficiency on SCs is reversible, since the plating medium contained normal levels of B6. To test this hypothesis, single fibers isolated from the muscles of the B6-deficient mice were cultured in the medium contained with or without B6. As a result, the number of MyoD + Pax7 + clusters on single fibers in the culture without B6 was lower than that with B6 (2.6 vs. 3.7 clusters/fiber, P < 0.05), indicating that SCs cultured without B6 barely proliferated and possibly underwent apoptosis. Conclusions B6 may play a role in proliferation and apoptosis prevention of SCs. This study is the first to show the effects of B6 on SC function and will pave the way for new research on the role of B6 in muscle regeneration in the future. Funding Sources None.

Assessment of Serum Vitamin B12 Levels and Other Metabolic Parameters in Subjects With Different Values of Bone Mineral Density.

BackgroundControversial experimental and clinical evidences have raised questions regarding the role of B12 and insulin-like growth factor 1 (IGF-1) on osteoblast function and bone health. In this study, we aimed to determine if the serum levels of B12, IGF-1 and procollagen type 1 N-terminal propeptide (P1NP) are associated with different degrees of bone mineral density (BMD).MethodsA total of 287 subjects (190 women and 97 men; mean age 53 years) volunteered for evaluation of BMD and serum levels of B12, IGF-1 and P1NP; BMD at lumbar spine and proximal femur was evaluated by means of dual-energy X-ray absorption (DEXA) and expressed as T-score; serum concentrations of vitamin B12 and IGF1 were measured with a chemiluminescent immunoassay on Access II Beckman Coulter and DiaSorin Liaison XL analyzers, respectively; P1NP was assessed in 61 women and 35 men with reduced T-score on Roche Modular platform.ResultsA total of 101 subjects (66 women and 35 men) had a reduced BMD (T-score < -1) or osteoporosis with a T-score < -2.5, while 186 (124 women and 62 men) had a normal BMD. No significant difference in the B12 levels was observed between the subjects with reduced BMD (mean 265.15 pg/mL, 95% CI: 236 - 294.25) and those with normal BMD (mean 243.91, 95% CI: 225.78 - 262.03) (P = 0.1990); lower levels of IGF-1 were observed in the group with reduced BMD (mean 138.7 pg/mL, 95% CI: 126.75 - 150.83) than in that with normal BMD (mean 167.34, 95% CI: 136.49 - 198.18) (P< 0.001); serum levels of P1NP were significantly lower in 22 subjects younger than 50 years (mean 44.8 ng/mL, 95% CI: 36.4 - 53.1) vs. 74 subjects > 50 years old (mean 53.3, 95% CI: 34.3 - 72.3) (P < 0.001), and in women (mean 45.3, 95% CI: 37.6 - 52.9) vs. men (mean 62, 95% CI: 23 - 101) (P < 0.001).ConclusionWe found no significant association between B12 levels and BMD, but significant associations of lower levels of IGF1 with reduced BMD and lower levels of P1NP with younger age and female sex were found; additional studies to further investigate the association of serum levels of B12, growth factors and biochemical turnover markers with human bone health are needed.

Role of B12 and Homocysteine Status in Determining BMD and Bone Turnover in Young Indians

Vitamin B12 (B12) deficiency and hyperhomocysteinemia (HHcy) are independent risk factors for low bone mineral density (BMD) and fracture risk. We studied the role of HHcy and B12 deficiency in determining the peak bone mass in Indians. Randomly selected 151 healthy young adult subjects (females 100, mean age: 26yr) underwent evaluation of dietary intake of calcium and B12; sun exposure; estimation of BMD by dual-energy X-ray absorptiometry at total hip, forearm, and lumbar spine; serum 25(OH)D3; intact parathyroid hormone; B12; homocysteine (Hcy); and bone turnover markers (BTMs) serum crosslaps, N-mid osteocalcin, and bone-specific alkaline phosphatase. Hypovitaminosis D (serum 25OHD3<20ng/mL) and serum ALP level >150IU/L were seen in 83% and 27%, respectively. Median serum B12 and Hcy levels were 140pg/mL (interquartile range [IQR]: 72–230pg/mL) and 18μmol/L (IQR 14–32μmol/L); B12 deficiency (serum B12<200pg/mL) and HHcy (serum Hcy>30μmol/L) were present in 71% and 68%, respectively. Low BMD (Z-score <−2.0) was present in 17% of subjects. There was no significant correlation between serum Hcy, folate, B12, BTM, and BMD. BMD was predicted by height, weight, and body mass index. Young Indian healthy adults have high prevalence of hypovitaminosis D, B12 deficiency, and HHcy. There is no correlation of serum B12, folate, and Hcy status with BTMs and BMD in young, healthy, vegetarian Indian adults. Anthropometric variables predict BMD in young Indians.

Advances in Vascular Cognitive Impairment

Advances in Vascular Cognitive Impairment

How B6 Helps B12: The Roles of B6, B12, and the Enzymes in Aminomutase-Catalyzed Reactions

How B₆ Helps B₁₂: The Roles of B₆, B₁₂, and the Enzymes in Aminomutase-Catalyzed Reactions