Protein-bound B12 Research Articles

Development of novel Vitamin B12 fortified yogurts using isolated and microencapsulated Vitamin B12

AbstractAdults aged > 50 years, which make up to 40% of the European population, are vulnerable to low vitamin B12 (B12) status due to age-related factors that impair digestion and absorption of protein-bound B12 from natural food sources. Older adults are recommended to meeting their dietary B12 intake through the consumption of B12-fortified foods or supplements because these products contain free B12. B12 seems most bioavailable from milk products compared to other food sources, showcasing dairy as a potential vehicle for B12 food fortification. Yogurt is a versatile, popular dairy product, making it a promising food vehicle for B12 fortification to enhance the availability of B12-fortified foods for population groups at risk of B12 deficiency. With the overall goal to develop a novel, B12-fortified dairy product, the objective of this project was to compare the shelf-life stability of different chemical forms of B12 added to yogurt either in isolated or in encapsulated form. For both fortification strategies, we compared methylcobalamin (MeCB), a naturally-occurring B12 form, and cyanocobalamin (CnCB), the synthetic form of B12. Encapsulated microparticles were created by spray-drying a maize starch-derived polymeric material (EUDRAGUARD Natural®) with 1% (w/V) MeCB or CnCB. The release of B12 from encapsulated microparticles was confirmed by in vitro simulated gastrointestinal digestion; maximum B12 release (103% recovery) was achieved under conditions simulating the small intestine, where B12 is absorbed in the human body. Yogurts were produced by incubating whole milk (3.25% milk fat) with yogurt starter bacteria at 43°C overnight; after fermentation and cooling down, isolated (I-MeCB or I-CnCB) or encapsulated B12 powders (E-MeCB or E-CnCB) in the concentration of 50μg of B12/175 g of yogurt were added, creating stirred yogurt. Yogurts were stored at 4°C for eight weeks, with intermittent sampling for B12 stability testing using RIDASCREEN immunoassay. For CnCB-fortified yogurts, I-CnCB and E-CnCB had similar B12 concentrations at baseline (48.3μg and 48.2μg, respectively) and week 8 (53.9μg and 51.4μg, respectively). Difference in B12 content between I-CnCB and E-CnCB was < 5% for both time-points. For MeCB, similar concentrations were found for I-MeCB (64.1μg) and E-MeCB (65.0μg) at baseline; however, at week 8, E-MeCB remained stable (69.8μg) while a pronounced decrease in B12 was observed with I-MeCB (33.3μg). At week 8, I-MeCB B12 concentrations were 52% lower than E-MeCB. In conclusion, CnCB was shown to be the more stable fortificant throughout shelf-life. Encapsulation techniques are a viable option to increase MeCB stability in fortified yogurts.

Forms and Amounts of Vitamin B12 in Infant Formula: A Pilot Study.

PurposeInfant formula is based on cow’s milk and designed to mimic breast milk for substitution. Vitamin B12 (B12) is bound to proteins in both breast milk and cow’s milk, and in milk from both species the vitamin occurs mainly in its natural form such as hydroxo-B12 with little or no synthetic B12 (cyano-B12). Here we test commercially available infant formulas.MethodsEleven commercially available infant formulas were measured for content of B12 and analyzed for the presence of B12-binding proteins and forms of B12 using size exclusion chromatography and HPLC.ResultsAll infant formulas contained B12 by and large in accord with the informations given on the package inserts. None of the formulas contained protein-bound B12, and cyano-B12 accounted for 19–78% of the total amount of B12 present, while hydroxo-B12 constituted more or less the rest.ConclusionsThis pilot study shows that infant formula differs from breast milk in providing the infant with free B12, rather than protein-bound B12, and by a relative high content of cyano-B12. The consequence of supplying the infant with synthetic cyano-B12 remains to be elucidated.

Letters: Omeprazole and Vitamin B_12

Letters1 July 1994Letters: Omeprazole and Vitamin B12Stefan P. Marcuard, MDStefan P. Marcuard, MDEast Carolina University School of Medicine; Greenville, NC 27858-4354Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-121-1-199407010-00022 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:Our study design to evaluate protein-bound B12 absorption before and during treatment with omeprazole is appropriate and is known as “self-pairing” [1, 2]. This method eliminates the variability between study patients and “controls.” Although we agree that a placebo group would have strengthened our results, our straightforward study design is adequate to show changes in vitamin B12 absorption during omeprazole therapy.Dr. Lavy's comments indicate a misunderstanding of vitamin B12 digestion and absorption. To correct protein-bound vitamin B12 malabsorption, hydrochloric acid (not vitamin B12) is added to the modified Schilling tests. In fact, this has been done by ...

The absorption of free vitamin B12 and R protein-bound vitamin B12 in the diagnosis of pancreatic exocrine insufficiency in rats.

Vitamin B12 (B12) absorption was studied in rats following biliopancreatic duct ligation. The absorption of free B12, as well as of hog R protein-bound B12, was markedly impaired after both intragastric and intraduodenal administration in these rats. The intraduodenal administration of a mixture of pancreatic extract and sodium bicarbonate (NaHCO3) improved the absorption of both free and R protein-bound B12. However, pancreatic extract without NaHCO3 was ineffective in this respect. Intraduodenal administration of NaHCO3 without pancreatic extract worsened the R protein-bound B12 absorption. This finding would indicate that the degradation of R protein by proteolytic enzymes, in the intestine of rats with pancreatic juice exclusion, is inhibited by NaHCO3.

Clinically significant vitamin B12 deficiency secondary to malabsorption of protein-bound vitamin B12

Protein- (chicken serum) bound [57Co]cyanocobalamin absorption was evaluated in five hypochlorhydric patients who had developed B12 deficiency despite having normal absorption of unbound crystalline vitamin B12. All five patients had decreased urinary excretion of protein-bound B12 (0.06--0.34%) as compared to twelve normal controls (0.61--5.6%), P less than .001. Improvement in protein-bound B12 absorption in four of the five patients occurred with the exogenous administration of hydrochloric acid, pepsin, gastric intrinsic factor, or a combination thereof. Vitamin B12 deficiency developing in the setting of hypochlorhydria may result from deficiency of acid-peptic digestion of B12 bound to protein and/or a relative deficiency of intrinsic factor. This digestive defect is not detected with tests which measure the absorption of unbound crystalline B12 but is detected by a simple test which employs B12 bound to chicken serum as the form of protein-bound B12.