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Dietary Pectin Shortens the Biologic Half-Life of Vitamin B-12 in Rats by Increasing Fecal and Urinary Losses^1,2,

Department of Nutritional Sciences, University of California, Berkeley, CA 94720

As little as 5% of pectin added to a fiber-free diet elevates urinary methylmalonic acid (MMA) severalfold in vitamin B-12—deprived rats. The present study examines whether increased urinary MMA reflects lower vitamin B-12 status or occurs only because of fermentation of pectin by intestinal bacteria and increased production of propionate, a precursor of MMA. By monitoring urinary and fecal excretion of ⁵⁷Co after a tracer dose of [⁵⁷Co]vitamin B-12, we found the biologic half-life of vitamin B-12 to be 59 d for rats fed a fiber-free diet and only 19 d for rats fed a 5% pectin diet. Also, pectin-fed rats oxidized only 12% of a 1-mmol dose of [¹⁴C]propionate to ¹⁴CO₂ in 2 h, whereas rats fed the fiber-free diet expired 33% of the dose. Finally, high urinary MMA persisted even after the removal of pectin from the diet. We conclude that dietary pectin accelerates vitamin B-12 depletion in rats, possibly by interfering with enterohepatic recycling of vitamin B-12. By stimulating microbial propionate production, pectin and other fermentable fibers may also contribute to increased urinary MMA in vitamin B-12 deficiency, but a larger propionate pool does not account for the other effects of pectin on vitamin B-12 status.

KEY WORDS: • vitamin B-12 • methylmalonate • propionate • radioactive isotopes • rat • pectin • dietary fiber • intestinal flora

¹ Supported in part by National Institutes of Health Grant AM-19970.

² These data are taken from the dissertation submitted by R. W. Cullen to the Graduate Division, University of California, Berkeley, in partial fulfillment of the requirements for the Ph.D. in Nutrition.

³ Present address: Dept. of Human Nutrition and Food Systems Management, Winthrop College, Rock Hill, SC 29733.

⁴ To whom reprint requests should be addressed.

Manuscript received 24 January 1989. Revision accepted 10 April 1989.