Effect of High Protein Consumption on Markers of B6 Status in a Rodent Model of Moderate Pyridoxine Deficiency

Abstract

Pyridoxal‐5‐phosphate (PLP) is the active form of pyridoxine (PN; B6). Increasing protein intake may affect B6 status by increasing PLP‐dependent enzymes in amino acid metabolism. These impacts may be more pronounced during moderate B6 deficiency, which is observed in 25% of North Americans. To this end, we examined the impact of changing the dietary carbohydrate:protein ratio in rodents consuming recommended vs. moderately deficient intakes of PN‐HCl, on plasma markers of B6 status. Weanling male Sprague‐Dawley rats (n=8/group) were randomized to one of four dietary groups for five weeks. A two factorial design used two levels of B6 (marginally deficient (MD): 0.7 vs. adequate (A): 7.0 mg PN‐HCl/kg diet), and two defined ratios of carbohydrate to protein: 60%: 20% (AIN‐93 standard; NP); and 40%: 40% (high protein diet; HP), with dietary fat held constant. Plasma B6 vitamers, including PN, pyridoxal (PL), PLP, and 4‐pyridoxic Acid (PA) were analyzed by reverse‐phase high‐pressure liquid chromatography in dark conditions. Decreasing dietary B6 intake significantly depressed all plasma B6 vitamers. Increasing dietary protein intake significantly depressed plasma PN (A‐NP=235; A‐HP=203; MD‐NP=181; MD‐HP=90 nM; SEM =21.8 nM). There were no significant interactions evident. Other markers of B6 status, including plasma homocysteine, were not significantly impacted. The current data provide evidence of an increased conversion of PN to PLP in the face of an increased dietary protein load. However, under moderate B6 deficient conditions, consuming high amounts of protein similar to the upper acceptable macronutrient distribution range does not significantly exacerbate B6 deficiency.