VITAMINS

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Vitamin deficiency does not become apparent immediately even if the diet is nutritionally defective. It usually takes from 1 week to 1 month for vitamin deficiency to become apparent. In the process of my studying on tryptophan metabolism, urine was realized to be a non-invasive biological sample. I knew that it was possible to deduce the disturbance of nutrient metabolism in the body before the appearance of symptoms from the amounts of metabolites excreted in urine. The amounts of vitamins excreted in urine have not been of great concern clinically for a long time because vitamin deficiency did not become apparent immediately even if the amount of vitamin in urine was almost zero. However, I realized the significance of the urinary excretion amounts of vitamins based on the thought that vitamins are essential to maintain health. Namely, the urinary excretion amounts of vitamins and their catabolic metabolites reflected the amounts of vitamins being stored in the body. From these findings, I proposed the values of urinary excretion of vitamins (biological index) for maintenance of health. Furthermore, I found that the urinary excretion of 2-oxo acids (functional biomarker) produced from energy-producing nutrients could be used as the indicator of vitamins really functioning in the body. Finally, I proposed the high-quality nutritional guidance using biomarker and functional biomarker.

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In mammals, polyunsaturated fatty acids (PUFAs) such as linoleic acid (18:2n-6) and α -linolenic acid (18:3n-3) cannot be synthesized de novo. Therefore, these PUFAs are essential fatty acids (EFAs). However, these PUFAs can be converted to arachidonic acid (20:4n-6) and eicosapentaenoic acid (20:5n-3). Mead acid (20:3n-9), is an unusual n-9 series PUFA, which is endogenously synthesized from oleic acid (18:1n-9) in an essential fatty acid (EFA)-deficiency state. In this study, we showed that Mead acid was produced from oleic acid by two desaturation enzymes (FADS1 and FADS2) and one elongation enzyme (ELOVL5), indicating that n-3, n-6, and n-9 PUFAs are metabolized by the same enzymes. Furthermore, ELOVL5 acquired an elongation activity towards oleic acid under EFA-deficient state, which allows it to synthesize Mead acid. We revealed a novel regulatory mechanism that the substrate preference of ELOVL5 was modified by a post-translational modification.
The function of Mead acid during EFA-deficiency is not known, but we showed that the inhibition of Mead acid synthesis induced hepatic triacylglycerol accumulation via the suppression of very low-density lipoprotein (VLDL) secretion in EFA-deficiency mice. From these results, it is possible that Mead acid functions as a substitute for the PUFA produced from EFAs in VLDL secretion during EFA-deficiency.

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