No abstract

SummaryAscorbate is a cofactor of two-enzyme hydroxylation in the pathway of carnitine biosynthesis. The purpose of this study was to investigate the contribution of ascorbate to endogenous carnitine in guinea pigs fed high-fat diets. The contents of carnitine in plasma, urine and tissues of guinea pigs supplemented with L-ascorbic acid were determined and compared with those supplemented with carnitine. Albino-Hartley guinea pigs were fed vitamin C-deficient diets containing lard throughout the experiment. They were administered orally with 5mg L-ascorbic acid/d/animal for 14d, and then divided into three groups and administered orally with the following supplements (/d/animal) for 14d; L (5mg L-ascorbic acid), LASA (100mg L-ascorbic acid), and LCAR (10mg carnitine plus 5mg L-ascorbic acid). As a control, a normal group was fed vitamin C-deficient diets and administered orally with 5mg L-ascorbic acid/d/animal for 28d. The animals fed high-fat diets (L group) had higher free-carnitine contents in the muscle and urine than the normal group. The groups of LCAR and LASA had significantly higher contents of acid-soluble carnitine (p<0.05) in plasma than the L group. Urinary excretion of carnitine in the LASA group was decreased to the same level as that in the normal group, although no significant difference between the groups of L and LCAR was observed. Moreover, the supplement of ascorbic acid, but not of carnitine, induced a significantly lower content of triacylglycerol in the plasma of the LASA group as compared to the L group (p<0.05). These data suggest that high doses of ascorbic acid in guinea pigs fed high-fat diets contribute to the enhancement of carnitine synthesis and improvement of the triacylglycerol content in the plasma.

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Pincer nails (PN) are defined as a transverse overcurvature of the nail plate. Although there have been advancements in therapeutic approaches, the precise underlying mechanisms for the development of PN are still not fully understood. Currently, PN are assumed to develop due to lack of upward mechanical force on the toes. We developed a novel wireless device to observe detailed gait motion. We analyzed trends of gait motion in healthy individuals without PN, healthy individuals with PN without a family history of PN, and healthy individuals with PN and a family history of PN. We found that a family history of PN is an independent risk factor for PN, irrespective of gait motion. Moreover, healthy individuals with PN but without a family history of PN exhibit strong and concentrated pressure on the first toe pad during walking. In sum, a family history of PN and excess upward mechanical forces on the first toe pad during walking may be risk factors for the development of PN.