ABSTRACT
OBJECTIVE: Pantothenic acid (PaA) is a vitamin that is an integral part of coenzyme A (CoA). CoA is an essential coenzyme in fat metabolism. The aim of this study was to determine whether PaA deficiency causes the accumulation of tissue fats and, if so, can refeeding of PaA decrease such accumulated fat. METHODS: Weaning rats were fed the PaA-free diet for 30 d. Rats were then divided into two groups. One group was continuously fed the PaA-free diet, and the other was fed the PaA-containing diet for an additional 13 d. At the end of the experiment, liver fat and perinephric fat were weighed, and plasma triglyceride levels measured. An additional similar experiment was conducted in which rats consumed 15% ethanol instead of water. RESULTS: Fat that accumulated by consuming the PaA-free diet for 30 d was decreased by consuming the PaA-containing diet for an additional 13 d. Ethanol feeding elicited much greater accumulation of liver, perinephric, and plasma fats if rats were fed the PaA-free diet. In such cases, administration of PaA could decrease the accumulated fat. CONCLUSION: PaA deficiency causes fat accumulation, and readministration of PaA decreases the tissue fat in rats fed the pantothenic acid-free diet. Ethanol accelerated the accumulation of fat in rats fed the PaA-free diet. PaA could be beneficial for decreasing accumulated tissue fat.
Subject(s)
Ethanol/adverse effects , Kidney/drug effects , Lipid Metabolism/drug effects , Lipids/blood , Liver/drug effects , Pantothenic Acid/therapeutic use , Vitamin B Deficiency/drug therapy , Animals , Coenzyme A/metabolism , Diet , Fatty Liver/etiology , Fatty Liver/metabolism , Kidney/metabolism , Liver/metabolism , Male , Pantothenic Acid/deficiency , Rats , Rats, Wistar , Vitamin B Complex/administration & dosage , Vitamin B Complex/therapeutic use , Vitamin B Deficiency/complications , Vitamin B Deficiency/metabolism , WeaningABSTRACT
We have reported previously that the urinary excretion of B-group vitamins reflects recent dietary intakes of these vitamins. We also proposed reference values for the urinary levels of B-group vitamins for human subjects, and used these for evaluating human nutritional status. However, the question arises as to whether the urinary excretion of B-group vitamins in animals or human subjects decreases immediately before they become B-group vitamin insufficient or when fed a diet low in vitamins. In the present study, rats were fed a vitamin-free diet for 5 d, and changes in the levels of B-group vitamins in urine and blood were monitored. Urinary excretion of vitamin B1, vitamin B2, 4-pyridoxic acid (a catabolite of vitamin B6), pantothenic acid, folate and biotin steeply decreased, and all of the values reached zero within 1-2 d. With respect to blood, the concentrations of only three of the eight B-group vitamins (vitamin B1, pyridoxal phosphate and biotin) decreased to 15 % (P < 0·0001), 7 % (P < 0·0001) and 2 % (P < 0·0001) on day 5, respectively, compared with the values at the beginning of the experiment. The decrease was more rapid and the changes were greater in the urine samples than in the blood samples. The present data complement our previous proposal that the urinary excretion of B-group vitamins reflects the nutritional status of these vitamins.
