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Nutrient Requirements of Nonhuman Primates: Second Revised Edition, 2003
TABLE 7-2 Estimates of Thiamin Requirement
Daily Air-Dry Diet Consumption
Type of Diet
Thiamin Levels Studied
No deficiency signs, maintained weight
15 µg·BWkg-1·d-1 for maintenance
Waisman and McCall, 1944
Waisman and McCall, 1944
Dose divided by time to replete deficient monkeys
15.5 µg·BWkg-1·d-1 for maintenance
Rinehart et al., 1948
Waisman (1944), Cooperman et al. (1945), and Greenberg and Moon (1963). The signs of deficiency in rhesus monkeys include growth failure, “freckled” dermatitis, incoordination, faulty grasping reflexes, impaired vision, scanty hair coat, reduced red-cell count, anemia, leukopenia, fatty liver, blindness, and eventual death. The dermatitis begins as small, dry, red spots about the face and progresses to dark scabs over the entire body. The severe anorexia seen in thiamin deficiency has not been observed.
There are two reports on the riboflavin requirement of macaques. The riboflavin concentration required to cure deficiency signs and allow excretion in the urine of animals weighing 3-4 kg was 25-30 µg·BWkg-1·d-1 (total intake, 90 µg) (Cooperman et al., 1945). In another investigation, the requirement of monkeys weighing 3 to 4 kg was estimated to be 41 µg·BWkg-1·d-1; this estimate was based on the difference in urinary excretion of riboflavin between animals receiving sufficient riboflavin and those fed a deficient diet for 5 weeks (Greenberg, 1970).
Mann et al. (1952) and Mann (1968) described riboflavin deficiency in capuchin monkeys (Cebus albifrons). Weight loss, dermatitis, alopecia, ataxia, and sudden death were the reported signs. Severe anemia did not develop in capuchin monkeys, although seen consistently in rhesus monkeys. The concentration of plasma riboflavin was considered a good indicator of riboflavin status. A riboflavin intake of 50-55 µg·BWkg-1·d-1 was required to restore maximal growth rate in deficient animals. That represented a daily supplement of 30-40 µg of riboflavin in a basal diet furnishing 10-15 µg·BWkg-1·d-1 (Mann et al., 1952). Although the weights of the animals were not specified, monkeys used in similar studies in the same report, but not involved in the requirement study, weighed 0.9-1.4 kg and consumed 40-60 g of diet per day.
Foy et al. (1964, 1972) and Foy and Kondi (1984) described riboflavin deficiency in the baboon (Papio anubis) as characterized by weight loss, apathy, severe dermatitis, anemia, gingivitis, diarrhea, and adrenal cortical hemorrhage. The dermatitis progressed to nodular lesions that formed mud-pack-like masses on the face, arms, legs, and feet. The lesions extended into the lower third of the esophagus (Foy and Kondi, 1984). An increased concentration of xanthurenic acid, but not of anthranilic acid (both are metabolites of tryptophan), was found in the urine of riboflavin-deficient baboons by Foy et al. (1964). Increased anthranilic acid but unchanged concentrations of xanthurenic acid in the urine were reported by Verjee (1971). No explanation for the different findings was offered. An erythroid aphasia characterized by a fall in marrow erythroid activity leading to reduced hemoglobin, packed-cell volume, and total blood volume was reported in baboons made riboflavin-deficient. A reversal of the albumin:globulin ratio also was observed (Foy et al., 1964, 1968; Foy and Kondi, 1968).
The signs of riboflavin deficiency in the baboon were reversed with a therapeutic dose of about 10-50 mg of riboflavin per animal per day for 3-7 days (Foy and Kondi, 1968). No attempt was made to see whether the same effect could be achieved with smaller doses.
There are insufficient data to show whether different species of primates have similar or different riboflavin requirements. The estimated riboflavin requirement of nonhuman primates has been set at 1.7 mg·kg-1 of dietary DM. That requirement is based on studies with purified diets fed to rhesus and capuchin monkeys, summarized in Table 7-3.
Pantothenic acid is a part of coenzyme A, which is involved in metabolic acetylation reactions. Coenzyme A serves as a cofactor in the tricarboxylic acid cycle, in fatty-acid synthesis and degradation, and in the formation of acetylcholine in nervous tissue (Plesofsky-Vig, 1996, 1999). Biologic availability of pantothenic acid in the average American human diet is estimated to be about 50% (Tarr et al., 1981; Institute of Medicine, 1998). The supplemental form usually added to diets is D-calcium pantothenate, equivalent in activity to 85% pantothenic acid.
McCall et al. (1946) reported that pantothenic acid deficiency in rhesus monkeys (Macaca mulatta) resulted in lack of growth, anemia, loss of hair, and ataxia. Only partial