1. Vitamin D-deficient rachitic rats were given [1-(3)H]cholecalciferol by gastric intubation. After 24hr., diethyl ether extracts of liver and kidney contained 5-11% and 4.5-20% respectively of total vitamin D apparently esterified with long-chain fatty acids. 2. A two-dimensional thin-layer chromatographic technique was devised that completely separated seven synthetic vitamin D esters according to the chain length and number of double bonds in the fatty acid component. When the ;vitamin D ester' fraction from liver or kidney was co-chromatographed with the standard esters, radioactivity appeared mainly in vitamin D palmitate, stearate, oleate and linoleate regions. The proportion of radioactivity in the saturated fatty acid esters was higher in kidney than in liver. 3. The same percentage of tissue vitamin D in the esterified form was found at each of two dosages of vitamin D. 4. The possible specificity of a vitamin D esterification mechanism is discussed.

Animals↗

PubMed1968

Investigations on vitamin D esters synthesized in rats. Turnover and sites of synthesis.

1. The tissue contents of vitamin D alcohol and ester were estimated in rats 5, 10, 24, 48 and 72hr. after peroral administration of [1-(3)H]cholecalciferol. 2. The total vitamin D in liver decreased in an exponential fashion from 19% of the dose at 5hr. to 0.6% at 72hr., but the ester content remained at a relatively constant low value from 5hr., so that by 72hr. it represented 67% of the total vitamin D. Vitamin D ester in kidney increased slowly to 48hr., but by 72hr. it was only 10% of the total vitamin D. 3. The small intestine, unlike liver and kidney, contained a higher content of vitamin D ester 10hr. after administration than at later times, and it is postulated that some vitamin D was esterified during absorption from the alimentary tract. 4. Plasma contained vitamin D ester at all time intervals, and it is suggested that ester found in liver and kidney could have been transported to these sites in the blood. 5. Thoracic-duct lymph was found to transport 43% of a peroral dose of vitamin D in 12hr., of which 1.4% was esterified. The fatty acid components of the lymph vitamin D ester, determined by two-dimensional thinlayer chromatography, were mainly palmitate (31%), stearate (25%), oleate (16%) and linoleate (16%). This pattern was similar to that previously found in liver.

Animals↗

PubMed1968

Enzyme studies on the esterification of vitamin D in rat tissues.

1. The mechanism of vitamin D esterification in the rat was studied with liver, small-intestinal mucosa, pancreatic juice and blood plasma as enzyme sources and [1-(3)H]cholecalciferol, [U-(14)C]ergocalciferol and [4-(14)C]cholesterol as substrates. 2. No esterification of vitamin D could be detected with liver preparations nor with homogenates or acetone-dried powder extracts of intestinal mucosa. 3. Pancreatic juice esterified [1-(3)H]cholecalciferol with oleic acid, and specificity studies indicated that a cholesterol-esterifying enzyme was using vitamin D as substrate. 4. Plasma cholesterol-esterifying enzyme also esterified vitamin D. 5. The specificity of the esterification reaction is discussed in relation to (a) the molecular structure of the substrates and (b) their availability, in a micellar solution, to the enzyme. 6. It is concluded that cholesterol-esterifying enzymes esterify vitamin D in vivo during absorption from the small intestine and while it is transported in blood.

Animals↗

PubMedDate not supplied

A new mechanism for induced vitamin D deficiency in calcium deprivation.

Synthesis of vitamin D in the skin in response to ultraviolet light is the main determinant of vitamin D status in man and it is therefore surprising that rickets and osteomalacia, clinical signs of vitamin D deficiency, remain common in tropical and subtropical countries. Skin pigmentation can reduce vitamin D formation but this is a negligible limitation in people exposed to abundant ultraviolet light. Earlier studies in animals and man suggested that another environmental factor, the low calcium/high cereal diet typical of susceptible populations, might affect the efficiency of vitamin D utilization. We show here in rats that the rate of inactivation of vitamin D in the liver is increased by calcium deprivation. The effect is mediated by 1,25-dihydroxyvitamin D, produced in response to secondary hyperparathyroidism, which promotes hepatic conversion of vitamin D to polar inactivation products that are excreted in bile. This finding has widespread implications both for understanding the pathogenesis of endemic rickets and in that it provides a unifying mechanism for the development of vitamin D deficiency in many clinical disorders.

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PubMedDate not supplied

Cornell University Leadership Program for veterinary students.

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Animals↗