In an attempt to create a model of human infantile beriberi, pregnant rats were fed, from the 10th day of pregnancy through lactation, a low-thiamine diet. Controls were either pair-fed or offered a nutritionally complete diet ad libitum. Dams exhibited symptoms of thiamine deficiency after 30 days on the experimental diet, whereas their pups displayed signs of thiamine deficiency from the 14th postnatal day. Brain transketolase activity was depressed in day-old thiamine-deficient pups, and brain pyruvic acid levels were elevated after the 7th postnatal day. From the 14th postnatal day, brains of thiamine-deficient pups contained less phospholipids, cerebrosides and cholesterol than those of both controls. On the 21st day, weight and lipid content of brains of thiamine-deficient and of pair-fed pups were lower than those of normal controls. In some rats rehabilitation with thiamine was begun on the 19th day, and after 23 days, brain cerebroside content was still lower in the experimental group than in both controls. Since cerebrosides are an essential component of myelin, this finding may suggest damage of the myelin sheath.
I . The interrelationships between dietary calcium, fluorine and vitamin D were studied in young rats.2. Rats maintained on a low-Ca diet gained less weight and had less ash in their bones. Their femurs incorporated more radioactive Ca than those of rats kept onacontrol diet. Supplementation of the diet with F slightly decreased growth and the content of bone ash without any effect on the content of Ca and phosphorus in the bone ash. The F supplement decreased uptake of radioactive Ca by bone. Addition of vitamin D to a low-Ca diet improved growth and, when added alone, increased uptake of radioactive Ca by bone without affecting the content in femurs of ash, Ca or P. Addition of F to a low-Ca diet supplemented with vitamin D diminished the uptake of radioactive Ca.3. Decrease of bone ash in rats fed the low-Ca diet was accompanied by an increase in bone nitrogen. The bones of the unsupplemented rats contained less citric acid per unit of dry, fat-free mass. Addition of F decreased citric acid, whereas addition of vitamin D increased it.4. The results are discussed and it is concluded that vitamin D added to a low-Ca diet does not exert a calcifying effect on bone, but rather increases Ca turnover. F, on the other hand, reduces the exchangeability of bone mineral.
The importance of lipid metabolism as related to calcification has received impetus by recent studies. While protein-polysaccharides have been implicated increasingly in the process of calcification ( 1 ) , Irving has made pertinent histochemical observations noting the presence of a lipopolysaccharide at the calcification front in cartilage ( 2 , 3). Howell and Carlson believe that these lipopolysaccharides are sulfated, and further studies by Howell have shown a striking difference in phospholipid profiles from rachitic and normal animal cartilage (4, 5). It has been postulated that vitamin D deficiency may cause changes in calcium translocation by affecting the selectivity of cation transfer (i.e., Ca2+) through membrane coated with phospholipid.Calcium binding has been shown to occur by a phospholipid protein complex (6). A regulatory function for lipids in cell membrane transport of electrolytes and other tissues has been extensively studied and a possible selective role for these compounds in mineralization or water transfer at calcifying sites has been theorized ( 7).On this basis it appeared worthwhile to study lipid metabolism in weanling rat epiphyseal cartilage, a structure which is rapidly undergoing sequential changes in calcification and which, would, therefore, lend itself to such a study.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.