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Biomedical subjects

C R Merril

Publications and source records attributed to C R Merril.

At least 145 records · Page 8Linked to original sources
PubMed1975

Galactose and glucose metabolism in galactokinase deficient, galactose-1-P-uridyl transferase deficient and normal human fibroblasts.

Despite the genetic interruption of the Leloir pathway both galactosemic patients and galactosemic fibroblasts can convert galactose to CO2 and TCA precipitable products, although at less than the normal rate. These observations stimulated investigations into the identity of the alternative metabolic routes which allows for galactose metabolism in the absence of in vitro galactose-1-P-uridyl transferase. Four lines of galactosemic cells, each without detectable gal-transferase, produced 14CO2 from [1-14C]-galactose (0.094 mumoles in 20 cc of medium) at approximately 39% +/- 16% the rate of transferase positive cells over a 48-hour period. However, galactokinase deficient fibroblasts produced 14CO2 and TCA precipitable products from [1-14C]-galactose or [U-14C]-galactose at only 3% to 9% the rate of normal fibroblasts. Therefore it seems likely that gal-transferase deficient fibroblasts must first synthesize galactose-1-P for further metabolism of galactose.

Adult↗
PubMed1975

Addition of leucine precursors to the diet of leucine-starved mice.

Leucine-starved mice placed on a diet supplemented with the immediate precursor of leucine, alpha-ketoisocaproic acid, regain lost weight. This weight gain is similar to that observed when the leucine-starved mice are provided with leucine in their diet. Mice on a leucine-free diet supplemented with alpha-ketoisovaleric acid, the first compound in the leucine biosynthetic pathway, continued to lose weight as quickly as mice on leucine-deficient diets.

Animals↗
PubMed1972

Galactose utilization in galactosemia.

Cultures of human galactosemic fibroblasts without detectable transferase activity were able to convert [1-(14)C]galactose to (14)CO(2) to the same extent as normal cells, but did so at a significantly slower rate. The utilization of galactose in both normal and galactosemic cells was strongly inhibited by glucose at physiologic concentrations.

Carbon Dioxide↗