Date of Award:

5-1978

Document Type:

Thesis

Degree Name:

Master of Science (MS)

Department:

Nutrition, Dietetics, and Food Sciences

Department name when degree awarded

Nutrition and Food Science

Committee Chair(s)

Deloy Hendricks

Committee

Deloy Hendricks

Committee

Arthur Mahoney

Committee

Thomas Blotter

Abstract

The effect of increasing the dietary protein and pyridoxine level on calcium balance and bone strength was studied in growing and adult rats. The loss of calcium due to urinary excretion of o-phosphoryl-ethanolamine on a high protein diet was also examined.

Three studies were conducted. In the first adult male rats were fed 40% protein diets with high or low pyridoxine or a low protein, low pyridoxine diet. Calcium balance and femur bending stress were determined. In the second study male weanling rats were given either 10 or 63% protein with 0.40 or 0.73% pyridoxine. Calcium and phosphorous balances were determined. Calcium, phosphorous, and ash content of the ulna, scapula, and caudal vertebrae were evaluated. Stress tests were carried out on the femur, tibia, humerus, and caudal vertebrae. Adult female rats were given 63% protein diets with or without pyridoxine in the third study. Calcium and phosphorous balances were determined. Urinary o-phosphorylethanolamine was checked.

The high protein diets caused a more positive calcium balance than the lower protein diets in all studies. The phosphorous balance became increasingly negative as the calcium balance became more positive. Pyridoxine level had no effect on the balance of either mineral. Diet had no effect on the mineral content of weight bearing bones. The high protein diet resulted in higher mineral values in the vertebrae than the lower protein diet. Diet did not effect resistance to stress in the bones of the adult rats. In the young rats, the stress results were not consistent. Pyridoxine had no effect on mineralization regardless of dietary protein level. No urinary excretion of o-phosphorylethan-olamine was found in a pyridoxine deficiency.

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