In 46 diabetic outpatients consisting of 20 males and 26 females not given thiamine treatment, the blood thiamine level was 46.9±28.5 ng/ml (mean±SD) and only 23.9% o of all cases had a value of more than the normal lower limit (50 ng/ml). Erythrocyte transketolase activity was 443.8±107.7 μg/ml/h and only 20.9% had a value of more than the normal lower limit (500 μg/ml/h), and the erythrocyte TPP effect was 16.6±13.2%. Moreover, there was a significant positive correlation (r=0.97) between the blood thiamine level and erythrocyte transketolase activity, and a significant inverse correlation (r=-0.525, r=-0.576) between blood thiamine level and/or erythrocyte transketolase activity and the erythrocyte TPP effect. In 24 diabetic outpatients consisting of 14 males and 10 females given thiamine treatment, the blood thiamine level was 96.5±44.5 ng/ml/h excluding one case (621.7 ng/ml), and it was higher than the normal lower limit in 83% of all cases. Erythrocyte transketolase activity was 513.9±133.4 μg/ml/h and it was higher than the normal lower limit in 58.3% Erythrocyte TPP effect was 5.84±8.39%. There was also a significant positive correlation (r=0.663) between blood thiamine level and erythrocyte transketolase activity, and a significant inverse correlation (r=-0.668, r=-0.834) between blood thiamine level and/or erythrocyte transketolase activity and erythrocyte TPP effect. Blood thiamine level and erythrocyte transketolase activity were significantly higher in diabetic outpatients given thiamine treatment than in diabetic outpatients not given thiamine treatment, while the erythrocyte TPP effect was significantly lower in diabetic outpatients given thiamine treatment than in diabetic outpatients not given thiamine treatment. There was no direct relationship between the lowered response of patellar tendon reflex and the biochemical status of thiamine. From the above findings it was concluded that diabetic outpatients tend to have a low blood thiamine level, with low erythrocyte transketolase activity and high erythrocyte TPP effect, and showed marginal thiamine deficiency.

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Forty-six diabetic outpatients consumed 1, 533±308 kcal (mean±SD) per day, 205±42g of carbohydrates, 73±18g of protein, 49±18g of fat, and 0.95±0.34 mg of thiamine. No significant correlation was found in 46 diabetics between blood thiamine level and the intake of dietary energy, carbohydrate or thiamine. In 13 healthy subjects given prepared diets, a significant correlation was found between blood thiamine level and dietary thiamine content, thiamine content per 1, 000 kcal, and 24-h urinary thiamine amount divided by urinary creatinine. When 9 healthy subjects (6 males, 3 females) consumed 1, 600 kcal with 0.6mg of thiamine for two days, their blood thiamine level was 47±29.1 ng/ml before and 29.7±7.1 ng/ml after eating the diet, showing low blood thiamine levels due to the low content of dietary thiamine. When 5 or 6 healthy female subjects consumed 1, 400 kcal with 1.6 mg of thiamine or 2, 000 kcal with 1.9 mg of thiamine for two days, their blood thiamine level was 45.3±4.8 ng/ml or 57.7±8.4 ng/ml before and 51.5±11.7 ng/ml or 56.4±11.7 ng/ml after eating the diets, respectively. In both diabetic outpatients and healthy subjects, a significant positive correlation was found between blood thiamine levels and dietary thiamine concentrations per 1, 000 kcal, and a significant positive correlation was also found between erythrocyte transketolase activity and dietary thiamine content. Thiamine content of food materials was 8.1 to 13.2% lower than the values given in the Japan Foodstuff Table. Moreover, 27.3 to 30% of the calculated thiamine content was lost during cooking procedures.

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β-Alanine-oxoglutarate aminotransferase from rat liver was mainly distributed in the mitochondrial fraction, while β-ureidopropionase, the last one of uracil-metabolizing enzymes to β-alanine, was predominantly distributed in the cytosolic fraction. When rat liver mitochondria were separated into submitochondrial fractions, β-alanineoxoglutarate aminotransferase was localized in the mitochondrial matrix. β-Alanine was transported into mitochondria with time and the influx of β-alanine into the matrix was 0.47 nmol/mg of mitochondrial protein at 2 min after incubation.

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Recovery from Mg deficiency was studied in adult Wistar rats fed a semisynthetic diet containing 0.04% Mg in the form of magnesium carbonate. Daily administration of a diet containing recommended levels of calcium carbonate to Mg-deficient rats led to the recovery, within the first seven days of treatment, of normal values in most of the parameters studied: gain in weight/day, and Mg retention and content in the Longissimus dorsi muscle and femur. Mg levels in whole blood, however, did not fully recover until the second week of treatment. Net Ca absorption (ADC) and balance were significantly higher in Mg-deficient rats than in controls and remained elevated although to a lesser extent in the femur. Longissimus dorsi muscle, blood and plasma were unchanged by Mg deficiency.

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