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Effect of thyroidectomy on pathways of glucose metabolism in lactating rat mammary gland.

ABSTRACT: 1. Assessment of the overall metabolic changes in lactating mammary gland after thyroidectomy has been made by measurement of the incorporation of (14)C from specifically labelled glucose, pyruvate and acetate into (14)CO(2) and (14)C-labelled lipid in the experimental rats and in sham-operated control animals. 2. Thyroidectomy depressed the oxidation of (14)C-labelled substrates, an effect still apparent when the control rats were pair-fed with thyroidectomized rats; however, the ratio of oxidation of [1-(14)C]glucose/oxidation of [6-(14)C]glucose was unaltered. In parallel with these studies it was revealed that the activities of hexokinase, glucose 6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and NADP-linked isocitrate dehydrogenase were all lower in the thyroidectomized group than in the pair-fed control group. 3. Thyroidectomy also lowered the incorporation of (14)C-labelled substrates into (14)C-labelled lipid, an effect further studied by measurement of the activities of citrate-cleavage enzyme and acetate thiokinase. Restricting the food intake of the control rats to that of the thyroidectomized group lowered the activity of citrate-cleavage enzyme, but no further depression was observed on thyroidectomy. The oxidized and reduced nicotinamide nucleotide content of mammary tissue was shown to be decreased in the thyroidectomized rats compared with the control rats.

SUBMITTER: Walters E

PROVIDER: S-EPMC1198353 | biostudies-other | 1967 Nov

REPOSITORIES: biostudies-other

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Project description:1. The overall metabolic changes in lactating mammary gland in alloxan-diabetic and anti-insulin-serum-treated rats were assessed by measurement of the incorporation of (14)C from specifically labelled glucose, pyruvate and acetate into carbon dioxide and lipid, together with measurements of enzymes concerned with the pentose phosphate pathway and with citrate metabolism. 2. Alloxan-diabetes depressed the rate of formation of (14)CO(2) from [1-(14)C]glucose and [2-(14)C]glucose to approx. 10% of the control rate; this was partially reversed by addition of insulin in vitro. The quotient Oxidation of [1-(14)C]glucose/Oxidation of [6-(14)C]glucose fell from a value of 17.6 in the control group to 3.9 in the diabetic group and was restored to 14.3 in the presence of insulin in vitro. In keeping with these results it was shown that glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activities were significantly decreased in alloxan-diabetic rats. 3. Alloxan-diabetes depressed the decarboxylation and the oxidation of labelled pyruvate, but not the oxidation of labelled acetate. 4. The synthesis of lipid from specifically labelled glucose was greatly decreased, that from [2-(14)C]pyruvate was almost unchanged and that from [1-(14)C]acetate alone was increased in alloxandiabetic rats. However, the stimulation of lipid synthesis from acetate by glucose was small in the alloxan-diabetic rats compared with the controls. Insulin in vitro partially reversed all these effects. Both citrate-cleavage enzyme and acetate thiokinase activities were decreased in alloxan-diabetic rats. 5. Treatment of rats with anti-insulin serum depressed the formation of (14)CO(2) from [1-(14)C]glucose and [2-(14)C]glucose, but increased that from [6-(14)C]glucose. This was completely restored by the presence of insulin in vitro. The quotient Oxidation of [1-(14)C]glucose/Oxidation of [6-(14)C]glucose fell from a value of 17.6 in the control group to 3.8 in the anti-insulin-serum-treated group. There were no changes in the activity of glucose 6-phosphate dehydrogenase or 6-phosphogluconate dehydrogenase, but the hexokinase distribution changed and the content of the soluble fraction increased significantly. 6. The synthesis of lipid from specifically labelled glucose was depressed in anti-insulin-serum-treated rats; this effect was completely reversed by addition of insulin in vitro to the tissue slices.

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Effect of thyroidectomy on pathways of glucose metabolism in lactating rat mammary gland.

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