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Biomedical subjects

D A York

Publications and source records attributed to D A York.

At least 145 records · Page 8Linked to original sources
PubMed1981

Effects of thyroid hormone and adrenalectomy on [Na+ + K+]ATPase in the ob/ob mouse.

The absence of the thyroid stimulation of hepatic [Na+ + K+]ATPase in obese (ob/ob) mice has been investigated. A wide range of tri-iodothyronine (T3) concentrations failed to enhance the hepatic [Na+ + K+]ATPase of ob/ob mice made hypothyroid by methimazole treatment but glycerophosphate dehydrogenase activity was maximally stimulated at low doses of T3. Adrenalectomy increased the basal activity of [Na+ + K+]ATPase to levels found in lean control mice and restored the response of this enzyme to T3. Body weight gain was unaffected by the induction of hypothyroidism in either lean or ob/ob mice. It is concluded that the adrenal steroids play an important role in the expression of [Na+ + K+]ATPase activity in the ob/ob mouse.

Adrenalectomy↗
PubMed1979

The relationship between protein turnover and energy balance in lean and genetically obese (ob/ob) mice.

1. Groups of lean and genetically obese (ob/ob) mice were adapted to varying energy intakes and the rates of total protein turnover in liver, gut and kidney were measured. 2. Lean mice gained less weight when fed above maintenance and lost less weight when fed below maintance than obese mice. 3. Hepatic protein turnover (mg/d) was sigmoidally related to digestible energy intake in lean mice but showed no significant changes with dietary intake in obese mice. 4. The changes in protein turnover resulted from changes in both the half-lives of protein synthesis and catabolism and in tissue protein content. 5. In the lean mice, protein turnover in kidney and gut was not significantly changed with increasing energy intake until the highest level was reached. 6. The findings suggest that protein turnover may be an important cycle for the regulation of energy balance in mice and that this cycle is impaired in the genetically obese (ob/ob) mice.

Animals↗
PubMed1978

Lipogenesis in situ in the genetically obese Zucker fatty rat (fa/fa): role of hyperphagia and hyperinsulinaemia.

In situ fatty acid synthesis has been measured with 3H2O in anaesthetised lean and obese Zucker (fa/fa) rats. The accumulation of fatty acids was increased in both the liver and adipose tissue of young fa/fa rats as a result of both an increased rate of lipogenesis and an increase in tissue mass. Whereas total hepatic lipogenesis increased with age, total adipose tissue lipogenesis decreased in older fa/fa rats. Experiments with hepatectomized rats showed that the liver was the major site of the excess fatty acid synthesis in fa/fa rats. The enhanced rate of lipogenesis in fa/fa rats was abolished by either pair-feeding or streptozotocin treatment. The results suggest that the increased fatty acid synthesis in fa/fa rats is secondary to the hyperphagia, hyperinsulinaemia, and increased mass of hepatic and adipose tissues.

Adipose Tissue↗
PubMed1978

An enzymatic defect in the obese (ob/ob) mouse: loss of thyroid-induced sodium- and potassium-dependent adenosinetriphosphatase.

Genetically obese (ob/ob) mice, mice that became obese after treatment with gold thioglucose, and lean animals were studied in the euthyroid state, after induction of hypothyroidism, and after treatment with triiodothyronine. The activity of glycerol 3-phosphate dehydrogenase (sn-glycerol-3-phosphate:(acceptor) oxidoreductase; EC 1.1.99.5] was reduced in the livers from hypothyroid animals and was increased by treatment with triiodothyronine in all groups. The activity of the ouabain-suppressible sodium- and potassium-dependent ATPase (ATP phosphohydrolase; EC 3.6.1.3) was increased by triiodothyronine and reduced by hypothyroidism in the lean and gold thioglucose-treated obese animals. In the obese (ob/ob) mice, on the other hand, treatment with triiodothyronine did not increase the activity of this enzyme, which remained at the level found in hypothyroid animals. This enzymatic activity was reduced in both liver and kidney. Adenylate cyclase [ATP pyrophosphate-lyase (cyclizing); EC 4.6.1.1] activity in liver membranes, however, was similar in all three groups of mice. This enzyme complex was activated by glucagon and was unaffected by treatment with thyroid hormones. The lack of a thyroid-dependent ouabain-suppressible (Na(+) + K(+))-ATPase in the tissues of the obese (ob/ob) mouse could explain most, if not all, of the abnormalities that have been described in this animal.

Adenosine Triphosphatases↗
PubMed1977

The generation and identification of the hemolysin of Trypanosoma congolense.

The hemolytic activity of Trypanosoma congolense appears to be due to the presence of free fatty acids generated by the action of phospholipase A on endogenous phosphatidyl choline. Some lysolecithin also contributes to the lytic activity. Trypanosoma lewisi, being devoid of phospholipase A, does not generate free fatty acids and is therefore non-hemolytic.

Animals↗
PubMed1977

Lipogenesis in hepatocytes of genetically obese rats.

A simple method for the preparation of hepatocytes in good yield from obese rats is described. Lipogenesis from [U-14C]-lactate, [U-14C]-glucose and tritiated water has been investigated in hepatocytes prepared from both genetically obese 'fatty' rats and their lean littermates. Hepatocytes from obese rats demonstrate elevated rates of fatty acid and sterol synthesis in contrast to hepatocytes from lean animals. The rate of fatty acid synthesis is sensitive to the dietary status of the animal prior to preparation. The enhanced lipogenesis in hepatocytes from obese rate depends on lactate as a source of carbon rather than glucose. The role of the liver in genetic obesity is discussed with particular reference to the major precursor for hepatic lipogenesis.

Animals↗
PubMed1976

Glycerol release in vitro from adipose tissue of obese (ob/ob) mice treated with thyroid hormones.

Glycerol release from adipose tissue of adult genetically obese (ob/ob) mice was greater than that from adipose tissue of lean litter-mates. However, a higher concentration of adrenaline was required to stimulate lipolysis in ob/ob adipose tissue. Since oxygen consumption and the uptake of radioactive iodine by the thyroid were reduced and the biological half-life of thyroidal radio-iodine was lengthened, it is suggested that ob/ob mice are hypothyroid. The poor sensitivity of ob/ob adipose tissue to low doses of adrenaline was improved by treatment with either tri-iodothyronine or thyroxine. The lipolytic responses to both dibutyryl 3':5'-cyclic adenosine monophosphate and aminophylline were enhanced in thyroid hormone-treated lean and ob/ob mice. A higher dose of tri-iodothyronine was required to enhance lipolysis in ob/ob mice than in lean controls. The possibility that hypothyroidism is responsible for the change in response of ob/ob adipose tissue to lipolytic hormones is discussed.

Adipose Tissue↗