1. Lactation results in a substantial fall in the rate of fatty acid synthesis in sheep adipose tissue. 2. Maintenance of adipose tissue from non-lactating sheep in tissue culture for 24 or 48 h with insulin increased the rate of fatty acid synthesis. Dexamethasone, a glucocorticoid analogue, alone inhibited the rate of fatty acid synthesis, but enhanced the stimulatory effect of insulin. Growth hormone (somatotropin) antagonized the increase in the rate of fatty acid synthesis induced by insulin or insulin plus dexamethasone. 3. Maintenance of adipose tissue from lactating sheep in tissue culture resulted in a small increase in the rate of fatty acid synthesis after 24 h, and then a large increase in rate between 24 and 48 h of culture. The increase during the second 24 h period was dependent on the presence of insulin; this effect was enhanced by dexamethasone and inhibited by growth hormone. 4. The increase in the rate of fatty acid synthesis in tissue from non-lactating sheep and in tissue from lactating sheep during the major increase in rate was prevented by actinomycin D, an inhibitor of transcription. 5. Effects of insulin and growth hormone were observed with physiological concentrations of the hormones. 6. The study suggests that known changes in the serum concentrations of insulin and growth hormone are the primary causes of the changes in fatty acid synthesis in adipose tissue during the lactation cycle in sheep. 7. During lactation, adipose tissue becomes refractory to insulin in sheep; responsiveness is partly restored by tissue culture in the presence of insulin and dexamethasone.

1-Methyl-3-isobutylxanthine↗

PubMed1988

Insulin, dexamethasone and their interactions in the control of glucose metabolism in adipose tissue from lactating and nonlactating sheep.

1. Lactation results in decreased glucose and acetate utilization and increased lactate output by sheep adipose tissue. 2. The ability of insulin to stimulate acetate uptake was lost in adipose tissue from lactating sheep, whereas both the response and the sensitivity (ED50) for insulin for stimulation of glucose conversion into products other than lactate were decreased. These impairments were partly restored by prolonged incubation of adipose tissue for 48 h. 3. The ability of insulin to stimulate lactate output was not altered by lactation. 4. Dexamethasone inhibited glucose uptake, lactate output and glycerol output in adipose tissue from both non-lactating and lactating sheep, with an ED50 of about 1 nM. Dexamethasone inhibited acetate uptake by adipose tissue from non-lactating sheep, but this effect was not observed with adipose tissue from lactating sheep. 5. Dexamethasone inhibited the stimulation of glucose uptake at all concentrations of insulin used; the effect varied with insulin concentration and resulted in an accentuation of the insulin dose-response curve. The insulin dose-response curve in the presence of dexamethasone was muted during lactation. 6. The overall effect of these adaptations is to ensure that glucose and acetate utilization by adipose tissue after an insulin surge is diminished during lactation.

Adipose Tissue↗

PubMed1988

Defect in signal transduction at the level of the plasma membrane accounts for inability of insulin to activate pyruvate dehydrogenase in white adipocytes of lactating rats.

1. The mechanism responsible for the failure of insulin to activate pyruvate dehydrogenase (PDH) in white adipose tissue in vivo during lactation was investigated. 2. Insulin failed to increase PDH in isolated adipocytes from lactating rats. 3. Insulin binding to plasma membranes from adipocytes was unchanged by lactation. 4. Incubation of plasma membranes plus permeabilized mitochondria from adipocytes in the presence of insulin resulted in activation of PDH when the plasma membranes were obtained from virgin rats, whereas no activation was observed when plasma membranes from lactating rats were used. 5. The results show that the failure of insulin to activate PDH in adipose tissue from lactating rats is due to a failure of the signal-transduction system in the plasma membrane at steps subsequent to insulin binding to the insulin receptor.

5'-Nucleotidase↗

PubMed1988

Fatty acid metabolism of the perfused caudate lobe from livers of fed and fasted non-pregnant and fasted late pregnant ewes.

1. Fatty acid metabolism has been compared in perfused liver lobes from fed and fasted non-pregnant sheep and fasted pregnant sheep to provide further information on the control of ketogenesis in this species. 2. Ketogenesis from exogenous palmitate was greatest in lobes from fasted pregnant sheep and least in lobes from fed non-pregnant sheep, whereas rates of ketogenesis from exogenous octanoate (0.4 mM) were similar in lobes from sheep in all three states. 3. High rates of ketogenesis from endogenous fatty acids occurred in perfused lobes from fasted pregnant sheep, apparently owing to enhanced lipolysis. 4. Activities of glycerol-3-phosphate acyltransferase, carnitine palmitoyl transferase (CPT) and other enzymes involved in ketone production did not change with physiological state; sheep differ markedly from rats in this respect. 5. The results suggest that the primary point of control of ketogenesis within the liver of sheep is at the level of CPT; the lack of change in maximum CPT activity suggests that control by modulators of this enzyme activity is even more important in sheep than in rats.

Animals↗

PubMed1988

Lipid metabolism in farm animals.

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Animals↗

PubMed1988

The legal ramifications of AIDS in the workplace.

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AIDS-Related Complex↗

PubMed1987

Protein metabolism in the mouse during pregnancy and lactation.

Protein synthesis was measured in vivo in the whole body and in a number of individual tissues in mice at various stages of pregnancy and lactation. The absolute rate of protein synthesis in the whole body increased from 640 mg/day in virgin mice to 1590 mg/day by day 18 of pregnancy, and to 2100 mg/day by day 15 of lactation. Large proportions of these increments were contributed by the rapidly growing foetuses and placentae in the pregnant animals and by protein synthesis in the mammary glands during lactation. In addition, a substantial stimulation of growth and protein synthesis was also observed in the liver and the gastrointestinal tract. Gastrocnemius muscle showed no changes in protein metabolism, indicating that in the well-fed mouse this tissue is not required to play a role as a protein reserve during pregnancy and lactation.

Animals↗

PubMed1987

Interactions of insulin and dexamethasone in the control of pyruvate kinase activity and glucose metabolism in sheep adipose tissue.

1. The Vmax. activity of pyruvate kinase of sheep adipose tissue increased during tissue culture up to 48 h; the increase was blocked by actinomycin D (an inhibitor of transcription) and was promoted by insulin and antagonized by dexamethasone. 2. In contrast with their effects on pyruvate kinase, insulin and dexamethasone acted synergistically to increase the activity of glucose-6-phosphate dehydrogenase of sheep adipose tissue maintained in culture. 3. Insulin stimulated, whereas dexamethasone inhibited, glucose utilization by sheep adipose tissue maintained in culture; the two agents were mutually antagonistic, and their effects were prevented by actinomycin D. 4. Antimycin A (an inhibitor of the electron-transport chain) stimulated glucose uptake and lactate output by sheep adipose tissue in the presence of dexamethasone and insulin, suggesting that the effects of dexamethasone on glucose utilization by sheep adipose tissue were not due to an inhibition of glucose transport. 5. Comparison of these findings with previous studies on the endocrine control of hepatic pyruvate kinase shows that there are major differences in the control of these Vmax. activities in liver and adipose tissue. 6. Although glucocorticoid hormones inhibit glucose utilization themselves and can antagonize the stimulatory effects of insulin on glucose utilization in adipose tissue from both sheep and rats, there appear to be major differences in the sites of action of these hormones in the two species.

Adipose Tissue↗

PubMed1987

Tissue-specific changes in the ability of insulin and noradrenaline to activate pyruvate dehydrogenase in vivo during lactation in the rat.

Changes are described in the total pyruvate dehydrogenase (PDH) activity, the proportion of PDH in the active state and its control by insulin and noradrenaline in vivo, in white adipose tissue, liver, skeletal muscle and mammary gland with pregnancy, lactation and on weaning. Lactation resulted in a decrease in total PDH in white adipose tissue and an increase in the mammary gland, whereas the proportion in the active state decreased in muscle and increased in the mammary gland. The ability of insulin to activate PDH of white adipose tissue was lost during lactation, whereas it was retained by the other tissues. The ability of noradrenaline to activate PDH was decreased in white adipose tissue but increased in liver during lactation. These various adaptations should limit the use of glucose and lactate carbon by adipose tissue and skeletal muscle during lactation and thereby facilitate their preferential utilization by the mammary gland.

Adipose Tissue↗

PubMed1987

Role of growth hormone in the adaptations of lipolysis in rat adipocytes during recovery from lactation.

Removal of the litter from lactating rats results in a fall in the rate of noradrenaline-stimulated lipolysis of adipocytes. This adaptation can be prevented by administration of growth hormone (somatotropin) to such rats and mimicked by injecting lactating rats with an antiserum to growth hormone, whereas lowering serum prolactin by injecting bromocriptine had no effect. The anti-lipolytic effect of adenosine is increased during lactation and is still increased by 2 days after litter removal. Injection of growth hormone into lactating rats decreased slightly the response to adenosine, whereas injection of growth hormone into rats after removal of their litters resulted in a much greater decrease in the response to adenosine, to that found in virgin and pregnant rats.

Adaptation, Physiological↗