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Roles of insulin and growth hormone in the adaptations of fatty acid synthesis in white adipose tissue during the lactation cycle in sheep.

ABSTRACT: 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.

SUBMITTER: Vernon RG

PROVIDER: S-EPMC1135497 | biostudies-other | 1988 Dec

REPOSITORIES: biostudies-other

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Project description:The mechanisms whereby growth hormone and dexamethasone modulate the stimulation of fatty acid synthesis by insulin in adipose tissue from lactating and non-lactating sheep have been investigated. Maintenance of adipose tissue from wethers (castrated male sheep) in tissue culture for 24 or 48 h with insulin resulted in an increased proportion of acetyl-CoA carboxylase being present in the active state; this effect was enhanced by dexamethasone and was antagonized by growth hormone. Lactation results in a decrease in both the total acetyl-CoA carboxylase of sheep adipose tissue and the proportion of the enzyme in the active state. Maintenance of adipose tissue from lactating sheep in tissue culture for 48 h in the presence of insulin plus dexamethasone increased markedly the proportion of acetyl-CoA carboxylase in the active state and increased slightly the total activity of the enzyme. Both of these effects were prevented by actinomycin D, and the change in activation status was prevented by growth hormone. Tissue culture for 6 days showed that growth hormone could also prevent the ability of insulin plus dexamethasone to increase the total activity of the enzyme. Analogous studies showed that insulin, dexamethasone and growth hormone modulated the activities of other lipogenic enzymes, but the effects were proportionately smaller than for acetyl-CoA carboxylase. Insulin also increased total protein synthesis in adipose tissue, but this was not antagonized by growth hormone. The results suggest that the fall in fatty acid synthesis in sheep adipose tissue during lactation is due to a decrease in both the total acetyl-CoA carboxylase activity and the proportion of the enzyme in the active state; these changes are probably induced by known changes in the serum concentrations of insulin and growth hormone. Lactation appears to result in the loss of a protein that is required for activation of acetyl-CoA carboxylase by insulin; production of this component appears to be prevented by growth hormone.

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Roles of insulin and growth hormone in the adaptations of fatty acid synthesis in white adipose tissue during the lactation cycle in sheep.

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