The hormonal control of lipid metabolism in sheep
type: CreativeWork
description: The hormonal control of lipid metabolism was investigated by incubation of ovine adipose tissue slices in the presence of hormones the in vitro. The effects of insulin, catecholamines, growth hormone (GH) and insulin-like growth factors (IGFs) on lipogenesis and lipid mobilization were studied to assess their likely individual contributions to overfatness in vivo. From the various measurements of lipid metabolism made, the rates of fatty acid accumulation in the tissue during the incubation were calculated. Since most of the fatty acid released by lipolysis appeared to be re-esterified, observation of glycerol data alone may give a false impression of the extent of fatty acid mobilization or the overall energy balance of the tissue. About 60 - 100% of fatty acid released by lipolysis could be recycled within the tissue, a phenomenon which is under hormonal control and is possibly linked with maintenance of non-shivering thermogenesis. Insulin stimulated the rate of lipogenesis (from acetate) by up to 6-fold, with the average stimulation about 70%, but it failed to affect the rate in tissue from one quarter of the animals tested. Also insulin stimulated the retention of fatty acid by the cell as well as fatty acid recycling, even in tissue in which it was not lipogenic. Thus observation of lipogenesis alone can give a false impression of the lipid-storing effects of a hormone. IGFs, when present at high concentrations, were lipogenic. However, because the binding proteins may restrict the activity of IGFs in vivo, low concentrations of IGF were tested and shown to be lipolytic. It is suggested that whereas the high concentrations of IGFs have been thought to act via the insulin receptor, low concentrations may mediate the lipolytic response via the IGF receptor. Similar states of negative energy balance in the tissue were caused by the presence of either IGF I, IGF II or adrenalin in the medium. GH sometimes stimulated a transient increase in the rate of lipolysis. I…
abstract: The hormonal control of lipid metabolism was investigated by incubation of ovine adipose tissue slices in the presence of hormones the in vitro. The effects of insulin, catecholamines, growth hormone (GH) and insulin-like growth factors (IGFs) on lipogenesis and lipid mobilization were studied to assess their likely individual contributions to overfatness in vivo. From the various measurements of lipid metabolism made, the rates of fatty acid accumulation in the tissue during the incubation were calculated. Since most of the fatty acid released by lipolysis appeared to be re-esterified, observation of glycerol data alone may give a false impression of the extent of fatty acid mobilization or the overall energy balance of the tissue. About 60 - 100% of fatty acid released by lipolysis could be recycled within the tissue, a phenomenon which is under hormonal control and is possibly linked with maintenance of non-shivering thermogenesis. Insulin stimulated the rate of lipogenesis (from acetate) by up to 6-fold, with the average stimulation about 70%, but it failed to affect the rate in tissue from one quarter of the animals tested. Also insulin stimulated the retention of fatty acid by the cell as well as fatty acid recycling, even in tissue in which it was not lipogenic. Thus observation of lipogenesis alone can give a false impression of the lipid-storing effects of a hormone. IGFs, when present at high concentrations, were lipogenic. However, because the binding proteins may restrict the activity of IGFs in vivo, low concentrations of IGF were tested and shown to be lipolytic. It is suggested that whereas the high concentrations of IGFs have been thought to act via the insulin receptor, low concentrations may mediate the lipolytic response via the IGF receptor. Similar states of negative energy balance in the tissue were caused by the presence of either IGF I, IGF II or adrenalin in the medium. GH sometimes stimulated a transient increase in the rate of lipolysis. I…
author: Lewis, Kae Jennifer
license: https://researchcommons.waikato.ac.nz/bitstreams/f00ba2af-7554-4da9-8d87-65ed6a40ad94/download
date published: 1987
date modified: 2026-07-24T05:57:27Z
provider: University Waikato
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: The University of Waikato