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Biomedical subjects

R G Vernon

Publications and source records attributed to R G Vernon.

At least 73 records · Page 4Linked to original sources
PubMed1992

Regional and interspecific differences in the ligand binding properties of beta-adrenergic receptors of individual white adipose tissue depots in the sheep and rat.

The ligand binding of beta-adrenergic receptors was characterized in the omental, subcutaneous and popliteal adipose tissue depots in the sheep, and the lumbar and parametrial depots in the rat. Displacement of [125I]iodocyanopindolol ([125I]ICYP) binding to sheep adipose tissue membranes by the beta-adrenergic antagonists CGP 20712A and ICI 118,551 (beta 1- and beta 2-antagonists, respectively) suggested only a single ligand binding site predominantly beta 2 in character in all three depots, but revealed differences in affinity for these ligands between depots. Lactation increased beta-receptor ligand binding in subcutaneous and omental but not popliteal sheep adipose tissue depots, but had no effect on beta-adrenergic receptor affinities for CGP 20712A and ICI 118,551 in the three sheep adipose tissue depots studied. In rat adipocyte membranes, displacement of [125I]ICYP by CGP 20712A and ICI 118,551 was biphasic, indicating high and low affinity sites; displacement profiles differed markedly between lumbar and parametrial depots, the former having a preponderance of beta 1-like receptors and the latter a preponderance of beta 2-like receptors. The properties of the beta-adrenergic receptor binding site thus show species and depot specific differences.

Adipose Tissue↗
PubMed1992

Growth-hormone-prolactin interactions in the regulation of mammary and adipose-tissue acetyl-CoA carboxylase activity and gene expression in lactating rats.

The factors and mechanisms responsible for the reciprocal changes in lipogenesis in rat mammary gland and adipose tissue during the lactation cycle have been investigated. Lactation decreased the activation status and mRNA concentration of acetyl-CoA carboxylase in adipose tissue. Litter removal decreased the mRNA concentration of acetyl-CoA carboxylase in the mammary gland and increased the enzyme's mRNA concentration and activation status in adipose tissue. Lowering serum prolactin concentration in lactating rats decreased the amount of mammary acetyl-CoA carboxylase mRNA and increased that of adipose tissue, and increased the activation status of the enzyme in adipose tissue. Decreasing serum growth hormone (GH) alone had little effect on acetyl-CoA carboxylase in lactating rats, although it did lower pup growth rate and serum concentration of insulin-like growth factor-I. Lowering serum GH concentration exacerbated the effects of decreasing serum prolactin on mammary-gland (but not adipose-tissue) acetyl-CoA carboxylase mRNA and further increased the rise in activation status of the adipose-tissue enzyme induced by decreasing serum prolactin. Changes in acetyl-CoA carboxylase mRNA in both mammary and adipose tissue were paralleled by changes in total enzyme activity except after litter removal, when there was a disproportionately large decrease in total enzyme activity of the mammary gland. Thus prolactin has a major and GH a minor role in the regulation of acetyl-CoA carboxylase activity during lactation. Changes in mammary activity in response to prolactin and GH are primarily due to alterations in gene transcription, whereas adaptation in adipose tissue involves both changes in gene transcription and activation status.

Acetyl-CoA Carboxylase↗
PubMed1992

Prostaglandin E2 in adipose tissue extracellular fluid of sheep.

Prostaglandin E2 concentration in perfusate from microdialysis tubing implanted in subcutaneous adipose tissue of sheep did not consistently change during feeding. Noradrenaline infused into this tissue produced a prompt increase of glycerol concentration in the perfusate, but this changed to a slight decrease towards the end of the infusion. At approximately the time of this decrease, levels of prostaglandin E2 in the perfusate increased.

Adipose Tissue↗
PubMed1992

The role of growth hormone, prolactin and insulin-like growth factors in the regulation of rat mammary gland and adipose tissue metabolism during lactation.

Inhibition of prolactin secretion with bromocriptine and neutralization of GH action with a specific antiserum to rat GH (rGH) were used to explore the modes of action of GH and prolactin in maintaining lactation in the rat. Treatment of dams with anti-rGH caused a small reduction in litter weight gain whilst bromocriptine reduced litter weight gain by 50%. When both treatments were combined, however, milk yield ceased completely and this was accompanied by a wide variety of effects on mammary lipid metabolism including decreases in the mRNA concentrations of acetyl CoA carboxylase, fatty acid synthase, malic enzyme and lipoprotein lipase. Activities of acetyl CoA carboxylase and lipoprotein lipase were also significantly reduced. Reciprocal changes were evident in adipose tissue with increases in acetyl CoA carboxylase and lipoprotein lipase activities. In conjunction with a decreased lipolytic response to noradrenaline in adipose tissue of animals given the combined treatment of bromocriptine and anti-rGH, this represented a co-ordinated series of changes to reduce lipid synthesis in the mammary gland and enhance lipogenesis and triglyceride storage in adipose tissue as milk production ceased. All of these effects could be prevented in part by concurrent treatment with GH, but insulin-like growth factor-I (IGF-I) and IGF-II failed to affect any of the parameters measured.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1991

Modulation of the activity of acetyl-CoA carboxylase and other lipogenic enzymes by growth hormone, insulin and dexamethasone in sheep adipose tissue and relationship to adaptations to lactation.

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.

Acetyl-CoA Carboxylase↗
PubMed1991

Chronic control of the beta- and alpha 2-adrenergic systems of sheep adipose tissue by growth hormone and insulin.

1. Sheep adipose tissue retained responsiveness to catecholamines when maintained in tissue culture for 48 h; both the rate of basal lipolysis and sensitivity to beta-agonists were increased after tissue culture. 2. Tissue culture in the presence of growth hormone resulted in an increased maximum response and sensitivity to the beta-agonist isoprenaline, but had no effect on basal lipolysis. 3. Tissue culture in the presence of insulin increased the basal rate of lipolysis and increased the ratio of the rate of noradrenaline-stimulated/isoprenaline-stimulated lipolysis, indicating a decrease in the 2-adrenergic effect of noradrenaline. 4. Tissue culture in the presence of growth hormone increased ligand binding to beta-adrenergic receptors. 5. Tissue culture in the absence of exogenous hormones increased ligand binding to alpha 2-adrenergic receptors; this was prevented by actinomycin D and partly prevented by insulin. 6. These studies show that both growth hormone and insulin chronically modulate the adrenergic system of sheep adipose tissue; the effects of growth hormone are primarily on the beta-adrenergic system, whereas insulin modulates the alpha 2-adrenergic system.

Adipose Tissue↗
PubMed1991

Depot specific endocrine control of fatty acid synthesis in adipose tissues of foetal lambs.

Chronic endocrine control of fatty acid synthesis in perirenal and subcutaneous adipose tissues of foetal lambs has been investigated. Maintenance of explants of subcutaneous adipose tissue in culture for 48 hr with insulin and dexamethasone (a glucocorticoid analogue), either singly or in combination showed that the two acted synergistically to increase the rate of fatty acid synthesis. Growth hormone inhibited the ability of insulin plus dexamethasone to increase the rate of fatty acid synthesis in explants of subcutaneous adipose tissue. In contrast neither insulin nor dexamethasone either singly or together increased the rate of fatty acid synthesis in perirenal adipose tissue; growth hormone also had no effect on the rate of fatty acid synthesis in this depot. These studies show that fatty acid synthesis is under distinct endocrine control in subcutaneous and perirenal adipose tissues in foetal lambs.

Adipose Tissue↗
PubMed1991

Insulin binding to skeletal muscle microsomes in lactating and dry sheep.

Microsomes were prepared from skeletal muscles taken from lactating and non lactating ewes. Insulin binding to these microsomes was not affected by reproductive status. There were significant differences in the ability of individual muscles to bind insulin. These differences correlated with the function of the muscle, as defined by the predominant muscle fibre type.

5'-Nucleotidase↗
PubMed1991

Adenosine and the control of adrenergic regulation of adipose tissue lipolysis during lactation.

Adenosine is a locally active factor that is produced intracellularly and extracellularly in adipose tissue. Adenosine binds to receptors in the plasma membrane of adipocytes; this activates a guanine triphosphate binding protein that inhibits adenylate cyclase activity and, hence, lipolysis. Lactation results in an enhanced responsiveness of adipocytes to beta-agonists, which stimulate lipolysis, and, paradoxically, to adenosine, which inhibits lipolysis. These adaptations are partly due to increases in ligand binding and to changes in postreceptor components of the signal transduction systems. Somatotropin is implicated in the chronic adaptations of the beta-adrenergic system, whereas insulin, somatotropin, glucocorticoids, and at least one unidentified factor have a role in the chronic control of the adenosine system of adipocytes.

Adenosine↗
PubMed1990

Insulin resistance of hind-limb tissues in vivo in lactating sheep.

1. The effects of varying the plasma insulin concentration by infusion while maintaining euglycaemia by infusion of glucose on nutrient arterio-venous differences across the hind-limb and mammary gland in lactating and non-lactating sheep were investigated. 2. Insulin infusion increased the glucose arterio-venous difference across the hind-limb; this effect of insulin was decreased by lactation, suggesting that lactation induces insulin resistance in skeletal muscle. 3. Lactation increased but insulin infusion decreased the plasma concentrations of acetate, beta-hydroxybutyrate and non-esterified fatty acids. 4. Insulin infusion decreased the arterio-venous differences of acetate and hydroxybutyrate across the hind-limb; this effect of insulin is probably indirect, resulting from the decrease in plasma concentrations of these metabolites. 5. Infusion of insulin had no effect on the glucose arterio-venous difference across the mammary gland, but did decrease the oxygen arterio-venous difference. 6. The results suggest that lactation results in insulin resistance in skeletal muscle, at least with respect to glucose utilization; this should facilitate the preferential utilization of glucose by the mammary gland.

Acetates↗
PubMed1990

Teladorsagia circumcincta egg output at the onset of natural and induced lactation in ewes.

Nineteen ewes maintained under 'worm-free' conditions received anthelmintic and 1 week later were dosed on 5 days each week with 500 Teladorsagia circumcincta larvae for between 10 and 12.5 weeks. Faecal egg counts were determined twice weekly. There were three groups: pregnant (P) ewes (n = 6) which each reared twin lambs, hormone-treated (H) ewes (n = 7) which were not pregnant and were given exogenous hormones (dexamethasone, oestradiol-17 beta, progesterone) for 37 days to induce udder development and milk production, and untreated barren (B) ewes (n = 6). The plasma concentrations of oestradiol-17 beta, prolactin and progesterone were measured. Starting 10-15 days before birth in Group P, there was a biphasic periparturient rise in egg count and the onset of the first peak in egg count preceded the parturient peak in plasma prolactin concentration by several days. Most Group H (5/7) and all Group B ewes remained highly resistant to Teladorsagia infection throughout, despite an induced rise in prolactin concentrations in Group H ewes. It was concluded that factors other than prolactin initiate the periparturient rise but that prolactin is one factor which maintains the response once lactation commences.

Animals↗