Endocrine - metabolic interrelationships in normal man and in liver disease
Endocrine - metabolic interrelationships in normal man and in liver disease
Endocrine influences on intermediary metabolism have been investigated in normal man and in liver disease, and the particular role of insulin in hepatic regeneration and metabolism after partial hepatectomy has been examined in the rat. Growth hormone and cortisol excess in normal subjects had delayed, but not acute, hyperglycaemic effects associated with increased insulin secretion. Suppression of insulin secretion with somatostatin exaggerated these actions and revealed a ketotic effect of both hormones. Hyperglucagonaemia also increased insulin secretion and only in somatostatin induced insulin deficiency was a rapid hyperglycaemic and transient hyperketonaemic action observed. Although the fasting blood glucose was normal, patients with chronic liver disease had impaired clearance of an exogenous glycerol load, suggesting a decreased capacity for gluconeogenesis. They also showed carbohydrate intolerance despite peripheral hyperinsulinaemia, but circulating ketone body concentrations were normal. The elevated circulating growth hormone, cortisol and glucagon concentrations in some patients may have contributed to the metabolic changes observed. Studies with simultaneous insulin and C-peptide estimations in peripheral blood suggested that the hyperinsulinaemia of cirrhosis resulted from decreased insulin degradation rather than hypersecretion. Partial hepatectomy in rats increased DNA synthesis, assessed by hepatic [3H] thymidine uptake. DNA synthesis was impaired in streptozotocin-diabetics and subcutaneous insulin therapy caused a delayed rise. Insulin was without effect in non-diabetic animals. The delayed metabolic effects of cortisol and growth hormone, and acute effects of glucagon, may assume particular importance when insulin secretion is low as in stress, starvation or diabetes and may contribute to the metabolic abnormalities in liver disease. While adequate insulin secretion is necessary for normal hepatic regeneration, additional insulin treatment does not modify the regenerative response in non-diabetic rats.
University of Southampton
Johnston, Desmond Geoffrey
652930df-0e03-47c9-91ab-29923b8b6125
1982
Johnston, Desmond Geoffrey
652930df-0e03-47c9-91ab-29923b8b6125
Johnston, Desmond Geoffrey
(1982)
Endocrine - metabolic interrelationships in normal man and in liver disease.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
Endocrine influences on intermediary metabolism have been investigated in normal man and in liver disease, and the particular role of insulin in hepatic regeneration and metabolism after partial hepatectomy has been examined in the rat. Growth hormone and cortisol excess in normal subjects had delayed, but not acute, hyperglycaemic effects associated with increased insulin secretion. Suppression of insulin secretion with somatostatin exaggerated these actions and revealed a ketotic effect of both hormones. Hyperglucagonaemia also increased insulin secretion and only in somatostatin induced insulin deficiency was a rapid hyperglycaemic and transient hyperketonaemic action observed. Although the fasting blood glucose was normal, patients with chronic liver disease had impaired clearance of an exogenous glycerol load, suggesting a decreased capacity for gluconeogenesis. They also showed carbohydrate intolerance despite peripheral hyperinsulinaemia, but circulating ketone body concentrations were normal. The elevated circulating growth hormone, cortisol and glucagon concentrations in some patients may have contributed to the metabolic changes observed. Studies with simultaneous insulin and C-peptide estimations in peripheral blood suggested that the hyperinsulinaemia of cirrhosis resulted from decreased insulin degradation rather than hypersecretion. Partial hepatectomy in rats increased DNA synthesis, assessed by hepatic [3H] thymidine uptake. DNA synthesis was impaired in streptozotocin-diabetics and subcutaneous insulin therapy caused a delayed rise. Insulin was without effect in non-diabetic animals. The delayed metabolic effects of cortisol and growth hormone, and acute effects of glucagon, may assume particular importance when insulin secretion is low as in stress, starvation or diabetes and may contribute to the metabolic abnormalities in liver disease. While adequate insulin secretion is necessary for normal hepatic regeneration, additional insulin treatment does not modify the regenerative response in non-diabetic rats.
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Published date: 1982
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Local EPrints ID: 460054
URI: http://eprints.soton.ac.uk/id/eprint/460054
PURE UUID: 90b181db-4b9c-4e93-8296-1146d4b5344f
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Date deposited: 04 Jul 2022 17:44
Last modified: 23 Jul 2022 00:58
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Author:
Desmond Geoffrey Johnston
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