Proceedings of the 1978 Laurentian Hormone Conference 1979
DOI: 10.1016/b978-0-12-571135-7.50016-3
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Hormonal Interactions in the Regulation of Blood Glucose

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Cited by 29 publications
(24 citation statements)
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“…When insulin is deficient (absolute or relative), hyperglycemia develops as a result of three processes: increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization by peripheral tissues (39)(40)(41)(42)(43)(44). Increased hepatic glucose production results from the high availability of gluconeogenic precursors, such as amino acids (alanine and glutamine; as a result of accelerated proteolysis and decreased protein synthesis) (45), lactate (as a result of increased muscle glycogenolysis), and glycerol (as a result of increased lipolysis), and from the increased activity of gluconeogenic enzymes.…”
Section: Carbohydrate Metabolismmentioning
confidence: 99%
“…When insulin is deficient (absolute or relative), hyperglycemia develops as a result of three processes: increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization by peripheral tissues (39)(40)(41)(42)(43)(44). Increased hepatic glucose production results from the high availability of gluconeogenic precursors, such as amino acids (alanine and glutamine; as a result of accelerated proteolysis and decreased protein synthesis) (45), lactate (as a result of increased muscle glycogenolysis), and glycerol (as a result of increased lipolysis), and from the increased activity of gluconeogenic enzymes.…”
Section: Carbohydrate Metabolismmentioning
confidence: 99%
“…This is augmented by transient insulin resistance due to the hormone imbalance itself as well as the elevated free fatty acid concentrations [8,10,26,[28][29][30][31][32][33][34][35][36][37][38][39]. Uncontrolled hepatic fatty acid oxidation in the liver to ketone bodies (beta-hydroxybutyrate and acetoacetate) results ketonemia and metabolic acidosis [40].…”
Section: Pathogenesismentioning
confidence: 99%
“…These hormonal changes increase glucose production from glycogenolysis and gluconeogenesis and impair glucose utilization by peripheral tissues, resulting in hyperglycemia, osmotic diuresis, electrolyte loss, dehydration, decreased glomerular filtration (further compounding hyperglycemia) and hyperosmolarity. [26,[30][31][32][33][34][35].…”
Section: Pathogenesismentioning
confidence: 99%
“…11 In DKA, the severe deficiency in insulin and increased counter-regulatory hormones lead to increased lipolysis and production of ketone bodies and resulting metabolic acidosis. 12 It is not known why people with HHS do not develop ketoacidosis, but it is postulated to be owing lower level of free fatty acids or higher portal vein insulin. 13 …”
mentioning
confidence: 99%