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Biological Responses in Context
Published in Arthur T. Johnson, Biology for Engineers, 2019
The concentration of glucose in human blood is maintained at about 90 mg/100 mL (or 0.9 kg/m3) by two pancreatic hormones: insulin and glucagon. Insulin lowers blood glucose levels by stimulating nearly all body cells (except those in the brain) to assimilate and consume blood glucose. It also slows the conversion of liver glycogen (an insoluble storage form of glucose) into glucose and inhibits the transformation of amino acids and fatty acids into glucose. Glucagon raises blood glucose levels by signaling liver cells to increase glycogen hydrolysis and to convert amino acids and fatty acids to glucose. The glucose is then released into the blood (Figure 6.20.7). The combination of these two hormones, both of which may be present in the blood at the same time, results in exquisite glucose control.
Hypoglycaemia and Hypoglycaemia Awareness
Published in Anthony N. Nicholson, The Neurosciences and the Practice of Aviation Medicine, 2017
The physiological processes that maintain blood glucose, described above, are under hormonal control. Insulin is the main regulatory hormone secreted from the [β-cells of the pancreatic islets (Rizza et al., 1981). Activation of insulin receptors in skeletal muscle and adipose tissue increases peripheral glucose uptake and storage. Insulin also suppresses glycogenolysis and gluconeogenesis, promoting hepatic and renal storage of glucose as glycogen. Conversely, falling insulin concentrations lead to a release of hepatic glucose and diminished peripheral glucose uptake. Glucose concentrations are also controlled by the actions of additional ‘counter-regulatory hormones’. The regulatory and glucose-lowering effects of insulin are opposed by the counter-regulatory hormones, glucagon, adrenaline, cortisol and growth hormone, as well as by activation of the sympathoadrenal system. Glucagon, released from the a-cells of the islet as glucose concentrations fall, stimulates hepatic glycogenolysis and so increases hepatic glucose uptake. It also stimulates hepatic gluconeogenesis, although, because it does not mobilize gluconeogenic precursors from peripheral tissue, the effect is somewhat limited.
Introduction to Physiological Regulators and Control Systems
Published in Robert B. Northrop, Endogenous and Exogenous Regulation and Control of Physiological Systems, 2020
In Chapter 7, another important physiological system that uses parametric control will be examined in detail: the blood glucose regulatory system. The pancreatic hormone insulin is seen to increase the rate at which glucose diffuses into insulin-sensitive cells by effectively increasing the transmembrane diffusion rate constant for glucose. The pancreatic hormone glucagon acts parametrically to increase blood glucose concentration by stimulating the production of key enzymes in liver cells that catalyze the breakdown of glycogen into glucose and increase its release rate into the bloodstream. Many other examples of parametric control and regulation will also be described in this text.
Adaptive controller based an extended model of glucose-insulin-glucagon system for type 1 diabetes
Published in International Journal of Modelling and Simulation, 2023
Mahour Saoussane, Tadjine Mohammed, Chakir Mesaoud
The level of blood glucose is mainly controlled by two hormones having opposite effects. While insulin clears out the blood glucose by stimulating its uptake by muscles and adipose tissues and storing it as a glycogen in the liver, glucagon supplies the bloodstream with glucose produced by liver gluconeogenesis and glycogenolysis. Consequently, any dysfunction in the secretion of insulin or glucagon will lead to problems in the control of glycemia. Despite the importance of glucagon in the control of glycemia. There are fewer studies in the literature on glucagon and α-cells than those on insulin and β-cells [9]. The use of insulin as the only control input may be insufficient in case of hypoglycemia, because a low glucose level cannot be raised by insulin action alone. It seems to be that in order to restore the desired glucose level, the administration of glucagon, as another control input is necessary. The block diagram of the glucose-insulin-glucagon regulatory system is given in Figure 2.
Closed-loop insulin delivery: update on the state of the field and emerging technologies
Published in Expert Review of Medical Devices, 2022
In addition to insulin, secretion of the hormones glucagon and amylin is impaired in people with type 1 diabetes. Glucagon is secreted in response to falling glucose levels and triggers release of glucose stored as glycogen from the liver. Amylin delays gastric emptying and reduces post-prandial hyperglycemic excursions. Dual-hormone systems aim to deliver one of these two hormones in addition to insulin, to further improve glucose control by allowing for more aggressive insulin delivery [108]. Barriers to dual-hormone systems include the need for a second or dual chamber pump, and the risk of gastrointestinal side-effects. Newer glucagon analogues are more stable at room temperature than previously available formulations, enabling continuous infusion without the need for daily set changes [109]. A 7-day study of 10 participants in the home setting using the iLet dual-hormone using dasiglucagon vs insulin-only showed higher time in range with dual-hormone (79% vs 72%), and lower time in hypoglycemia [110]. Amylin’s synthetic analogue pramlintide has been trialed in adult inpatient dual-hormone closed-loop studies, and results showed improvements in time in range compared to insulin-only systems [111]. Larger, pivotal trials of dual-hormone systems are in the pipeline.
Closed-loop insulin delivery: current status of diabetes technologies and future prospects
Published in Expert Review of Medical Devices, 2018
Mitigating hypoglycaemia burden and improving postprandial performance has prompted evaluation of co-administration of glucagon for the former or amylin for the latter, alongside insulin, in dual-hormone CLS [9]. Glucagon is produced by the pancreas and is a counter-regulatory hormone which prevents hypoglycaemia by converting hepatic glycogen stores to glucose (glycogenolysis) [73]. El-Khatib et al. compared dual-hormone CLS with usual care (SAP or CSII alone) in adults with T1D and showed that dual-hormone CLS resulted in significant reductions in mean glucose and time spent hypoglycaemic [74]. In a randomized three-way crossover trial in adults, dual-hormone CLS was compared with single-hormone CLS and SAP. The primary outcome (time spent <4 mmol/L) was significantly reduced by both dual-hormone and single-hormone CLS compared to SAP. A greater reduction in the primary outcome was observed by dual-hormone CLS when compared to single-hormone CLS, but did not reach statistical significance [75]. Similar findings have also been seen in the pre-adolescent and adolescent cohorts [76,77]. Results from these and other day-and-night dual-hormone CLS studies are summarized in Table 1.