China 
Africa 
Explore chapters and articles related to this topic
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.
Diabetes Monitoring System
Published in Rajarshi Gupta, Dwaipayan Biswas, Health Monitoring Systems, 2019
The glucose-insulin control system in the human body is regulated by a complex neuro-hormonal control system. Insulin is the primary regulator of glucose homeostasis that promotes glucose utilization and inhibits glucose production from stored resources in the body. Working at different scales, counter-regulatory hormones like glucagon, epinephrine, cortisol, and growth hormone defend the body from life-threatening hypoglycemia. Insulin control and hypoglycemia counter-regulation are balanced by neuro-modulation. Glucose in the body is produced by the liver and utilized in both insulin-dependent (e.g., central nervous system and red blood cells) and insulin-independent tissues (e.g., muscle and adipose tissues). Insulin is secreted by the beta cells in the pancreas, then reaches the system circulation after liver degradation, and is finally cleared by the kidney. The glucose and insulin systems interact by feedback control signals; for example, during glucose perturbation after a meal, the beta cells secrete more insulin after sensing high plasma glucose concentration, thereby promoting glucose utilization and inhibiting glucose production to balance the plasma glucose. Insulin sensitivity and beta-cell responsitivity progressively deteriorate in type 2 diabetes. In type 1 diabetes, the beta cells don’t respond to glucose perturbation, and therefore, insulin must be provided exogenously into the patient’s body to compensate for hyperglycemia. However, insulin treatment is often risky and may lead to severe hypoglycemia. Therefore, for type 1 diabetic patients it is a challenge to maintain reduced hyperglycemia without risking hypoglycemia; blood glucose level is the measured quantity in such optimization. Several control models have been developed to assist diabetes control, which are reviewed in the following section.
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.
An extensible mathematical model of glucose metabolism. Part I: the basic glucose-insulin-glucagon model, basal conditions and basic dynamics
Published in Letters in Biomathematics, 2018
Caleb L. Adams, D. Glenn Lasseigne
The healthy state of the human body depends on tightly regulated glucose metabolism. Two important counter-regulatory hormones of glucose metabolism include insulin and glucagon. In a healthy individual, the glucose regulatory system manages the body’s blood glucose concentration (typically between 70 and 120 mg/dl) despite input from eating and additional use of internal glucose stores. Defects in this regulatory system, if left untreated or poorly treated, lead to a life-threatening disease state (Type I diabetes) or may lead to long-term complications, ill-health and possible early death (impaired fasting glucose tolerance and insulin resistance leading to Type II diabetes).
Why are physical activity breaks more effective than a single session of isoenergetic exercise in reducing postprandial glucose? A systemic review and meta-analysis
Published in Journal of Sports Sciences, 2021
Glucose counterregulation involves the physiological processes that increase hepatic glucose production via counterregulatory hormones (e.g. glucagon and epinephrine) to prevent or correct hypoglycaemia (Gerich, 1988). Glucose counter-regulation may occur in response to exercise due to an increase in counterregulatory hormones (Galassetti et al., 2001). Given that none of the studies in this meta-analysis directly measured hepatic glucose production or counterregulatory hormone concentrations, we defined the occurrence of glucose counterregulation as the elevated blood glucose levels during or after a session of exercise compared to the uninterrupted sitting condition.