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Diabetes Mellitus (DM) can be considered as the 21st century pandemic and it therefore represents an alarming threat to public health with rising trends and severity worldwide. DM comprises a set of metabolic disorders, which share the phenotype of hyperglycaemia (increment in blood glucose concentration). Blood glucose concentration fluctuates considerably in response of food intake, hormonal cycles, or behavioral factors. These fluctuations may range from 70 to 180 mg/dL for most normal subjects, although blood glucose concentration remains within the normo glycaemic zone (10-110 mg/dL) for most of the time. The internal physiological regulation of these wide fluctuations is a complex and multifactorial process. The most critical regulatory role is played by the pancreas, wich upon sensing an elevation of blood glucose concentration, secretes insulin through its beta cells, while an opposite change in the glucose causes the secretion of glucagon through its alpha cells. The secreted insuline assists the uptake of glucose by the cells and then storage the excess of glucose in the liver in the form of glycogen. Secreted glucagon assists the catabolism of glycogen into glucose that is released from the liver into the bloodstream, while insulin inhibits glycogen synthase. Furthermore, free fatty acids in blood potentiate the short-term responsiveness of pancratic beta cells to glucose oscillations, but may inhibit long-term responsiveness. Finally, blood glucose concentration and its relation to insulin concentration depend on the action of several other hormones (e.g. epinephrine, norepinephrine, and cortisol, making the complexity of this multifactorial regulatory system evident. The primary effect of blood glucose is exercised by insulin, and most efforts to date have focused on the study of this causal relation. Prolonged hyperglycaemia is normally caused by defects in insulin secretion by the pancreatic beta cells or in the efficiency of insulin-facilitated glucose uptake by the cells. The exact quantitative nature of the dependence between blood glucose concentration and the action of the other hormones mentioned above, or factors such as diet, endocrine cycles, exercise, stress and so on, remains largely unknown (primarily because of the lack of appropriate data), although the qualitative effect has been established, the aggregate effects of all these factors for modeling purposes set the basis for the study of glucose variability.
Modelling the Variability in the Insuline-Glucose Feedback System
Modelling the Variability in the Insuline-Glucose Feedback System
Vicente RIBAS-RIPOLL
Shockomics talk about planned analysis.
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Diabetes Mellitus (DM) can be considered as the 21st century pandemic and it therefore represents an alarming threat to public health with rising trends and severity worldwide. DM comprises a set of metabolic disorders, which share the phenotype of hyperglycaemia (increment in blood glucose concentration). Blood glucose concentration fluctuates considerably in response of food intake, hormonal cycles, or behavioral factors. These fluctuations may range from 70 to 180 mg/dL for most normal subjects, although blood glucose concentration remains within the normo glycaemic zone (10-110 mg/dL) for most of the time. The internal physiological regulation of these wide fluctuations is a complex and multifactorial process. The most critical regulatory role is played by the pancreas, wich upon sensing an elevation of blood glucose concentration, secretes insulin through its beta cells, while an opposite change in the glucose causes the secretion of glucagon through its alpha cells. The secreted insuline assists the uptake of glucose by the cells and then storage the excess of glucose in the liver in the form of glycogen. Secreted glucagon assists the catabolism of glycogen into glucose that is released from the liver into the bloodstream, while insulin inhibits glycogen synthase. Furthermore, free fatty acids in blood potentiate the short-term responsiveness of pancratic beta cells to glucose oscillations, but may inhibit long-term responsiveness. Finally, blood glucose concentration and its relation to insulin concentration depend on the action of several other hormones (e.g. epinephrine, norepinephrine, and cortisol, making the complexity of this multifactorial regulatory system evident. The primary effect of blood glucose is exercised by insulin, and most efforts to date have focused on the study of this causal relation. Prolonged hyperglycaemia is normally caused by defects in insulin secretion by the pancreatic beta cells or in the efficiency of insulin-facilitated glucose uptake by the cells. The exact quantitative nature of the dependence between blood glucose concentration and the action of the other hormones mentioned above, or factors such as diet, endocrine cycles, exercise, stress and so on, remains largely unknown (primarily because of the lack of appropriate data), although the qualitative effect has been established, the aggregate effects of all these factors for modeling purposes set the basis for the study of glucose variability.
Modelling the Variability in the Insuline-Glucose Feedback System
Modelling the Variability in the Insuline-Glucose Feedback System
Vicente RIBAS-RIPOLL
Shockomics talk about planned analysis.
Shockomics milano april_2016_v2
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