Development of an Undergraduate Control Engineering Design Project: PID Control of Blood Glucose Levels in Type 1 Diabetes Mellitus Subjects

Author(s):  
Richard Jones ◽  
Ming Tham ◽  
Alexander James Barnes
2012 ◽  
Vol 97 (11) ◽  
pp. 4193-4200 ◽  
Author(s):  
A. J. Fahey ◽  
N. Paramalingam ◽  
R. J. Davey ◽  
E. A. Davis ◽  
T. W. Jones ◽  
...  

Context: Recently we showed that a 10-sec maximal sprint effort performed before or after moderate intensity exercise can prevent early hypoglycemia during recovery in individuals with type 1 diabetes mellitus (T1DM). However, the mechanisms underlying this protective effect of sprinting are still unknown. Objective: The objective of the study was to test the hypothesis that short duration sprinting increases blood glucose levels via a disproportionate increase in glucose rate of appearance (Ra) relative to glucose rate of disappearance (Rd). Subjects and Experimental Design: Eight T1DM participants were subjected to a euglycemic-euinsulinemic clamp and, together with nondiabetic participants, were infused with [6,6-2H]glucose before sprinting for 10 sec and allowed to recover for 2 h. Results: In response to sprinting, blood glucose levels increased by 1.2 ± 0.2 mmol/liter (P < 0.05) within 30 min of recovery in T1DM participants and remained stable afterward, whereas glycemia rose by only 0.40 ± 0.05 mmol/liter in the nondiabetic group. During recovery, glucose Ra did not change in both groups (P > 0.05), but glucose Rd in the nondiabetic and diabetic participants fell rapidly after exercise before returning within 30 min to preexercise levels. After sprinting, the levels of plasma epinephrine, norepinephrine, and GH rose transiently in both experimental groups (P < 0.05). Conclusion: A sprint as short as 10 sec can increase plasma glucose levels in nondiabetic and T1DM individuals, with this rise resulting from a transient decline in glucose Rd rather than from a disproportionate rise in glucose Ra relative to glucose Rd as reported with intense aerobic exercise.


Metabolism ◽  
2001 ◽  
Vol 50 (6) ◽  
pp. 657-660 ◽  
Author(s):  
O. Kordonouri ◽  
R.W. James ◽  
B. Bennetts ◽  
A. Chan ◽  
Y.L. Kao ◽  
...  

2021 ◽  
Vol 64 (6) ◽  
pp. 425-431
Author(s):  
Jieun Lee

Background: In contrast to type 2 diabetes, type 1 diabetes mellitus (T1DM) requires insulin treatment to control blood glucose. As the incidence and prevalence of T1DM have steadily increased; therefore, T1DM is increasingly being diagnosed not only in children and adolescents, but also in adults. Therefore, the importance of accurate diagnosis and optimal management of T1DM is being recognized in clinical practice.Current Concepts: T1DM is caused by insulin deficiency, following the destruction of insulin-producing pancreatic <i>β</i>-cells. Diagnosis of diabetes is based on the following criteria: fasting blood glucose levels ≥126 mg/dL, random blood glucose levels ≥200 mg/dL accompanied by symptoms of hyperglycemia, an abnormal 2-hour oral glucose tolerance test, or glycated hemoglobin ≥6.5%. Accurate diagnosis of T1DM based on patients’ clinical characteristics, serum C-peptide levels, and detection of autoantibodies against <i>β</i>-cell autoantigens is important for optimum care and to avoid complications. A target glycated hemoglobin level is recommended in children, adolescents, and young adults with access to comprehensive care. The availability of insulin analogues and mechanical technologies (insulin pumps and continuous glucose monitors) has improved the management of T1DM, and these are useful for the prevention of microvascular complications. Screening for microvascular complications should commence at puberty or 5 years after diagnosis of T1DM.Discussion and Conclusion: Effective cooperation and coordination between patient, parents, and healthcare providers are necessary to achieve a successful transition from pediatric to adult care in patients with T1DM. Diabetic management for T1DM should be individualized based on patients’ lifestyle, as well as psychosocial, and medical circumstances.


2014 ◽  
Vol 4 (5) ◽  
pp. 20140042 ◽  
Author(s):  
Marie Csete ◽  
John Doyle

Blood glucose levels are controlled by well-known physiological feedback loops: high glucose levels promote insulin release from the pancreas, which in turn stimulates cellular glucose uptake. Low blood glucose levels promote pancreatic glucagon release, stimulating glycogen breakdown to glucose in the liver. In healthy people, this control system is remarkably good at maintaining blood glucose in a tight range despite many perturbations to the system imposed by diet and fasting, exercise, medications and other stressors. Type 1 diabetes mellitus (T1DM) results from loss of the insulin-producing cells of the pancreas, the beta cells. These cells serve as both sensor (of glucose levels) and actuator (insulin/glucagon release) in a control physiological feedback loop. Although the idea of rebuilding this feedback loop seems intuitively easy, considerable control mathematics involving multiple types of control schema were necessary to develop an artificial pancreas that still does not function as well as evolved control mechanisms. Here, we highlight some tools from control engineering used to mimic normal glucose control in an artificial pancreas, and the constraints, trade-offs and clinical consequences inherent in various types of control schemes. T1DM can be viewed as a loss of normal physiologic controls, as can many other disease states. For this reason, we introduce basic concepts of control engineering applicable to understanding pathophysiology of disease and development of physiologically based control strategies for treatment.


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