Terminal Synergetic Control for Blood Glucose Regulation in Diabetes Patients

2018 ◽  
Vol 140 (10) ◽  
Author(s):  
A. Hachana ◽  
M. N. Harmas
Keyword(s):  
Blood Glucose ◽  
Sliding Mode ◽  
Type I Diabetes ◽  
System Stability ◽  
Diabetic Patients ◽  
Type I ◽  
Continuous Control ◽  
Control Scheme ◽  
Synergetic Control ◽  
Diabetes Patients

In this paper, a new robust terminal synergetic control scheme is proposed to regulate blood glucose level in diabetic patients (type I diabetes), based on recently developed synergetic control and a terminal attractor technique. The technique presented has the advantage of using a continuous control law. Moreover, the proposed control scheme, besides being chattering free, has the characteristics of finite time convergence. Lyapunov synthesis is adopted to ensure controlled system stability. Simulation results of terminal synergetic control are compared to classic synergetic and second-order sliding mode control (SMC) performance, demonstrating that the proposed control method allows for rapidly achieving normoglycemia in type I diabetes patients.

β-Adrenoceptor Blockade and Recovery from Hypoglycaemia in Diabetic Subjects: Normalization after Lactate and Glycerol Infusions

1982 ◽  
Vol 62 (2) ◽  
pp. 131-136 ◽  
Author(s):  
I. Lager ◽  
U. Smith
Keyword(s):  
Blood Glucose ◽  
Recovery Rate ◽  
Type I Diabetes ◽  
Diabetic Patients ◽  
Type I ◽  
Insulin Dependent ◽  
Propranolol Treatment ◽  
Glucose Recovery ◽  
Insulin Dependent Diabetic ◽  
Gluconeogenic Substrates

1. Previous studies have shown that non-selective β-adrenoceptor blockade attenuates the blood glucose recovery rate after hypoglycaemia in type I diabetes. Apart from possible effects on hepatic glycogenolysis propranolol also inhibits the release of the important gluconeogenic substrates lactate and glycerol. 2. To determine whether the effect of non-selective β-adrenoceptor blockade on glucose recovery could be associated with diminished availability of gluconeogenic substrates, lactate and glycerol were infused during hypoglycaemia in four insulin-dependent diabetic patients. Comparisons were made of the blood glucose recovery on placebo, propranolol and propranolol combined with the infusion. 3. The blood glucose recovery rate after hypoglycaemia was less on propranolol than with placebo but was significantly improved and not different from placebo when propranolol treatment was combined with lactate and glycerol infusions. Thus, at least for type I diabetic patients, in whom gluconeogenesis is proportionally greater than in healthy subjects, non-selective β-adrenoceptor blockade attenuates the glucose recovery rate from hypoglycaemia mainly by reducing the availability of gluconeogenic substrates.

The increase in sympathetic nerve activity after glucose ingestion is reduced in type I diabetes

2000 ◽  
Vol 98 (5) ◽  
pp. 627-632 ◽  
Author(s):  
Jan FAGIUS ◽  
Christian BERNE
Keyword(s):  
Sympathetic Activity ◽  
Type I Diabetes ◽  
Diabetic Patients ◽  
Type I ◽  
Sympathetic Outflow ◽  
Control Subjects ◽  
Glucose Ingestion ◽  
Muscle Nerve ◽  
Normal Strength ◽  
Diabetes Patients

Food intake is followed by an increase in baroreflex-governed sympathetic outflow to muscle vessels. It is established that insulin contributes to this stimulation; however, the increase occurs (to a lesser degree) even in the absence of enhanced insulin secretion. To further elucidate the role of insulin, muscle nerve sympathetic activity was recorded by microneurography, and the increase after an oral 100-g glucose load in eight C-peptide-negative patients with type I diabetes without any signs of neuropathy was compared with that in 16 healthy control subjects. The level of sympathetic activity at rest was similar in the two groups (type I diabetes patients, 19.5±2.4 bursts/min; controls, 20.4±4.8 bursts/min; means±S.D.). Following glucose intake there was a significant increase in activity in both groups, with maximum values at 30 min of 24.3±3.7 bursts/min for type I diabetes patients and 34.4±9.1 bursts/min for controls. The summarized response (during 90 min) of the diabetic patients was less than half that of the control subjects (P = 0.0003). It is concluded that the response of muscle nerve sympathetic activity to glucose ingestion is reduced to about half of its normal strength in the absence of insulin, and that there is no difference in sympathetic outflow at rest between healthy subjects and diabetic patients without polyneuropathy.

Skin Microcirculation in Patients with Type I Diabetes with and without Neuropathy after Neurovascular Stimulation

1998 ◽  
Vol 94 (3) ◽  
pp. 255-261 ◽  
Author(s):  
Thomas Forst ◽  
Andreas Pfützner ◽  
Thomas Kunt ◽  
Thomas Pohlmann ◽  
Ulrike Schenk ◽  
...  
Keyword(s):  
Blood Flow ◽  
Diabetic Neuropathy ◽  
Type I Diabetes ◽  
Capillary Blood ◽  
Capillary Blood Flow ◽  
Diabetic Patients ◽  
Type I ◽  
Skin Microcirculation ◽  
Skin Perfusion ◽  
Diabetes Patients

1. Neurovascular inflammation is impaired in patients suffering from diabetic neuropathy. The aim of our study was to evaluate the distribution of nutritive and total skin blood flow in diabetic patients with and without neuropathy after neurovascular stimulation with acetylcholine. 2. Twenty patients with Type I diabetes, 10 with and 10 without neuropathy, and 10 age-matched non-diabetic control subjects, underwent microvascular investigations before and after neurovascular stimulation by intracutaneous application of acetylcholine. The capillary blood cell velocity in the nailfold of the hallux was measured by videophotometric capillaroscopy, and the total skin microcirculation in the same area by laser Doppler flowmetry. 3. The increase in total skin blood flow was significantly impaired in the group of neuropathic diabetic patients compared with the non-neuropathic diabetic patients (17.5 ± 83 versus 51.0 ± 16.2; P < 0.05) and the non-diabetic subjects (17.5 ± 8.3 versus 67.8 ± 19.7; P < 0.01). The increase in capillary blood flow was not significantly impaired in Type 1 diabetes patients with neuropathy. 4. The ratio between capillary blood flow and total skin perfusion decreased significantly in the control group (from 0.82 ± 0.15 to 0.47 ± 0.11; P < 0.005) and in the Type I diabetes patients without neuropathy (from 0.79 ± 0.12 to 0.43 ± 0.12; P < 0.05), whereas the decrease in the neuropathic group was statistically insignificant (from 1.05 ± 0.19 to 0.72 ±0.16). 5. Diminished total skin perfusion in the foot after intracutaneous stimulation with acetylcholine in Type I diabetes patients is associated with diabetic neuropathy, indicating a disturbance in the neurovascular reflex arc. This impaired neurovascular response is caused by a diminished total and sub-papillary blood flow and not by a diminished nutritive capillary flow. There is no evidence of a diminished nutritive capillary blood flow during neurogenic inflammation in Type I diabetes patients suffering from diabetic neuropathy.

scholarly journals Selfcare in Type I Diabetes with Continuous Glucose Monitoring

2019 ◽  
Vol 8 (1) ◽  
pp. 5
Author(s):  
Elham Nazari ◽  
Somaye Nazari
Keyword(s):  
Blood Glucose ◽  
Type I Diabetes ◽  
Blood Glucose Control ◽  
Glucose Monitoring ◽  
Blood Glucose Monitoring ◽  
Control Group ◽  
Diabetic Patients ◽  
Type I ◽  
Online Data ◽  
Data Set

Introduction: The number of diabetes patients are increasing. If the blood glucose is not controlled in diabetics, patients will face with complications. Self-care is important to control the blood glucose of diabetic patients and prevention of complications such as neurological complications, heart, eye disease, amputations and so on. Therefore aim of this study is to identify the effect of Continuous blood Glucose Monitoring or CGM on the blood glucose control in type I diabetes.Materials and methods: The study was done on 20 patients chosen from an online data set available in http://www.jaeb-diabetes.net/ . These patients used CGM to test blood glucose and the result of three month test was measured. To analyze the data, the software SPSS 21, independent Mann- Whitney test was used.Results: The results showed that blood glucose in patients of the experimental group reduced significantly rather than patient of the control group in the second and third month. Also, HbA1C of the patients has reduced.Conclusion: The CGM has an effective role in controlling blood glucose and prevention of complications. Therefore it is recommended that educational programs on the use of monitoring blood glucose, such as CGM as a requirement to be developed.

Effects of nisoldipine and lisinopril on microvascular dysfunction in hypertensive Type I diabetes patients with nephropathy

1998 ◽  
Vol 95 (6) ◽  
pp. 709-717 ◽  
Author(s):  
V. B. SØRENSEN ◽  
P. ROSSING ◽  
L. TARNOW ◽  
H.-H. PARVING ◽  
T. NØRGAARD ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Diabetic Nephropathy ◽  
Vascular Resistance ◽  
Antihypertensive Treatment ◽  
Type I Diabetes ◽  
Diabetic Patients ◽  
Type I ◽  
Once Daily ◽  
Control Subjects ◽  
Diabetes Patients

1. Our objective was to compare the effect of a long-acting calcium antagonist (nisoldipine) compared with an angiotensin-converting enzyme inhibitor (lisinopril) on the non-neurogenic regulation of the microvascular blood flow in hypertensive Type I diabetes patients with diabetic nephropathy. 2. We performed a 1-year double-blind, double-dummy randomized controlled study comparing nisoldipine (20–40 mg once daily) with lisinopril (10–20 mg once daily) in 48 hypertensive Type I diabetes patients with diabetic nephropathy. For comparison, 22 age-matched normotensive healthy control subjects were included. Measurements were performed at baseline and after 1 year of antihypertensive treatment. The minimal vascular resistance and distensibility (stiffness) of resistance vessels in skin and skeletal muscle were measured using the local isotope washout method. 3. Mean arterial pressure was reduced to the same extent in both groups: nisoldipine, 113±2.1 to 105±1.6 mmHg (P< 0.001); lisinopril, 110±2.7 to 101±2.1 mmHg (P< 0.002) (controls, 88±2.2 mmHg; P< 0.0001 compared with diabetic patients). Nisoldipine improved the skin vascular distensibility from 28±3.3 to 43±3.8% (P< 0.005) and decreased skin minimal vascular resistance from 16.9±1.0 to 13.6±0.8 mmHg·ml-1·min·100 g (P< 0.02). Lisinopril had no significant effect on skin vascular distensibility (40±4.0% and 41±4.4%), but minimal vascular resistance tended to diminish (18.1±0.9 to 15.8±1.3 mmHg·ml-1·min·100 g (P =0.09). Nisoldipine significantly increased the skin distensibility (P = 0.05) after 1 year of antihypertensive treatment compared with lisinopril. 4. The control group had a skin vascular distensibility of 54±3.2% and a minimal vascular resistance of 10.8±0.7 mmHg·ml-1·min·100 g, both significantly different from the values in the diabetic groups (P< 0.0001 for all). Skeletal muscle vascular distensibility was unaltered after 1 year of treatment with both nisoldipine (22±3.3% and 19±2.7%) and lisinopril (19±2.1% and 24±2.5%), but was reduced compared with a control value of 43±3.7% (P< 0.0001 for diabetes patients versus controls). However, neither nisoldipine nor lisinopril had any effect on the increased minimal vascular resistance or the reduced skeletal muscle distensibility. 5. Enhanced thickening of the basement membranes of the terminal arteriolar wall was found in skin biopsy specimens in 91% of diabetic patients and 38% only in control subjects (P< 0.000001 both before and after treatment for diabetic patients versus controls). There was no significant effect of antihypertensive treatment on arteriolar hyalinosis. 6. The reduction in systemic blood pressure was identical during 1 year of treatment with nisoldipine or lisinopril. The abnormal arteriolar stiffness was more pronounced in the group treated with nisoldipine than with lisinopril and only nisoldipine compared with lisinopril improved the abnormal arteriolar stiffness and minimal vascular resistance in the skin. This suggests that nisoldipine can reverse the peripheral skin perfusion and thereby improve the local protection against development of ischaemic skin lesions in Type I diabetes patients with clinical diabetic nephropathy.

Backstepping Sliding Mode Gaussian Insulin Injection Control for Blood Glucose Regulation in Type I Diabetes Patient

2018 ◽  
Vol 140 (9) ◽  
Author(s):  
Akshaya Kumar Patra ◽  
Pravat Kumar Rout
Keyword(s):  
Blood Glucose ◽  
Sliding Mode ◽  
Type I Diabetes ◽  
State Space Model ◽  
Hybrid Approach ◽  
Insulin Injection ◽  
Diabetes Patient ◽  
Type I ◽  
Closed Loop Systems ◽  
Continuous Glucose Monitors

New efforts have been made to build up prototypes of subcutaneous closed-loop systems for controlling blood glucose (BG) levels in type I diabetes mellitus (TIDM) patients with the development of clinically accurate continuous glucose monitors, automated micro-insulin dispenser (MID), and control algorithms. There is an urgency to develop new control algorithm to determine the desired dose of insulin for maintaining normal BG levels. As a solution to the above issue, a novel backstepping sliding mode Gaussian controller (BSMGC) is proposed whose gains vary dynamically with respect to the error signal. A feedback control law is formulated by a hybrid approach based on BSMGC. A ninth-order linearized state-space model of a nonlinear TIDM patient with the MID is formulated for the design of the BSMGC. This controller is evaluated, and the results are compared with other recently published control techniques. The output responses clearly reveal the better performance of the proposed method to control the BG level within the range of normoglycaemia in terms of accuracy, robustness and handling uncertainties.

Current Approaches in Diabetes Treatment and Other Strategies to Reach Normoglycemia

2020 ◽  
Vol 20 (32) ◽  
pp. 2922-2944
Author(s):  
Worood Sirhan ◽  
Ron Piran
Keyword(s):  
Blood Glucose ◽  
Current Knowledge ◽  
Type I Diabetes ◽  
Current Status ◽  
Control Individual ◽  
Diabetic Patients ◽  
Regulation Mechanism ◽  
Type I ◽  
Glucose Levels ◽  
Blood Glucose Levels

: Cells are mainly dependent on glucose as their energy source. Multicellular organisms need to adequately control individual glucose uptake by the cells, and the insulin-glucagon endocrine system serves as the key glucose regulation mechanism. Insulin allows for effective glucose entry into the cells when blood glucose levels are high, and glucagon acts as its opponent, balancing low blood glucose levels. A lack of insulin will prevent glucose entry to the cells, resulting in glucose accumulation in the bloodstream. Diabetes is a disease which is characterized by elevated blood glucose levels. All diabetes types are characterized by an inefficient insulin signaling mechanism. This could be the result of insufficient insulin secretion, as in the case of type I diabetes and progressive incidents of type II diabetes or due to insufficient response to insulin (known as insulin resistance). We emphasize here, that Diabetes is actually a disease of starved tissues, unable to absorb glucose (and other nutrients), and not a disease of high glucose levels. Indeed, diabetic patients, prior to insulin discovery, suffered from glucose malabsorption. : In this mini-review, we will define diabetes, discuss the current status of diabetes treatments, review the current knowledge of the different hormones that participate in glucose homeostasis and the employment of different modulators of these hormones. As this issue deals with peptide therapeutics, special attention will be given to synthetic peptide analogs, peptide agonists as well as antagonists.

Sign in / Sign up

Export Citation Format

Share Document