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.

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.

Effects of somatostatin on the behaviour of thromboxane B2 and β-thromboglobulin in type I diabetes

1985 ◽  
Vol 109 (1) ◽  
pp. 104-107 ◽  
Author(s):  
G. Gragnoli ◽  
A. M. Signorini ◽  
I. Tanganelli
Keyword(s):  
Platelet Function ◽  
Type I Diabetes ◽  
Thromboxane B2 ◽  
Diabetic Patients ◽  
Base Line ◽  
Type I ◽  
Control Subjects ◽  
Pharmacological Studies ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic

Abstract. Pharmacological studies have shown that the addition of somatostatin to insulin promotes a more rapid recovery from diabetic ketoacidosis. However, contradictory results have been reported concerning the action of somatostatin on platelet function, frequently deranged in diabetes. Therefore the plasma levels of thromboxane B2, a stable metabolite of proaggregatory thromboxane A2 and of β-thromboglobulin, a marker of platelet activation, were studied in 9 control subjects and in 13 insulin-dependent diabetic patients before and during somatostatin injection, administered as an initial 250 μg iv bolus followed by infusion of 300 μg over 3 h. In both groups, after somatostatin infusion thromboxane B2 and β-thromboglobulin levels showed, respectively, a progressive fall and an increase up to the second hour. Over the next hour thromboxane B2 increased and μ-thromboglobulin decreased but their levels did not return to basal values. During this experiment β-thromboglobulin plasma values in diabetic patients did not differ from those of control subjects. In contrast, thromboxane B2, decreased in relation to pharmacological treatment, maintained elevated levels. Our data, however, demonstrate that the dose of somatostatin used, produced in the diabetic patients a normal fall of thromboxane B2 in terms of percentage of base-line values, but increases of β-thromboglobulin lower than in control subjects. It is suggested that platelet function should be evaluated when somatostatin is used in the treatment of poorly controlled type I diabetes.

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.

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.

Stem Cell-Based Therapies: A New Ray of Hope for Diabetic Patients

2019 ◽  
Vol 14 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Junaid Khan ◽  
Amit Alexander ◽  
Mukta Agrawal ◽  
Ajazuddin ◽  
Sunil Kumar Dubey ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Drug Therapy ◽  
Type I Diabetes ◽  
Embryonic Stem ◽  
Health Concern ◽  
Future Research ◽  
Diabetic Patients ◽  
Successful Implementation ◽  
Type I

Diabetes and its complications are a significant health concern throughout the globe. There are physiological differences in the mechanism of type-I and type-II diabetes and the conventional drug therapy as well as insulin administration seem to be insufficient to address the problem at large successfully. Hypoglycemic swings, frequent dose adjustments and resistance to the drug are major problems associated with drug therapy. Cellular approaches through stem cell based therapeutic interventions offer a promising solution to the problem. The need for pancreatic transplants in case of Type- I diabetes can also be by-passed/reduced due to the formation of insulin producing β cells via stem cells. Embryonic Stem Cells (ESCs) and induced Pluripotent Stem Cells (iPSCs), successfully used for generating insulin producing &#946; cells. Although many experiments have shown promising results with stem cells in vitro, their clinical testing still needs more exploration. The review attempts to bring into light the clinical studies favoring the transplantation of stem cells in diabetic patients with an objective of improving insulin secretion and improving degeneration of different tissues in response to diabetes. It also focuses on the problems associated with successful implementation of the technique and possible directions for future research.

A program to reduce onset distress in unselected type I diabetic patients: effects on psychological variables and metabolic control

1995 ◽  
Vol 132 (5) ◽  
pp. 580-586 ◽  
Author(s):  
K Spiess ◽  
G Sachs ◽  
P Pietschmann ◽  
R Prager
Keyword(s):  
Patient Education ◽  
Metabolic Control ◽  
Type I Diabetes ◽  
Intensive Treatment ◽  
Medical Psychology ◽  
Diabetic Patients ◽  
Type I ◽  
Psychological Variables ◽  
Reduction Program

Spiess K, Sachs G, Pietschmann P, Prager R. A program to reduce onset distress in unselected type I diabetic patients: effects on psychological variables and metabolic control. Eur J Endocrinol 1995;132:580–6. ISSN 0804–4643 This paper reports the results of a prospective controlled trial of a program addressing reduction of onset distress and better future adaptation in adults who were enrolled at the time of diagnosis of type I diabetes mellitus. Patients were assigned randomly to either standard intensive treatment and patient education with the distress reduction program (N = 10) or to standard intensive treatment and patient education without this program (N = 13). Prospective follow-up of patients with multiple validated measures of treatment outcome showed less anxious coping behavior, less depression and less denial at the 9-month follow-up and less denial at the 15-month follow-up in the group with the distress reduction program, but no differences in metabolic control between the two groups at any time. We conclude that our program has a positive impact on the crisis at diabetes onset; the lower denial in the treatment group may lead to improved regimen adherence in the long term. Klaus Spiess, Institute of Medical Psychology, University of Vienna, Severingasse 9, A-1090-Vienna, Austria

scholarly journals Calcium Homeostasis in Ventricular Myocytes of Diabetic Cardiomyopathy

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Lina T. Al Kury
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Cardiomyopathy ◽  
Contractile Function ◽  
Type I Diabetes ◽  
Heart Function ◽  
Diabetic Rat ◽  
Diabetic Patients ◽  
Type I ◽  
High Blood Glucose ◽  
Cardiac Contractile

Diabetes mellitus (DM) is a chronic metabolic disorder commonly characterized by high blood glucose levels, resulting from defects in insulin production or insulin resistance, or both. DM is a leading cause of mortality and morbidity worldwide, with diabetic cardiomyopathy as one of its main complications. It is well established that cardiovascular complications are common in both types of diabetes. Electrical and mechanical problems, resulting in cardiac contractile dysfunction, are considered as the major complications present in diabetic hearts. Inevitably, disturbances in the mechanism(s) of Ca2+ signaling in diabetes have implications for cardiac myocyte contraction. Over the last decade, significant progress has been made in outlining the mechanisms responsible for the diminished cardiac contractile function in diabetes using different animal models of type I diabetes mellitus (TIDM) and type II diabetes mellitus (TIIDM). The aim of this review is to evaluate our current understanding of the disturbances of Ca2+ transport and the role of main cardiac proteins involved in Ca2+ homeostasis in the diabetic rat ventricular cardiomyocytes. Exploring the molecular mechanism(s) of altered Ca2+ signaling in diabetes will provide an insight for the identification of novel therapeutic approaches to improve the heart function in diabetic patients.

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