Reduced number of angiotensin II receptors on platelets in insulin-dependent diabetes

1986 ◽  
Vol 71 (2) ◽  
pp. 217-220 ◽  
Author(s):  
J. M. C. Connell ◽  
Yu-An Ding ◽  
B. M. Fisher ◽  
B. M. Frier ◽  
P. F. Semple
Keyword(s):  
Angiotensin Ii ◽  
Type I Diabetes ◽  
Plasma Concentrations ◽  
Normal Subjects ◽  
Insulin Dependent Diabetes ◽  
Angiotensin Ii Receptors ◽  
Diabetic Patients ◽  
Type I ◽  
Angiotensin Ii Receptor ◽  
Insulin Dependent

1. Angiotensin II receptors on platelets were studied in 13 patients with uncomplicated type I diabetes mellitus and in 15 age-matched normal subjects. 2. Receptor density on cells from the diabetic patients was 15% lower than the normal subjects (5.2 ± 0.8 sd sites/platelet in diabetic patients and 6.4 ± 0.8 in normals, P < 0.001), but there were no differences in receptor affinity as measured by Kd (4.9 ± 1.5 × 10−10 mol/l in diabetic patients and 5.4 ± 1.4 × 10−10 mol/l in normals). 3. Plasma concentrations of renin and angiotensin II were similar in both groups. 4. The reduced density of angiotensin II receptors on platelets from patients with insulin-dependent diabetes may reflect a generalized abnormality of angiotensin II receptor regulation.

scholarly journals FTIR Spectroscopic Investigation of Mineral Structure of Streptozotocin Induced Diabetic Rat Femur and Tibia

2003 ◽  
Vol 17 (2-3) ◽  
pp. 627-633 ◽  
Author(s):  
Handan Boyar ◽  
Belma Turan ◽  
Feride Severcan
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Diabetic Rat ◽  
Carbonate Content ◽  
Diabetic Patients ◽  
Type I ◽  
Mineral Density ◽  
Insulin Dependent

Diabetes mellitus (DM) can be accepted as a heterogenous multi organ disorder that can affect various systems of the human body. Disorders include retinopathy, neuropathy, cardiomyopathy, musculoskeletal abnormalities such as diminished bone formation and bone healing retardation. Low bone mineral density is often mentioned as a complication for patients with insulin dependent diabetes mellitus (type I DM). Streptozotocin (STZ) induced diabetic rats are good models for investigation of the complications of insulin dependent diabetes. In the present study, the effects of STZ induced diabetes on the mineral environment of rat bones namely femur and tibia were studied by Fourier transform infrared (FTIR) spectroscopic technique. The results revealed that mineral crystal sizes increased and carbonate content decreased for diabetic femur and tibia. These changes can be due to the formation of osteoporosis which is widely seen in diabetic 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.

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.

scholarly journals Electroacupuncture at the Zusanli (ST-36) Acupoint Induces a Hypoglycemic Effect by Stimulating the Cholinergic Nerve in a Rat Model of Streptozotocine-Induced Insulin-Dependent Diabetes Mellitus

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Yu-Chen Lee ◽  
Te-Mao Li ◽  
Chung-Yuh Tzeng ◽  
Ying-I Chen ◽  
Wai-Jane Ho ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Insulin Signaling ◽  
Type I Diabetes ◽  
Insulin Dependent Diabetes ◽  
Type I ◽  
Signaling Proteins ◽  
Glucose Levels ◽  
Before And After ◽  
Insulin Dependent ◽  
Adrenalectomized Rats

Animal studies have shown that electroacupuncture (EA) at Zusanli (ST-36) and Zhongwan (CV-12) acupoints reduces plasma glucose concentrations in rats with type II diabetes. However, whether EA reduces plasma glucose levels in type I diabetes is still unknown. In this study, we explore the various non-insulin-dependent pathways involved in EA-induced lowering of plasma glucose. Streptozotocin (STZ) (60 mg kg−1, i.v.) was administered via the femoral vein to induce insulin-dependent diabetes in non-adrenalectomized and in adrenalectomomized rats. EA (15 Hz) was applied for 30 min to bilateral ST-36 acupoints after administration of Atropine (0.1 mg kg−1i.p.), Eserine (0.01 mg kg−1i.p.), or Hemicholinium-3 (5 μg kg−1i.p.) in non-adrenalectomized rats. Rats administered acetylcholine (0.01 mg kg−1i.v.) did not undergo EA. Adrenalectomized rats underwent EA at bilateral ST-36 acupoints without further treatment. Blood samples were drawn from all rats before and after EA to measure changes in plasma glucose levels. Expression of insulin signaling proteins (IRS1, AKT2) in atropine-exposed rats before and after EA was measured by western blot. Atropine and hemicholinium-3 completely blocked the plasma glucose lowering effects of EA, whereas eserine led to a significant hypoglycemic response. In addition, plasma glucose levels after administration of acetylcholine were significantly lower than the fasting glucose levels. In STZ-adrenalectomized rats, EA did not induce a hypoglycemic response. EA stimulated the expression of IRS1 and AKT2 and atropine treatment blocked the EA-induced expression of those insulin signaling proteins. Taken together, EA at the ST-36 acupoint reduces plasma glucose concentrations by stimulating the cholinergic nerves.

New approach for in vivo detection of insulitis in type I diabetes: activated lymphocyte targeting with 123I-labelled interleukin 2

1994 ◽  
Vol 131 (4) ◽  
pp. 431-437 ◽  
Author(s):  
Alberto Signore ◽  
Marco Chianelli ◽  
Elisabetta Ferretti ◽  
Anna Toscano ◽  
Keith E Britton ◽  
...  
Keyword(s):  
Gamma Camera ◽  
Type I Diabetes ◽  
Interleukin 2 ◽  
Nod Mice ◽  
Insulin Dependent Diabetes ◽  
Type I ◽  
New Approach ◽  
In Vivo Detection ◽  
Insulin Dependent

Signore A, Chianelli M, Ferretti E, Toscano A, Britton KE, Andreani D, Gale EAM, Pozzilli P. New approach for in vivo detection of insulitis in type I diabetes: activated lymphocyte targeting with 123I-labelled interleukin 2. Eur J Endocrinol 1994;131:431–7. ISSN 0804–4643 Insulitis is considered the histopathological hallmark of type I (insulin-dependent) diabetes. In the nonobese diabetic (NOD) mouse, diabetes has never been observed in the absence of insulitis. The in vivo detection of insulitis could be of relevance for early prediction of diabetes. As approximately 15% of islet-infiltrating lymphocytes express interleukin 2 receptors, we have labelled recombinant interleukin 2 with 123I and used this radiopharmaceutical to detect insulitis by gamma camera imaging. We studied 71 prediabetic NOD and 27 normal Balb/c mice. Labelled α-lactalbumin was used as the control protein. In the first set of experiments we studied the tissue distribution of radiolabelled interleukin 2 in isolated organs from animals sacrificed at different time points. Higher radioactivity was detected in the pancreas of NOD mice injected with labelled interleukin 2, as compared to NOD mice receiving labelled α-lactalbumin (p < 0.003 at 20 min; p< 0.001 at 40 min; p< 0.0001 at 60 min) or Balb/c mice injected with labelled interleukin 2 (p< 0.05 at 40 min; p< 0.001 at 60 min). In another set of experiments, gamma camera images have been acquired after injection of 123I-labelled interleukin 2. Radioactivity in the pancreatic region of prediabetic NOD and Balb/c mice showed similar kinetics to those observed by single organ counting, with higher accumulation in the pancreatic region of NOD mice (p < 0.04 after 22–45 min in NOD mice vs Balb/c mice). Finally, a positive correlation was found between the radioactivity in the pancreas and the extent of lymphocytic infiltration (p < 0.01 for pancreas radioactivity counted in vitro and p< 0.004 for pancreas radioactivity counted in vivo by gamma camera). This study demonstrates that 123I-labelled interleukin 2 administered iv accumulates specifically in the inflamed pancreas of diabetes-prone NOD mice, suggesting its potential application in human insulin-dependent diabetes mellitus. A Signore, Servizio Speciale di Medicina Nucleare, II Clinica Medica, Policlinico Umberto I, 00161 Roma, Italy

Anti-goat immunoglobulin antibodies in diabetic children at diagnosis and follow-up: comparison with islet cell antibodies and other autoantibodies

1989 ◽  
Vol 120 (3) ◽  
pp. 326-330 ◽  
Author(s):  
U. Di Mario ◽  
L. Crisa ◽  
E. Anastasi ◽  
G. Contreas ◽  
D. Andreani ◽  
...  
Keyword(s):  
Islet Cell ◽  
Solid Phase ◽  
Type I Diabetes ◽  
Islet Cell Antibodies ◽  
Normal Subjects ◽  
Islet Cell Antibody ◽  
Diabetic Patients ◽  
Type I ◽  
Recent Onset

Abstract. The presence of antibodies reacting with human as well as animal immunoglobulins in sera from recent onset Type I diabetic patients has been recently demonstrated by some of our group. In the present study, the occurrence of these antibodies has been evaluated in sera from 19 Type I diabetic patients, at diagnosis and at follow-up within three years, and from 26 normal subjects, and has also been compared with the presence of islet cell antibodies and other organ-specific autoantibodies. A solid-phase radioimmunoassay has been used: serum was incubated in goat immunoglobulin-coated wells and the binding of 125-I-anti-human immunoglobulin antibodies was evaluated. Anti-goat immunoglobulin antibodies were above the 90th percentile of normal values in all diabetic patients at diagnosis (median, interquartile range, in μg 125I-antibody bound/1 serum: 83, 77.5–88, versus 51.5, 44.5–62 in normal subjects, P < 0.001) and significantly declined with time after diagnosis (P < 0.001). Islet cell antibodies were present in 79% of patients at diagnosis, whereas at least one other auto-antibody was found in 21% of patients. In the follow-up study the decline in anti-goat immunoglobulin antibody levels was different from that of islet cell antibody positivity. A circulating immunoglobulin reacting with other immunoglobulins is thus present in the early stages of Type I diabetes and may well play a part in the complex immunopathogenetic interactions.

scholarly journals Hepatobiliary function in children with insulin-dependent diabetes mellitus

1995 ◽  
Vol 41 (4) ◽  
pp. 15-17
Author(s):  
Ye. B. Kravets ◽  
Ye. A. Biryulina ◽  
Z. G. Mironova
Keyword(s):  
Diabetes Mellitus ◽  
Type I Diabetes ◽  
Diagnostic Methods ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Main Role ◽  
Type I ◽  
Hepatobiliary System ◽  
Insulin Dependent ◽  
Bile Excretion

The hepatobiliary system plays the crucial role in the development of metabolic disorders in diabetics. Involvement of the hepatobiliary system may develop at the early stages of diabetes mellitus. The present study was aimed at elucidation of the specific features of bile excretion and production in children with type I diabetes making use of present-day diagnostic methods. Fifty-two patients with type 1 diabetes aged 6 to 15 and 20 healthy controls were examined. Besides common clinical studies, fractionated duodenal probing followed by biochemical analysis of the bile, ultrasonic examination of the hepatobiliary system, and dynamic hepatobiliscintigraphy were carried out. Typical changes in liver parenchyma developing after fatty hepatosis type were found to play the main role in the structure of hepatobiliary involvement occurring in insulin-dependent diabetes. Disorders of bile excretion are caused by dyskinetic disorders of extrahepatic bile duct and choleresis changes. Bile excretion arrhythmia manifests most frequently as hypertensive dyskinesia. In patients with a longstanding disease bile excretion changes are mainly due to increased tone of the sphincter of Oddi and decelerated contractility of the gallbladder. Biochemical composition of the bile was characterized by decreased concentration of bile acids, phospholipids, and bilirubin, by a lower cholate-cholesterol coefficient, and increased levels of cholesterol and total lipids.

The effect of insulin withdrawal on intermediary metabolism in patients with diabetes secondary to chronic pancreatitis

1991 ◽  
Vol 124 (5) ◽  
pp. 510-515 ◽  
Author(s):  
Steen Larsen ◽  
Jannik Hilsted ◽  
Else K. Philipsen ◽  
Bente Tronier ◽  
Meta Damkjær Nielsen ◽  
...  
Keyword(s):  
Chronic Pancreatitis ◽  
Cell Function ◽  
Blood Glucose Concentration ◽  
Insulin Dependent Diabetes ◽  
Diabetic Patients ◽  
Type I ◽  
Secondary Diabetes ◽  
Patients With Diabetes ◽  
Insulin Dependent ◽  
Beta Hydroxybutyrate

Abstract. Insulin was withdrawn from 7 patients with Type I (insulin-dependent) diabetes and 4 patients with insulin-dependent diabetes secondary to chronic pancreatitis, both groups without residual beta-cell function. Median plasma glucagon concentrations rose slightly, but significantly after withdrawal of insulin in Type I diabetic patients (from 14 (range: 11-16) to 19 (14-25) pmol/l by 6 h), but not in the patients with secondary diabetes. This was accompanied by a significantly higher increase in blood glucose concentration from 5.1 (4.9-5.7) to 15.2 (12.9-18.1) mmol/1 by 6 h in Type I diabetic patients compared with patients with secondary diabetes (from 4.9 (4.3-6.7) to 13.1 (10.9-13.5) mmol/l) (p<0.01). Beta-hydroxybutyrate increased to a similar extent in the two groups, whereas no significant increases were found in glycerol and lactate in any of the groups. Increased secretion of glucagon is not essential for the development of hyperglycemia and ketonemia in patients with diabetes secondary to chronic pancreatitis, but may augment the degree of hyperglycemia in Type I diabetic patients compared with patients having secondary diabetes.

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