scholarly journals Effect of Type I Diabetes on the Proteome of Mouse Oocytes

2016 ◽  
Vol 39 (6) ◽  
pp. 2320-2330 ◽  
Author(s):  
Guangjian Jiang ◽  
Guangli Zhang ◽  
Tian An ◽  
Zhongchen He ◽  
Lihua Kang ◽  
...  

Background: Type I diabetes is a global public health concern that affects young people of reproductive age and can damage oocytes, reducing their maturation rate and blocking embryonic development. Understanding the effects of type I diabetes on oocytes is important to facilitate the maintenance of reproductive capacity in female diabetic patients. Methods: To analyze the effects of type I diabetes on mammalian oocytes, protein profile changes in mice with streptozotocin-induced type I diabetes were investigated using proteomic tools; non-diabetic mouse oocytes were used as controls. Immunofluorescence analysis for the spindle and mitochondria of oocytes. Results: We found that type I diabetes severely disturbed the metabolic processes of mouse oocytes. We also observed significant changes in levels of histone H1, H2A/B, and H3 variants in diabetic oocytes (fold change: > 0.4 or < -0.4), with the potential to block activation of the zygotic genome and affect early embryo development. Furthermore, diabetic oocytes exhibited higher abnormal spindle formation and spatial remodeling of mitochondria than observed in the controls. Conclusion: Our results indicate that type I diabetes disrupts metabolic processes, spindle formation, mitochondria distribution and modulates epigenetic code in oocytes. Such effects could have a major impact on the reproductive dynamics of female patients with type I diabetes.

2019 ◽  
Vol 14 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Junaid Khan ◽  
Amit Alexander ◽  
Mukta Agrawal ◽  
Ajazuddin ◽  
Sunil Kumar Dubey ◽  
...  

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.


1995 ◽  
Vol 132 (5) ◽  
pp. 580-586 ◽  
Author(s):  
K Spiess ◽  
G Sachs ◽  
P Pietschmann ◽  
R Prager

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


2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Lina T. Al Kury

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.


1997 ◽  
Vol 7 (3) ◽  
pp. 283-287 ◽  
Author(s):  
J. Nawrocki ◽  
W. Chrzanowski ◽  
D. Koch ◽  
K. Dziegielewski

The present paper reports our first results after pars plana vitrectomy in patients with diabetic retinopathy and hemodialysis with a follow-up of 6 to 24 months. Between January 1992 and October 1994 we performed vitreoretinal surgery with silicone oil tamponade in nine eyes of seven patients with diabetic nephropathy on hemodialysis. All patients had had type I diabetes for 19–32 years. Over the observation period the retina was completely attached in eight eyes. Final visual acuity of 0.1 - 0.7 was attained in four eyes, 0.06 two, hand movements in one eye. Two eyes had no useful final visual acuity because of redetachment of the retina or secondary glaucoma with rubeosis iridis. The small number of complications shows that pars plana vitrectomy can be done in diabetic patients with nephropathy on hemodialysis. This significantly improves their quality of life


1987 ◽  
Author(s):  
B JUDE ◽  
A WATEL ◽  
D FONTAINE ◽  
P FONTAINE ◽  
A COSSON

Hypercoagulability is one of the possible factors reported in genesis or aggravation of vascular complications in diabetes mellitus. We therefore examined procoagulant activity (PCA) of disrupted monocytes frcm 26 patients with Type I diabetes and 6 with Type II, versus 32 control subjects (male/ female ratio = 1 in each group).Diabetes monocytes exhibited a slight but detectable PCA before any incubation or in vitro stimulation, whereas control monocytes did not. Data obtained with coagulation factor deficient plasmas or phospholipase C indicated that PCA was tissue factor (TF) alone in 22 cases and TF associated with a significant amount of factor VII/VIIa activity in 10 cases.Incubation in serum free medium led to significant raise of PCA in diabetes cells when stimulated with endotoxin or not, and in control cells only after stimulation. Furthermore, PCA appeared earlier in diabetes monocytes than in control ones, (4 hours, versus 20 hours). PCA frcm control cells was FT-like. PCA frcm diabetes cells was FT-like when no VII/VIIa activity was present on non-stimulated cells, and prothrombinase-like when VII/VIIa activity was early associated with the cells. In the latter case, trace amounts of factor X activity were also detectable. Whether factor VII and factor X activities were of plasmatic origin and associated to the cells, or synthesized in vitro by the cells remains unclear. The characteristics of PCA were net correlated with clinical features (age, diabetic complications) nor with the type of diabetes.Our data suggest that in diabetes patients, monocytes exhibit an increased PCA, possibly corresponding to a baseline stimulation, or at least a higher responsiveness to undergoing stimuli in vitro.


2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Ebru Atalar ◽  
Cuneyd Gunay ◽  
Hakan Atalar ◽  
Tugba Tunc

A 49-year-old male presented with acute midthoracic severe back pain following a witnessed nocturnal convulsion attack. There was no history of trauma and the patient had a 23-year history of Type I diabetes mellitus. MRI scans of the thoracic spine revealed compression fractures at T5, T6, T7, and T8 vertebrae. The patient was treated conservatively. At 17 months after the initial diagnosis, the complaints of back pain had been resolved and the patient was able to easily undertake daily living activities. Hypoglycaemia is a common problem in diabetic patients treated with insulin. Convulsions may occur as a consequence of insulin-induced hypoglycemia. Nontraumatic compression fractures of the thoracic spine following seizures are a rare injury. Contractions of strong paraspinal muscles can lead to compression fracture of the midthoracic spine. Unrecognized hypoglycaemia should be considered to be a possible cause of convulsions in insulin-dependent diabetic patients. The aim of this report is to point out a case of rarely seen multilevel consecutive vertebrae fractures in a diabetic patient after a nocturnal hypoglycaemic convulsion attack.


1982 ◽  
Vol 62 (2) ◽  
pp. 131-136 ◽  
Author(s):  
I. Lager ◽  
U. Smith

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.


2001 ◽  
Vol 101 (1) ◽  
pp. 59-64 ◽  
Author(s):  
Abram KATZ ◽  
Karin EKBERG ◽  
Bo-Lennart JOHANSSON ◽  
John WAHREN

The purpose of this study was to quantify the extent to which skin blood flow (SBF) responses to application of endothelium-dependent and -independent vasodilating agents differ between Type I diabetic patients and healthy subjects. Patients and matched controls were studied after an overnight fast. SBF was determined with laser Doppler perfusion imaging before and after iontophoresis of acetylcholine (Ach; endothelium-dependent) and sodium nitroprusside (SNP; endothelium-independent). Basal SBF did not differ significantly between groups. Iontophoresis of ACh and SNP increased SBF 20-fold in controls. In the patients, the increases in SBF following iontophoresis of ACh and SNP were reduced by 18% and 19%, respectively, versus controls (P < 0.05 for both). These data demonstrate that Type I diabetic patients have similar diminished SBF responses to iontophoresis of ACh and SNP, which suggests that non-endothelial-dependent factors are primarily responsible for the diminished SBF responses.


1985 ◽  
Vol 109 (1) ◽  
pp. 104-107 ◽  
Author(s):  
G. Gragnoli ◽  
A. M. Signorini ◽  
I. Tanganelli

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.


2001 ◽  
Vol 102 (1) ◽  
pp. 69-75 ◽  
Author(s):  
Nicholas J.M. FARDON ◽  
Robert WILKINSON ◽  
Trevor H. THOMAS

Microalbuminuria in Type I diabetes involves a cell membrane abnormality and is associated with a large increase in cardiovascular risk. The hypothesis that the membrane abnormality alters granule exocytosis in neutrophils, which could contribute to the increased incidence of cardiovascular disease, was investigated. PMA-stimulated expression of CD11b and CD69 on neutrophils from normal controls (NC), long-term uncomplicated Type I diabetic control patients (DC) and diabetic nephropathy patients (DN) was determined by fluorescence activated cell scanning. Neutrophils from DN were faster than neutrophils from either NC or DC to exocytose primary granules with CD69 following initial expression of the adhesion molecule CD11b. However, a larger proportion of neutrophils from DN failed to withdraw CD11b from the cell membrane after 90min incubation. The protein kinase C (PKC) inhibitor, bisindolylmaleimide (BIM), showed that a larger proportion of neutrophils from DN, compared with DC or NC, exocytosed primary granules independent of PKC. The calpain inhibitor, E64d, showed that a larger proportion of neutrophils from both groups of diabetic patients, compared with NC, exocytosed primary granules independent of calpain. Cytoskeletal disruption with cytochalasin D had an effect on CD11b and CD69 exocytosis similar to that of BIM and E64d. The pathways controlling granule exocytosis in neutrophils from diabetic patients are abnormal. A change characteristic of DN causes rapid exocytosis of primary granules, and also causes the adhesion molecule CD11b to persist on an increased proportion of neutrophils. This will make an important contribution to increased vascular damage in these patients.


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