scholarly journals Effect of omega-3 supplementation on neuropathy in type 1 diabetes

Neurology ◽  
2017 ◽  
Vol 88 (24) ◽  
pp. 2294-2301 ◽  
Author(s):  
Evan J.H. Lewis ◽  
Bruce A. Perkins ◽  
Leif E. Lovblom ◽  
Richard P. Bazinet ◽  
Thomas M.S. Wolever ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Nerve Conduction ◽  
Sensory Function ◽  
Omega 3 ◽  
Open Label ◽  
Pufa Supplementation ◽  
Corneal Confocal Microscopy ◽  
Seal Oil

Objective:To test the hypothesis that 12 months of seal oil omega-3 polyunsaturated fatty acids (ω-3 PUFA) supplementation will stop the known progression of diabetic sensorimotor polyneuropathy (DSP) in type 1 diabetes mellitus (T1DM).Methods:Individuals with T1DM and evidence of DSP as determined by a Toronto Clinical Neuropathy Score ≥1 were recruited to participate in a single-arm, open-label trial of seal oil ω-3 PUFA supplementation (10 mL·d−1; 750 mg eicosapentaenoic acid, 560 mg docosapentaenoic acid, and 1,020 mg docosahexaenoic acid) for 1 year. The primary outcome was the 1-year change in corneal nerve fiber length (CNFL) measured by in vivo corneal confocal microscopy, with sensory and nerve conduction measures as secondary outcomes.Results:Forty participants (53% female), aged 48 ± 14 years, body mass index 28.1 ± 5.8 with diabetes duration of 27 ± 18 years, were enrolled. At baseline, 23 participants had clinical DSP and 17 did not. Baseline CNFL was 8.3 ± 2.9 mm/mm2 and increased 29% to 10.1 ± 3.7 mm/mm2 (p = 0.002) after 12 months of supplementation. There was no change in nerve conduction or sensory function.Conclusions:Twelve months of ω-3 supplementation was associated with increase in CNFL in T1DM.ClinicalTrials.govidentifier:NCT02034266.Classification of evidence:This study provides Class IV evidence that for patients with T1DM and evidence of DSP, 12 months of seal oil omega-3 supplementation increases CNFL.

In Vivo Corneal Confocal Microscopy and Prediction of Future-Incident Neuropathy in Type 1 Diabetes: A Preliminary Longitudinal Analysis

2015 ◽  
Vol 39 (5) ◽  
pp. 390-397 ◽  
Author(s):  
Leif E. Lovblom ◽  
Elise M. Halpern ◽  
Tong Wu ◽  
Dylan Kelly ◽  
Ausma Ahmed ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Confocal Microscopy ◽  
Longitudinal Analysis ◽  
Corneal Confocal Microscopy

scholarly journals Using in vivo corneal confocal microscopy to identify diabetic sensorimotor polyneuropathy risk profiles in patients with type 1 diabetes

2017 ◽  
Vol 5 (1) ◽  
pp. e000251 ◽  
Author(s):  
Evan J H Lewis ◽  
Bruce A Perkins ◽  
Lief E Lovblom ◽  
Richard P Bazinet ◽  
Thomas M S Wolever ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Confocal Microscopy ◽  
Risk Profiles ◽  
Sensorimotor Polyneuropathy ◽  
Corneal Confocal Microscopy

scholarly journals Early Alterations of Corneal Subbasal Plexus in Uncomplicated Type 1 Diabetes Patients

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Domenico Schiano Lomoriello ◽  
Irene Abicca ◽  
Mariacristina Parravano ◽  
Daniela Giannini ◽  
Benedetta Russo ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Diabetic Retinopathy ◽  
Confocal Microscopy ◽  
Nerve Fiber ◽  
Fiber Length ◽  
Diabetes Complications ◽  
Corneal Confocal Microscopy ◽  
Subbasal Nerve Plexus

Purpose. The purpose of our study is to describe the in vivo corneal confocal microscopy characteristics of subbasal nerve plexus in a highly selected population of patients affected by type 1 diabetes mellitus (T1DM) without any microvascular diabetes complications.Methods. We included 19 T1DM patients without diabetic peripheral neuropathy, diabetic autonomic neuropathy, diabetic retinopathy, and microalbuminuria. All patients underwent in vivo corneal confocal microscopy and blood analysis to determine subbasal nerve plexus parameters and their correlation with clinical data. We compared the results with 19 healthy controls.Results. The T1DM group showed a significant decrease of the nerve fiber length (P=0.032), the nerve fiber length density (P=0.034), the number of fibers (P=0.005), and the number of branchings (P=0.028), compared to healthy subjects. The nerve fiber length, nerve fiber length density, and number of fibers were directly related to the age at onset of diabetes and inversely to the duration of DM. BMI (body mass index) was highly related to the nerve fiber length (r = −0.6,P=0.007), to the nerve fiber length density (r = −0.6,P=0.007), and to the number of fibers (r = −0.587,P=0.008). No significant correlations were found between the corneal parameters and HbA1c.Conclusions. Early subclinical fiber corneal variation could be easily detected using in vivo corneal confocal microscopy, even in type 1 diabetes without any microvascular diabetes complications, including diabetic peripheral neuropathy, diabetic autonomic neuropathy, diabetic retinopathy, and microalbuminuria.

scholarly journals Effect of Coxsackievirus B4 Infection on the Thymus: Elucidating Its Role in the Pathogenesis of Type 1 Diabetes

2021 ◽  
Vol 9 (6) ◽  
pp. 1177
Author(s):  
Abdulaziz Alhazmi ◽  
Magloire Pandoua Nekoua ◽  
Hélène Michaux ◽  
Famara Sane ◽  
Aymen Halouani ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
T Cell ◽  
Viral Infections ◽  
Lymphoid Organ ◽  
Thymic Epithelial Cells ◽  
Central Tolerance ◽  
Coxsackievirus B4

The thymus gland is a primary lymphoid organ for T-cell development. Various viral infections can result in disturbance of thymic functions. Medullary thymic epithelial cells (mTECs) are important for the negative selection of self-reactive T-cells to ensure central tolerance. Insulin-like growth factor 2 (IGF2) is the dominant self-peptide of the insulin family expressed in mTECs and plays a crucial role in the intra-thymic programing of central tolerance to insulin-secreting islet β-cells. Coxsackievirus B4 (CVB4) can infect and persist in the thymus of humans and mice, thus hampering the T-cell maturation and differentiation process. The modulation of IGF2 expression and protein synthesis during a CVB4 infection has been observed in vitro and in vivo in mouse models. The effect of CVB4 infections on human and mouse fetal thymus has been studied in vitro. Moreover, following the inoculation of CVB4 in pregnant mice, the thymic function in the fetus and offspring was disturbed. A defect in the intra-thymic expression of self-peptides by mTECs may be triggered by CVB4. The effects of viral infections, especially CVB4 infection, on thymic cells and functions and their possible role in the pathogenesis of type 1 diabetes (T1D) are presented.

scholarly journals A C-peptide complex with albumin and Zn2+ increases measurable GLUT1 levels in membranes of human red blood cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
M. Geiger ◽  
T. Janes ◽  
H. Keshavarz ◽  
S. Summers ◽  
C. Pinger ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Amino Acid ◽  
Blood Cells ◽  
Glucose Transporter ◽  
Peptide Binding ◽  
C Peptide ◽  
Amino Acid Peptide ◽  
Human Red Blood Cells

Abstract People with type 1 diabetes (T1D) require exogenous administration of insulin, which stimulates the translocation of the GLUT4 glucose transporter to cell membranes. However, most bloodstream cells contain GLUT1 and are not directly affected by insulin. Here, we report that C-peptide, the 31-amino acid peptide secreted in equal amounts with insulin in vivo, is part of a 3-component complex that affects red blood cell (RBC) membranes. Multiple techniques were used to demonstrate saturable and specific C-peptide binding to RBCs when delivered as part of a complex with albumin. Importantly, when the complex also included Zn2+, a significant increase in cell membrane GLUT1 was measured, thus providing a cellular effect similar to insulin, but on a transporter on which insulin has no effect.

scholarly journals The DNA Sensor AIM2 Protects against Streptozotocin-Induced Type 1 Diabetes by Regulating Intestinal Homeostasis via the IL-18 Pathway

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 959 ◽  
Author(s):  
Jefferson Antônio Leite ◽  
Gabriela Pessenda ◽  
Isabel C. Guerra-Gomes ◽  
Alynne Karen Mendonça de Santana ◽  
Camila André Pereira ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Gut Microbiota ◽  
Bacterial Translocation ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Dna Sensor ◽  
Proinflammatory Response

Pattern recognition receptors (PRRs), such as Nod2, Nlrp3, Tlr2, Trl4, and Tlr9, are directly involved in type 1 diabetes (T1D) susceptibility. However, the role of the cytosolic DNA sensor, AIM2, in T1D pathogenesis is still unknown. Here, we demonstrate that C57BL/6 mice lacking AIM2 (AIM2−/−) are prone to streptozotocin (STZ)-induced T1D, compared to WT C57BL/6 mice. The AIM2−/− mice phenotype is associated with a greater proinflammatory response in pancreatic tissues, alterations in gut microbiota and bacterial translocation to pancreatic lymph nodes (PLNs). These alterations are related to an increased intestinal permeability mediated by tight-junction disruption. Notably, AIM2−/− mice treated with broad-spectrum antibiotics (ABX) are protected from STZ-induced T1D and display a lower pancreatic proinflammatory response. Mechanistically, the AIM2 inflammasome is activated in vivo, leading to an IL-18 release in the ileum at 15 days after an STZ injection. IL-18 favors RegIIIγ production, thus mitigating gut microbiota alterations and reinforcing the intestinal barrier function. Together, our findings show a regulatory role of AIM2, mediated by IL-18, in shaping gut microbiota and reducing bacterial translocation and proinflammatory response against insulin-producing β cells, which ultimately results in protection against T1D onset in an STZ-induced diabetes model.

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