Human Amnion-Isolated Cells Normalize Blood Glucose in Streptozotocin-Induced Diabetic Mice

2003 ◽  
Vol 12 (5) ◽  
pp. 545-552 ◽  
Author(s):  
Jun Ping Wei ◽  
Tian Shu Zhang ◽  
Shigeyuki Kawa ◽  
Toru Aizawa ◽  
Masao Ota ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Type I Diabetes ◽  
Cell Mass ◽  
Mouse Tissue ◽  
Fetal Membrane ◽  
Type I ◽  
Diabetic Mice ◽  
Human Specific

Whole pancreas or β-cell transplantation has opened the way for the treatment of advanced stage of diabetes mellitus. However, it is always limited by the scarcity of transplantation materials. The amniotic membrane is part of the fetal membrane and is composed of amniotic epithelium (HAE) and mesenchymal (HAM) cells that are derived from the inner cell mass in the blastocyst. Thus, HAE and HAM cells may have the potential to differentiate into various organs. The aim of our study was to assess the possibility of HAE cells differentiating into insulin-producing cells. In vitro, HAE cells stimulated with nicotinamide induced insulin mRNA in the culture cells. In vivo, HAE cells were capable of normalizing the blood glucose level of diabetic mice after several weeks of implantation into streptozotocin-induced diabetic mice. The distribution of human cells and human insulin secretion in mouse tissue studied by immunohistochemistry for anti-human-specific β-2-microglobulin and anti-human-specific insulin shows the same location in mouse tissue. These studies suggest that HAE cells have the potential to differentiate into β-cells in vivo, and hence that HAE cells have therapeutic potential for the treatment of type I diabetes mellitus.

Sitagliptin (Januvia)

Top Drugs ◽  
2015 ◽  
Author(s):  
Jie Jack Li
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Type Ii Diabetes ◽  
Kidney Diseases ◽  
Type I Diabetes ◽  
Glycosylated Hemoglobin ◽  
Insulin Injection ◽  
Type I ◽  
Type Ii ◽  
Ancient Times

Diabetes has been known since antiquity. In fact, the term “diabetes mellitus” comes from the Greek meaning “siphon and honey” due to the excess excretion (siphon or faucet) of hyperglycemic (sweetened, or honeyed) urine associated with diabetes. In ancient times, diabetes was mostly type I, which usually manifests acutely in the young, secondary to certain underlying insults (possibly infections) to the islet cells of the pancreas resulting in an absolute lack of insulin. Insulin was discovered by Banting and Best in 1921, and insulin injection has literally saved millions of lives since then. With the wondrous efficacy that insulin bestows, type I diabetes is largely controlled because type I diabetes is insulindependent. However, type II diabetes, a more prevalent form of diabetes, is not insulin-dependent. In ancient times, when nutrition was scarce and obesity was not prevalent, type II diabetes mellitus (T2DM) was extremely rare. Indeed, type II diabetes is a disease more frequently associated with maturity, obesity, and gradually increasing blood glucose concentrations, and it may be asymptomatic for some time, only discovered on routine glucose screening. In fact, with the increasing body weight of the general population of the developed world, type II diabetes is becoming an epidemic. Serious complications of diabetes include nephropathy (kidney diseases), neuropathy (nerve damage), and retinopathy (blindness). Diabetes is the most common cause of blindness and amputation in the elderly in the United States. Oral diabetes drugs are required for most type II diabetic patients. Diabetes drugs may be classified into four categories: (a) agents that augment the supply of insulin such as sulfonylureas; (b) agents that enhance the effectiveness of insulin such as biguanides and thiazolidinediones; (c) GLP agonists; and (d) DPP4 Inhibitors. The efficacy of all the antidiabetic drugs can be monitored by measuring glycosylated hemoglobin (HaA1c) as a long term marker of elevated blood glucose. The amount of HaA1c reflects the average level over the last 120 days, the life span of a red blood cell, and should remain below 7%.

scholarly journals Type I diabetes mellitus decreases in vivo macrophage-to-feces reverse cholesterol transport despite increased biliary sterol secretion in mice

2011 ◽  
Vol 53 (3) ◽  
pp. 348-357 ◽  
Author(s):  
Jan Freark de Boer ◽  
Wijtske Annema ◽  
Marijke Schreurs ◽  
Jelske N. van der Veen ◽  
Markus van der Giet ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Reverse Cholesterol Transport ◽  
Type I Diabetes ◽  
Type I Diabetes Mellitus ◽  
Cholesterol Transport ◽  
Type I

Nocturnal Blood Glucose Control in Type I Diabetes Mellitus

Diabetes Care ◽  
1993 ◽  
Vol 16 (Supplement_3) ◽  
pp. 71-89 ◽  
Author(s):  
G. B. Bolli ◽  
G. Perriello ◽  
C. G. Fanelli ◽  
P. De Feo
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Glucose Control ◽  
Type I Diabetes ◽  
Blood Glucose Control ◽  
Type I Diabetes Mellitus ◽  
Type I

scholarly journals Contribution of Trem2 Signaling to the Development of Painful Diabetic Neuropathy by Mediating Microglial Polarization in Mice

2021 ◽  
Author(s):  
Xin Chen ◽  
Yue Le ◽  
Wan-you He ◽  
Jian He ◽  
Yun-hua Wang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Neuropathy ◽  
Mechanical Allodynia ◽  
Type I Diabetes ◽  
Intraperitoneal Administration ◽  
Thermal Hyperalgesia ◽  
Lumbar Spinal Cord ◽  
Type I ◽  
Painful Diabetic Neuropathy ◽  
Diabetic Mice

Abstract Background Painful diabetic neuropathy (PDN) is a common and intractable complication of diabetes mellitus, with little effective treatment. PDN has been associated with spinal neuroinflammation characterized by microglial activation. Recently, the triggering receptor expressed on myeloid cells 2 (TREM2), specifically localized on microglia, has been identified as a vital factor in modulating neuroinflammation and microglial phenotypes in neural diseases. Therefore, we hypothesized that spinal TREM2 might contribute to PDN and neuroinflammation by regulating microglial activity and phenotypes. Methods Type I diabetes mellitus was elicited by a single intraperitoneal administration of streptozotocin (STZ) in mice. The pain behaviors were reflected by paw mechanical withdrawal thresholds (PMWT) and thermal withdrawal latency (PTWL). Results We demonstrated that up-regulation of microglial TREM2 and amplification of both microglial M1 and M2 response was along with the presence of diabetes-related mechanical allodynia and thermal hypersensitivity. Moreover, we found that overexpression of TREM2 in microglia aggravated the symptom of PDN, amplified microglia M1 response, and suppressed microglia M2 polarization in the lumbar spinal cord of diabetic mice. However, inhibition of TREM2 with anti-TREM2 neutralizing antibodies attenuated mechanical allodynia and thermal hyperalgesia in diabetic mice. Besides, we identified Galectin-3 (GLT-3) as the potential ligand of the TREM2 receptor in facilitating the progression of PDN. Conclusions TREM2 could be a critical microglial membrane molecule that modulates microglial phenotypes pain hypersensitivity in PDN. GLT-3 might act as a specific ligand to trigger TREM2 signaling in PDN or other neuropathic pain.

scholarly journals Trisk 95 as a Novel Skin Mirror for Normal and Diabetic Systemic Glucose Level

2019 ◽  
Author(s):  
Nsrein Ali ◽  
Hamid Reza Rezvani ◽  
Diana Motei ◽  
Sufyan Suleman ◽  
Walid Mahfouf ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Type I Diabetes ◽  
Glucose Monitoring ◽  
Calcium Flux ◽  
Luciferase Reporter ◽  
Type I ◽  
Skin Wound Healing ◽  
High Blood Glucose ◽  
Increased Risk

AbstractCoping with diabetes requires frequent and even today mostly invasive blood glucose-based monitoring. Partly due to this invasive nature and the associated reduced skin wound healing and increased risk of infection, non-invasive glucose monitoring technologies would represent considerable progress. Edited keratinocytes may enable such a function.To address this hypothesis, we conducted a proteomic screen in the skin by making use of the experimental in vivo mouse model of type I diabetes alongside controls. We identified Trisk 95 as the only protein whose expression is induced in response to high blood glucose. A luciferase reporter assay demonstrated that induction of Trisk 95 expression occurs not only at the protein level but also transcriptionally. This induction was associated with a marked elevation in the Fluo-4 signal, suggesting a role for intracellular calcium changes in the signalling cascade. Strikingly, these changes lead concurrently to fragmentation of the mitochondria. As judged from the knockout findings, both the calcium flux and the mitochondrial phenotype were dependent on Trisk 95 function, since the phenotypes in question were abolished.The data demonstrate that the skin represents an organ that reacts robustly and thus mirrors changes in systemic blood glucose levels. The findings are also consistent with a channelling model of Trisk 95 that serves as an insulin-independent but glucose-responsive biomarker taking part in releasing calcium from the cellular stores in the skin. The skin cells may thus provide a novel mean for glucose monitoring when analysing changes in labelled Trisk 95 and calcium. By that, this study is the first proof of the concept of our registered patent (No. PCT FI2016/050917), which proposes the use of cells as biosensors for developing personalized health-monitoring devices.

Diminished insulin clearance during late pregnancy in patients with Type I diabetes mellitus

1998 ◽  
Vol 95 (3) ◽  
pp. 317-323 ◽  
Author(s):  
Anders O. BJÖRKLUND ◽  
Ulf K. C. ADAMSON ◽  
Per-Eric S. LINS ◽  
L. Magnus R. WESTGREN
Keyword(s):  
Diabetes Mellitus ◽  
Steady State ◽  
Blood Glucose ◽  
Clearance Rate ◽  
Insulin Infusion ◽  
Type I Diabetes ◽  
Type I ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Insulin Levels

1.Intensive insulin treatment of patients with Type I diabetes mellitus during pregnancy is associated with a high frequency of serious hypoglycaemic events. A potential change in insulin metabolism during pregnancy may affect both the frequency and the severity of insulin-induced hypoglycaemia. 2.In 10 patients with Type I diabetes, during the third trimester of pregnancy and 5 to 13 months after delivery, hypoglycaemia was induced by the hyperinsulinaemic hypoglycaemic clamp technique. A constant high-dose intravenous insulin infusion was administered for 150 ;min and arterial blood glucose was clamped at 2.2 ;mmol/l by counterregulation with intravenous glucose. During the experiment venous samples were collected for later analysis of free plasma insulin, whereby the metabolic clearance rate of insulin could be calculated. 3.The desired blood glucose level was approached after approximately 60 ;min of insulin infusion. After just 30 ;min the insulin levels were significantly higher during pregnancy compared with after delivery. In addition, the steady-state insulin level from 90 to 150 ;min was significantly higher during pregnancy. 4.From the steady-state insulin levels at 90 to 150 ;min, the metabolic clearance rate of insulin was calculated, being 24% higher after delivery. 5.We conclude that there is a decreased metabolic clearance rate of insulin during pregnancy. This might be due to altered blood-flow distribution, decreased hepatic insulin extraction and relative increase in body fat during pregnancy. A decreased clearance of insulin will contribute to the risk for serious hypoglycaemic events in patients with Type I diabetes during pregnancy.

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