Insulin-dependent Diabetes
Insulin-dependent Diabetes - Related Videos
16:59
Neo-Islet Formation in Liver of Diabetic Mice by Helper-dependent Adenoviral Vector-Mediated Gene Transfer
0 Views •
Cited by 5 •
2012
We describe hepatic neo-islet formation in STZ (streptozotocin)-induced diabetic mice by gene transfer of Neurogenin3 (Ngn3) and Betacellulin (Btc) using helper-dependent adenoviral vector (HDAd) and the reversal of hyperglycemia. Our method takes advantages of helper-dependent adenoviral vectors with their highly efficient in vivo transduction and the long lasting gene expression.
16:26
Regulatory T cells: Therapeutic Potential for Treating Transplant Rejection and Type I Diabetes
0 Views •
Cited by 2 •
2007
14:39
A Quantitative Assay for Insulin-expressing Colony-forming Progenitors
0 Views •
Cited by 11 •
2011
A three-dimensional clonogenic assay that allows pancreatic-like progenitors to differentiate into insulin-expressing colonies is described. This method takes advantage of semi-solid media containing methylcellulose, Matrigel and growth factors, in which single progenitors proliferate and differentiate in vitro, permitting quantification of the number of functional progenitors in a population.
12:08
Improving IV Insulin Administration in a Community Hospital
0 Views •
Cited by 7 •
2012
When compared to the previous paper protocol, implementation of a computerized glucose management system results in a substantial increase in blood glucose concentration measurements within the target range. Using a computerized glucose management system to monitor blood glucose levels, decreases in severe hypoglycemia (<40 mg/dL), clinical hypoglycemia (<70 mg/dL), and hyperglycemia (>180 mg/dL) also can be observed.
10:43
Transplantation of Pancreatic Islets Into the Kidney Capsule of Diabetic Mice
0 Views •
Cited by 98 •
2007
Our protocol was developed to cleanly and easily deliver islets or cells under the kidney capsule of mice. Cells are concentrated into pellets in the final tubing used for transplanting the cells under the kidney capsule. The ease of this technique reduces stress to the cells and the mouse.
FAQs
The key endocrine disruption begins when pancreatic beta-cell loss occurs. These cells normally supply insulin, so their loss removes the signal that coordinates glucose regulation with the body's energy needs. In the common type 1 form, immune-mediated damage can produce absolute insulin deficiency. This explains why restoring insulin is central to management rather than relying on lifestyle measures alone.
Without sufficient insulin signaling, glucose stays in the bloodstream instead of being taken up efficiently by insulin-responsive tissues. This separates blood glucose availability from effective cellular access to that fuel. The resulting imbalance is therefore both a circulation problem and an energy-balance problem, which is why treatment aims to regulate glucose rather than address a single isolated episode.
Research focuses on immune regulation, because type 1 diabetes involves immune-mediated destruction of beta cells. Understanding how that immune activity might be controlled could preserve or protect insulin-producing cells. This line of investigation addresses the underlying cellular cause and differs from management strategies that replace missing insulin after beta-cell function has already declined.
Persistent disruption of blood-glucose control can contribute to complications involving the eyes, kidneys, nerves, and cardiovascular system. These targets show that insulin-dependent diabetes has consequences beyond immediate glucose levels: dysregulation can affect multiple organ systems. Monitoring, insulin replacement, nutrition planning, and physical activity therefore have a preventive purpose, not merely a role in responding to abnormal measurements.
Management requires a continuing plan rather than a one-time intervention. Lifelong insulin replacement addresses the missing hormonal signal, while glucose monitoring helps track blood sugar. Nutrition planning and physical activity are incorporated alongside these measures. The combined approach is intended to support blood-glucose control and lower the likelihood of complications, making regular self-management a central part of care.
Two research directions highlighted for future therapy are immune regulation and beta-cell replacement. Immune-focused work seeks to address the process that damages insulin-producing cells, whereas replacement approaches aim to restore the cellular source of insulin. These strategies target different points in the disease process, and either could complement existing management based on insulin replacement, monitoring, nutrition, and activity.