Diabetes Therapy
Diabetes Therapy - Related Videos
16:26
Regulatory T cells: Therapeutic Potential for Treating Transplant Rejection and Type I Diabetes
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Cited by 2 •
2007
10:43
Transplantation of Pancreatic Islets Into the Kidney Capsule of Diabetic Mice
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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.
11:13
Adenoviral Gene Therapy for Diabetic Keratopathy: Effects on Wound Healing and Stem Cell Marker Expression in Human Organ-cultured Corneas and Limbal Epithelial Cells
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Cited by 27 •
2016
An example of adenoviral gene therapy in the human diabetic organ-cultured corneas is presented towards the normalization of delayed wound healing and markedly reduced epithelial stem cell marker expression in these corneas. It also describes the optimization of this process in stem cell-enriched limbal epithelial cultures.
16:59
Neo-Islet Formation in Liver of Diabetic Mice by Helper-dependent Adenoviral Vector-Mediated Gene Transfer
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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.
10:03
A Zebrafish Model of Diabetes Mellitus and Metabolic Memory
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Cited by 69 •
2013
Metabolic memory is the phenomenon by which diabetic complications persist and progress unimpeded even after euglycemia is achieved pharmaceutically. Here we describe a diabetes mellitus zebrafish model which is unique in that it allows for the examination of the mitotically transmissible epigenetic components of metabolic memory in vivo.
FAQs
Treatment selection reflects how glucose regulation is disrupted in a particular person. Some approaches replace missing insulin, whereas others increase insulin availability, improve tissue sensitivity to insulin, slow glucose entry from the intestine, or promote glucose loss through urine. Matching the intervention to these biological features helps researchers and clinicians evaluate glucose control alongside disease progression.
Insulin sensitivity describes how effectively tissues respond to insulin. When sensitivity improves, glucose uptake and energy use can change even without simply increasing insulin availability. This distinction helps separate therapies that act primarily on insulin action from those that supply or stimulate insulin, making insulin sensitivity an important biological variable in treatment research and metabolic assessment.
Pancreatic beta cells provide a biological context for understanding insulin availability. Studying their function helps researchers examine whether glucose regulation reflects impaired insulin production, altered insulin action, or both. Diabetes therapy therefore serves not only as clinical management but also as a framework for investigating beta-cell function, metabolism, and how these processes change as disease progresses.
Nutrition changes the amount and timing of glucose entering the circulation, while physical activity alters glucose uptake and energy use. These effects can complement medication-based mechanisms without acting through the same pathway. Considering these variables together gives a broader view of glucose regulation and helps interpret why glucose levels and variability may change during therapy.
Researchers and clinicians assess treatment using glycated hemoglobin, glucose variability, and indicators of organ health. Glycated hemoglobin provides an assessment of glucose exposure over time, while variability captures fluctuations that an average may not show. Organ-health measures add a broader outcome perspective, helping determine whether improved glucose regulation is associated with reduced complications.
Comparisons focus on the biological process each intervention changes and the resulting glucose outcomes. A study may distinguish insulin replacement from approaches that improve sensitivity, slow intestinal absorption, or promote urinary glucose excretion. Researchers can then relate those mechanisms to beta-cell function, metabolism, glycated hemoglobin, glucose variability, and organ health rather than relying on one measurement alone.
Therapy is relevant whenever researchers examine how altered glucose regulation affects metabolism, pancreatic beta-cell function, or organ health over time. Tracking treatment alongside these biological features can show how disease-related processes and clinical outcomes change together. This context supports investigations of progression rather than limiting evaluation to a single glucose measurement.
Glucose variability describes fluctuations in glucose rather than only the longer-term average represented by glycated hemoglobin. Including both measures can provide a more complete assessment of treatment response, because two individuals may have similar average exposure but different patterns of change. Researchers can also interpret these results alongside organ health and metabolic findings.