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Related Concept Videos

Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1 diabetes is an...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
Tissue Renewal without Stem Cells01:23

Tissue Renewal without Stem Cells

After cellular or tissue damage, the resident stem cells present in the human body can locally repair and regenerate the damaged tissue or organ. However, even though some tissues do not have stem cells, they can repair and regenerate with the help of pre-existing cells. For example, beta cells of the pancreas and hepatocytes of the liver can divide to renew and regenerate the tissue. Here, both cell division and cell death are well regulated by homeostasis.
However, failure of such a system...
Diabetes Mellitus: Introduction01:26

Diabetes Mellitus: Introduction

Diabetes mellitus consists of chronic metabolic disorders characterized by persistent hyperglycemia. This elevated blood glucose results from defects in insulin secretion, impaired insulin action, or both. Insulin, produced by pancreatic β-cells, is essential for maintaining glucose homeostasis by facilitating cellular glucose uptake for energy or storage. Disruptions in insulin production or function lead to glucose accumulation in the bloodstream, causing the clinical features and long-term...

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Bioluminescent Monitoring of Graft Survival in an Adoptive Transfer Model of Autoimmune Diabetes in Mice
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Making progress: preserving beta cells in type 1 diabetes.

Mary Pat Gallagher1, Robin S Goland, Carla J Greenbaum

  • 1Naomi Berrie Diabetes Center, Columbia University, College of Physicians and Surgeons, New York, New York, USA.

Annals of the New York Academy of Sciences
|January 4, 2012
PubMed
Summary
This summary is machine-generated.

Researchers are exploring new treatments to preserve insulin secretion in type 1 diabetes (T1D) by targeting the immune system. Promising agents show utility in new-onset T1D, though prevention trials need further development.

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Published on: November 5, 2016

Area of Science:

  • Immunology
  • Endocrinology
  • Diabetes Research

Background:

  • Type 1 diabetes (T1D) management has improved, but complete blood sugar normalization remains elusive.
  • Preserving pancreatic beta cell function is a key goal for improving T1D care and achieving a cure.
  • The immune system's attack on beta cells is a primary driver of T1D pathogenesis.

Purpose of the Study:

  • To review progress in clinical trials aimed at preserving insulin secretion in T1D.
  • To evaluate immunomodulatory strategies targeting the autoimmune assault on pancreatic beta cells.
  • To assess the efficacy of experimental agents in new-onset T1D and prevention studies.

Main Methods:

  • Review of clinical trial data for immunomodulatory agents in T1D.
  • Analysis of agents with diverse mechanisms: anti-T cell, anti-B cell, and costimulation blockade.
  • Examination of studies in both new-onset T1D and T1D prevention cohorts.

Main Results:

  • Successful trials in new-onset T1D demonstrated the utility of experimental agents in preserving insulin secretion.
  • Three agents with distinct mechanisms (anti-T cell, anti-B cell, costimulation blockade) showed promise.
  • Prevention studies have not yet yielded positive results but confirmed feasibility and identified new agents.

Conclusions:

  • Immunomodulatory therapies show potential for preserving insulin secretion in new-onset T1D.
  • Further research is needed to translate these findings into effective T1D prevention strategies.
  • Ongoing research focuses on novel agents and refining approaches to protect beta cells in T1D.