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Type I Diabetes I: Introduction

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 I Diabetes II: Pathophysiology

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...

Diabetes: Management and Pharmacotherapy

Diabetes: Management and Pharmacotherapy

The therapy for diabetes aims to alleviate hyperglycemia-related symptoms, prevent acute metabolic decompensation, and reduce chronic end-organ complications. Glycemic control is evaluated through short-term (self-monitoring, continuous glucose monitoring) and long-term (A1c, fructosamine) metrics, enabling near real-time tracking of blood glucose levels and reflecting glycemic control over specific time frames.
Insulin remains the cornerstone of treatment for most patients with type 1 and many...

Glucagon-like Receptor Agonists

Glucagon-like Receptor Agonists

Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...

Insulin: Dosing Regimen and Adverse Effects

Insulin: Dosing Regimen and Adverse Effects

Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...

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Related Experiment Video

Updated: Jun 16, 2026

High-Efficiency Generation of Antigen-Specific Primary Mouse Cytotoxic T Cells for Functional Testing in an Autoimmune Diabetes Model

High-Efficiency Generation of Antigen-Specific Primary Mouse Cytotoxic T Cells for Functional Testing in an Autoimmune Diabetes Model

Published on: August 16, 2019

Teplizumab therapy for type 1 diabetes.

Umesh B Masharani¹, Joseph Becker

¹Division of Endocrinology and Metabolism, Department of Medicine, University of California-San Francisco, 400 Parnassus Avenue, San Francisco, CA 94143, USA. umeshm@medicine.ucsf.edu

Expert Opinion on Biological Therapy

|January 26, 2010

Summary

Teplizumab, an anti-CD3 antibody, slowed beta-cell function loss in new-onset type 1 diabetes (T1D). This immunological intervention improved glycemic control and reduced insulin needs in patients with T1D.

Related Experiment Videos

Last Updated: Jun 16, 2026

High-Efficiency Generation of Antigen-Specific Primary Mouse Cytotoxic T Cells for Functional Testing in an Autoimmune Diabetes Model

High-Efficiency Generation of Antigen-Specific Primary Mouse Cytotoxic T Cells for Functional Testing in an Autoimmune Diabetes Model

Published on: August 16, 2019

Area of Science:

Immunology
Endocrinology
Autoimmune Diseases

Background:

Type 1 diabetes mellitus (T1D) is an autoimmune condition characterized by T-cell mediated destruction of pancreatic beta cells.
Current T1D treatments focus on managing glucose levels, highlighting the need for interventions that preserve beta-cell function.

Purpose of the Study:

To review preclinical and clinical research on teplizumab and anti-CD3 antibodies for preserving beta-cell function in new-onset T1D.
To examine the mechanism of action of teplizumab based on animal and human studies.

Main Methods:

Systematic review of research published between 1992 and 2009.
Analysis of data from animal models and human clinical trials involving teplizumab.

Main Results:

Phase I/II trials demonstrated that teplizumab slowed the rate of beta-cell function loss over two years in new-onset T1D patients.
Teplizumab treatment led to improved glycemic control and reduced insulin requirements.
Reported adverse events were mild and transient.

Conclusions:

Teplizumab shows promise in inducing disease-specific tolerance and preserving beta-cell function in T1D.
Further Phase III trials are ongoing to validate these findings and explore optimal dosing strategies.